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["Relation","Type","Sentence","MedLine Reference","Connectivity","# of References","Owner","Effect"]
["TGFB1 --+> TGFBR2","Expression","These data indicate that TGFB1-insensitivity in LbetaT2 cells results from a deficiency in Tgfbr2 expression., Expression of the transforming growth factor-beta type II receptor (TGF-beta RII) is highly regulated and is a critical determinant of the cellular response to TGF-beta., Dysregulated TGF-beta signalling may result from mutations in TGFBR1 and TGFBR2 genes, thus resulting in degenerative changes in the vessel wall., TGF-beta1 treatment increased the expression of TGF-beta1, TbetaR-I and TbetaR-II in mesenchymal cells in the cambium layer at 7 days in culture. <more data available...>","16384533:13, 11179682:0, 18550062:2, 12038632:8, 10861501:5, 9167190:2, 9516449:3, 11290556:6, 12198207:11, 19088080:4 <more data available...>",2,24,null,"positive"]
["TGFB1 --+> HSPB1","Expression","Retinoic acid enhanced the TGF-beta-induced increase of mRNA for HSP27., The TGF-beta-stimulated increase in the level of mRNA for HSP27 was also attenuated by T(3)., The TGF-beta1-induced down-regulation of LEDGF, Hsp27, and alphaB-crystallin promoters activity was reversed by cotransfection with a plasmid expressing LEDGF., SP600125, a specific inhibitor of stress-activated protein kinase /c-Jun N-terminal kinase (JNK), markedly reduced the HSP27 expression induced by TGF-beta., TGF-ß1 incubation resulted in increased expression of HSP-27 and decreased expression of HSP-72. <more data available...>","11909638:7, 12706291:3, 12649267:8, 18407296:5, 18577533:1198, 18596079:1181, 16055503:1191",2,7,null,"positive"]
["TGFB1 --+> TGFBR1","Expression","Interestingly, TGF-beta1 differentially stimulated or inhibited the expression of TbetaR-I and TbetaR-II mRNA in the gliomas., Dysregulated TGF-beta signalling may result from mutations in TGFBR1 and TGFBR2 genes, thus resulting in degenerative changes in the vessel wall., Furthermore, this truncated Smad4 functioned as a dominant negative form in TGF-beta1-mediated reporter activity and TGF-beta1 receptor expression., TGF-beta1 treatment increased the expression of TGF-beta1, TbetaR-I and TbetaR-II in mesenchymal cells in the cambium layer at 7 days in culture. <more data available...>","10048979:3, 18550062:2, 12860278:5, 12038632:8, 10861501:5, 9516449:3, 12198207:11, 19091788:9, 19038005:5, 15546867:6 <more data available...>",2,30,null,"positive"]
["TGFB1 --+> MET","Expression","In contrast, a combination of IL-6 and TGFbeta1 down-regulated c-met expression as well as Sp1 DNA binding activity., Real-time RT-PCR and Northern and Western blot analyses revealed that TGF-beta1 significantly induced c-met expression in HKC cells, which primarily took place at the gene transcriptional level., With respect to gene expression, fibrotic genes like transforming growth factor-beta (TGF-beta) and collagen Ialpha (Col-1alpha) were down-regulated by pirfenidone and increased expression of regenerative genes like hepatocyte growth factor (HGF) and c-met . <more data available...>","11469916:13, 15339794:3, 18652820:6, 15770602:6",2,4,null,"positive"]
["TGFB1 --+> A2M","Expression","It was blocked when bovine adrenocortical cells were exposed to 5,6-dichlorobenzimidazole riboside, a potent inhibitor of RNA polymerase II, suggesting that TGF-beta 1 acts as an activator of alpha 2-M gene expression at the transcriptional level., This is supported by the following observations: (i) Treatment of adrenocortical cells by FGF-2 resulted in a time-dependent and dose-dependent increase of alpha 2M synthesis, (ii) FGF-2 did not modify alpha 2M secretion rate; (iii) The induction of alpha 2M synthesis by FGF-2 was not observed in the presence of the transcription inhibitor DRB; (iv) The amount of alpha 2M mRNA was increased by 2 to 3 fold under either FGF-2 or TGF beta 1 treatment; (v) Optimal doses of TGF beta and FGF-2 synergistically increased alpha 2M synthesis. <more data available...>","1689294:5, 7524573:1, 9570034:1745, 15618353:1348",2,4,null,"positive"]
["TGFB1 --+> INPP5D","Expression","Activin/TGF-beta-induced expression of SHIP results in intracellular changes in the pool of phospholipids, as well as in inhibition of both Akt/PKB (protein kinase B) phosphorylation and cell survival., TGF-beta1 treatment does not increase IRAK-M or SHIP1 protein expression in shSMAD4 THP-1 cells, whereas it does so in shLUC THP1 cells, indicating that TGF-beta1 regulates IRAK-M and SHIP1 expression through a SMAD4-dependent pathway., lipopolysaccharide also upregulates the secretion and activation of TGFß, which, in turn, activates the transcription of the negative regulator SHIP. <more data available...>","12447389:5, 20404275:8, 15308103:1213, 15604218:1211, 17947710:1361, 16636301:1257, 19139077:265, 19139077:274, 19542365:220, 15778380:183 <more data available...>",2,16,null,"positive"]
["TGFB1 --+> THBS2","Expression","Using this assay, we observed that thrombospondin-1 and CISP/thrombospondin-2 syntheses were respectively stimulated threefold and twofold by a 24-h treatment with 2 ng/ml TGF beta 1., Further, p38 MAPK mediated induction of collagen I and TSP-2 expression by TGF-beta1 was still achieved in the presence of dexamethasone, showing that dexamethasone does not block p38 while it delays Smad2 phosphorylation and antagonizes stimulation of a Smad3/Smad4 dependent TGF-beta reporter construct., Further, the observation that TGFß can stimulate TSP-1 and -2 expression in bovine adrenal tissue [58] provides evidence to support further studies regarding the potential role of TGFß in regulating Thrombospondin expression in bovine follicles.","7698241:4, 15905080:5, 15616224:1300",2,3,null,"positive"]
["TGFB1 --+> VIM","Expression","Furthermore, induction of vimentin expression by TGF-beta1 and hypoxia was evaluated in gastric cancer cells., Here, we suggest a mechanism to explain how TGFbeta1 contributes to the up-regulation of vimentin expression while blocking myogenesis., Western blotting analysis showed that TGF-beta1 decreased cytokeratin and increased vimentin levels, while DMSO decreased both cytokeratin and vimentin., TGF-beta/IL-1beta treatment induced epithelial to mesenchymal-like phenotype transition (EMT), changing cell morphology and expression of vimentin and E-cadherin. <more data available...>","20358301:4, 17270292:2, 10580588:7, 20671927:3, 19213777:6, 1879463:2, 19116990:5, 19659836:8, 11752026:1166, 16382155:1202 <more data available...>",2,35,null,"positive"]
["LGALS3 --+> CCND1","Expression","Recombinant galectin-3 induced cardiac fibroblast proliferation, collagen production, and cyclin D1 expression., Interestingly, galectin-3 induces cyclin D1 expression (an early G1 cyclin) and its associated kinase activity in the absence of cell anchorage., We found that galectin-3 induces cyclin D(1) promoter activity in human breast epithelial cells independent of cell adhesion through multiple cis-elements, including the SP1 and CRE sites., Finally, we demonstrated that silencing of galectin-3 enhanced apoptosis induction with chemotherapeutic agents by further reducing the expression of anti-apoptotic and/or cell survival molecules such as survivin, cyclin D1, and XIAP, and increasing the expression of pro-apoptotic XAF-1. <more data available...>","15520318:6, 10463621:6, 12439750:3, 19843071:10, 17403142:1279, 11062152:1156, 11724777:1188, 19190323:249, 15867344:44",2,9,null,"positive"]
["TLR3 --+> CXCL10","Expression","Both TLR3 and RIG-I are required for CXCL10 expression., We established that stimulation of TLR3-positive cell lines and primary human endometrial epithelial cells with dsRNA leads to TLR3-dependent expression of interleukin -6, IL-8, interferon -inducible protein 10, RANTES, and IFN-beta., Furthermore, IRF-3 is thought to be required for Toll-like receptor3-induced type I IFN and IP-10 production., In addition to IFNß, activation of the TLR3/4 pathway also leads to the production of other mediators such as IP-10 and RANTES. <more data available...>","18258184:5, 15935884:5, 17660379:1240, 14580333:1257, 15315972:1197, 12453406:1108, 17785432:1346, 17170125:1102, 17332880:1148, 18188453:1255 <more data available...>",2,15,null,"positive"]
["CEBPD --+> CEBPA","Expression","Previous investigations indicated that transcription of the C/EBPalpha gene is sequentially activated during differentiation, initially by C/EBPbeta and C/EBPdelta and later by C/EBPalpha (autoactivation)., Nuclear expression of the 36-kilodalton C/EBP delta protein increases immediately after birth, followed first by increases in the 38-kilodalton C/EBP beta protein expression and then by increases in the 42-kilodalton C/EBP alpha protein expression., These data demonstrate that Myc specifically inhibits the terminal stages of the adipogenic program and suggest that Myc may act by blocking C/EBPbeta- and C/EBPdelta-directed activation of C/EBPalpha and PPARgamma2 expression, although the precise molecular mechanism is not understood. <more data available...>","10373535:1, 7910803:4, 10623469:4, 18703634:1194, 18930917:1043, 18653467:1203, 12138207:1046, 12186946:1140, 16154099:1059, 17273556:1253 <more data available...>",2,43,null,"positive"]
["STAT3 --+> CEBPA","Expression","Gene expression profile and quantitative PCR analysis of G-CSF-stimulated cell lines revealed that the expression of C/EBPalpha was up-regulated by the activation of Stat3., Treatment of freshly isolated adult rat hepatocytes with 10-100 mM ethanol rapidly (< 3 min) inhibits interleukin-6 (IL-6)-induced STAT3 activation, tyrosine and serine phosphorylation and IL-6-induced CCAAT enhancer binding protein (C/EBP) alpha and beta mRNA expression., One is that activated Stat3 binds to the promoter region of C/EBPa and induces the transcription of C/EBPa. <more data available...>","15664994:3, 10486586:2, 15664994:261, 15664994:66, 15664994:47, 15664994:255, 15664994:266",2,7,null,"positive"]
["CD44 --+> MET","Expression","CD44 isoforms bearing heparin sulfate chains can bind to HGF/SF and facilitate its presentation to c-Met., A blocking antibody to CD44v6 decreased HGF-induced c-Met phosphorylation as well as enhanced random- and site-directed migration., In this paper, we demonstrate that the activation of c-Met induced by InlB is dependent on CD44v6, a member of the CD44 family of transmembrane glycoproteins., In several types of cells, the activation of the receptor tyrosine kinase c-Met by its ligand hepatocyte growth factor (HGF) requires the coreceptor CD44v6. <more data available...>","12670907:1, 20357818:6, 19432801:3, 17065554:0, 17923692:2, 12183053:4, 10485493:1212",2,7,null,"positive"]
["LGALS3 --+> TGFB1","Expression","Gal-3 increased transforming growth factor-ß1, -ß2, and -ß3 expression in left ventricle compared with vehicle group; Ac-SDKP inhibited this effect., Thus disruption of the Galectin-3gene blocks fibrosis despite similar expression levels of TGF-ß.","19098114:1203, 16549783:134",2,2,null,"positive"]
["TGFB1 --+> S100A4","Expression","TGF-beta1 increased S100A4 expression in cultured ileal fibroblasts., Furthermore, TGFbeta1 up-regulated epithelial markers CTNNB1 and CTNND1, but suppressed mesenchymal markers, such as S100A4, FGF1 and FGF2., Consistent with these observations, S100A4 increases cell invasion ability induced by TGF-beta in MCF10CA1a.cl1 cells, and depletion of the protein in MDA-MB-231 cells inhibits it., In vitro experiments using human dermal microvascular endothelial cells demonstrated that TGF-beta1 induced myofibroblastic features in human dermal microvascular endothelial cells, including spindle cell morphology, reduction of CD34 expression, and induction of S100A4, alpha-smooth muscle actin, and COL1A1 expression, as well as the increased nuclear expression of phospho-Smad2. <more data available...>","20489045:10, 20592463:9, 20070253:8, 19608867:2, 17974953:1193, 12163453:1072, 16889607:1246, 14747385:1161, 19487818:1150, 17562716:291 <more data available...>",2,11,null,"positive"]
["CTSD --+> ABCA1","Expression","Conversely, expression of CTSD increased both ABCA1 mRNA expression and cellular ABCA1 protein.","17032648:6",2,1,null,"positive"]
["TGFB1 --+> CYBB","Expression","Transfection of wild-type mouse cardiac fibroblasts with AAV/TGFbeta (ACT)(1) markedly enhanced the expression of NADPH oxidases (p22(phox), p47(phox), and gp91(phox) subunits) and LOX-1, formation of reactive oxygen species, and collagen synthesis, concomitant with an increase in the activation of p38 and p44/42 mitogen-activated protein kinases ., TGF-ß1 upregulates the expression of p22phox, p47phox, p67phox, and gp91phox in rat mesangial cells (Figure 2B) and p22phox mRNA in tubular epithelial cells (Figure 2C), suggesting that TGF-ß1-induced reactive oxygen species may be NADPH oxidase dependent. <more data available...>","18182394:3, 12874439:1080, 12482831:1145",2,3,null,"positive"]
["CCND1 --+> HSPB8","Expression","The transient transfection with cyclin D1 increased HSPB8 levels ~2-fold when these blots were quantified in image analysis; the HSPB8 knockdown was ~8-fold in each case.","18006821:1234",2,1,null,"positive"]
["STAT1 --+> MCL1","Expression","Further, mutation of STAT1/STAT2 prevented the effect of both Abeta and SGK1 on Mcl-1 expression.","19609277:10",2,1,null,"positive"]
["TGFB1 --+> ITGB5","Expression","Thus, TGF-beta increases expression of the integrin beta(5) gene by mechanisms involving Sp1/Sp3 and Smad transcription factors., We investigated the effects of PPARalpha ligands on TGF-beta-induced beta3 and beta5 integrin expression and potential interaction between PPARalpha and TGF-beta signaling., In that scenario, however, Peroxisome proliferator-activated receptor-a activation antagonized transforming growth factor-ß-induced ß5-integrin transcription in vascular smooth muscle cells., Agonists of peroxisome proliferator-activated receptor-a inhibit TGFß-responsive ß5 integrin expression and disrupt formation of the Sp1-Smad4 complex, in parallel with induction of peroxisome proliferator-activated receptor-a/Smad4 interaction (43). <more data available...>","10964912:9, 12456495:3, 17098824:1241, 16249187:1329, 14684628:1206, 12130649:44",2,6,null,"positive"]
["CSF1 --+> NFATC1","Expression","Furthermore, anti-CD11b antibodies inhibited NFATc1 expression induced by M-CSF and RANKL in BMMs., S3 shows the normal osteoclast differentiation and expression of NFATc1 in NFATc2-/- monocyte/macrophage precursor cells that were stimulated with RANKL/M-CSF., Inhibition of c-Fos and NFATc1 expression induced by RANKL and M-CSF in RAGE-deficient prefusion osteoclasts To further understand how RAGE regulates osteoclast maturation and function, we examined expression of transcriptional factors essential for osteoclastogenesis, including c-Fos and NFATc1 (39, 40). <more data available...>","18775427:4, 16275763:1202, 16606672:1165, 17403683:264",2,4,null,"positive"]
["TGFB1 --+> CSF1","Expression","Anti-TGF-beta 1 decreased (p < 0.05) M-CSF induced colonies in 5/6 donors., Transforming growth factor beta (TGF-beta) increased both the synthesis of CSF-1 and its accumulation in the matrix., The M-CSF activity in the conditioned medium of mouse osteoblast-like MC3T3-E1 cells was increased by TGF-beta as well as interleukin-1 treatment., Here we show that TGF-beta1 induces the expression of macrophage-CSF (M-CSF) in vascular endothelial cells via a signaling pathway(s) involving hydrogen peroxide (H2O2)., Other agents, including PTH (35), tumor necrosis factor-alpha (36), and transforming growth factor-beta (37), have been shown to increase MCSF expression at the level of gene transcription. <more data available...>","7804125:8, 8591991:10, 8048485:1, 9278333:1, 9492032:1246, 16707491:363, 17332318:77",2,7,null,"positive"]
["TGFB1 --+> RBP1","Expression","In both cell populations, transforming growth factor-beta 1 treatment increased CRBP-1 expression., We also demonstrate that CRBP-1 expression by fibroblasts is regulated in vitro by retinoic acid and transforming growth factor-beta1., The expression of CRBP-1 is regulated at the transcriptional level by TGF-beta and retinoic acid but not synergistically, suggesting a possible common pathway., TGF-ß1 should be capable of diffusing through the microporous membrane, subsequently modulating CRBP-1 transcription.","12004002:12, 9403724:10, 11319755:4, 12419830:1201",2,4,null,"positive"]
["NCF1 --+> TLR2","Expression","Small inhibitory RNA to p47Phox in THP-1 cells abrogated high-glucose-induced TLR2 and TLR4 expression.","18650365:10",2,1,null,"positive"]
["CD44 --+> TGFB1","Expression","CD44 costimulation increased production of IL-10 in a partially IL-2-dependent manner and also promoted cell surface TGF-beta expression., Mechanistically, we demonstrate that CD44WT cells generated more active TGFbeta than CD44KO cells and that CD44 promotes the activation of TGFbeta via an MMP-dependent mechanism., We previously demonstrated in renal proximal tubular cells that the engagement of the extracellular polysaccharide hyaluronan with its receptor CD44 attenuated TGF-beta1 signaling., Gelatine zymography and immunofluorescent stain evidenced that elevated MMP-2 and MMP-9 activity and serum-dependent CD44 expression and its membranous localization may contribute to TGF-beta1 activation. <more data available...>","19635906:4, 18397995:3, 15084590:1, 19457680:7, 15574511:12, 15387373:2",2,6,null,"positive"]
["CD74 --+> CCND1","Expression","CD74 up-regulates expression of cyclin D and cyclin E in HEK293 cells (Fig. 5C)., Our studies document that inhibition of the MIF and/or CD74 decreases cyclin D1 gene expression.","18941249:1274, 17142775:1398",2,2,null,"positive"]
["CEBPA --+> CSF1","Expression","For example, when expressed alone, RUNX1, C/EBPa, and PU.1 are poor activators of the M-CSF promoter.","15988004:1056",2,1,null,"positive"]
["CSF1 --+> CEBPA","Expression","Ectopic expression of THOC5 mimicked M-CSF mediated cell maturation and enhanced protein expression of the myeloid transcription factors C/EBPbeta, C/EBPalpha, Pu-1 and also GAB2 (a PI-3 Kinase and macrophage development regulator)., M-CSF and G-CSF use separate pathways to activate ERK and modify C/EBPa .","19015024:4, 19587381:1161",2,2,null,"positive"]
["CD14 --+> CD86","Expression","In contrast, immature dendritic cells cultured in G4 plus human pancreatic RNase or eosinophil-derived neurotoxin for 48 h, although still CD14-, up-regulated the surface expression of CD83, CD86, and HLA-DR, indicating that human pancreatic RNase and eosinophil-derived neurotoxin treatment induced phenotypic maturation of DCs (Fig. 7A).","15528350:1252",2,1,null,"positive"]
["TGFB1 --+> SOX9","Expression","Moreover, exogenous TGF-beta can induce Sox9 expression in the mandibular arch., In addition, up-regulation of Fibronectin and suppression of Sox9 expression by TGF-beta1 was also found to be mediated by CTGF., Transforming growth factor-beta treatment increased MAPK activity and Sox-9, aggrecan, and collagen type II gene expression., TGF-beta1 increased the Sox9 messenger ribonucleic acid expression to 180% compared to control group in intervertebral disc tissue., TGF-beta1-stimulated gene expression of chondrogenic regulators, Sox9, Runx2 and Ihh, was also affected by activity of PD98059 and SB203580, to different degrees. <more data available...>","18684439:6, 17111364:7, 15564911:11, 20157375:7, 20590658:6, 18496879:5, 16575901:3, 17525254:5, 18602912:6, 19321054:8 <more data available...>",2,15,null,"positive"]
["TGFB1 --+> NCF1","Expression","In addition, LPS-induced ERK phosphorylation and subsequent Ser345 phosphorylation on p47phox were significantly inhibited by TGF-beta1 pretreatment., TGF-beta1 at 10 ng/mL significantly increased the intercellular reactive oxidative species production and p47phox expression (P < 0.05)., Transfection of wild-type mouse cardiac fibroblasts with AAV/TGFbeta (ACT)(1) markedly enhanced the expression of NADPH oxidases (p22(phox), p47(phox), and gp91(phox) subunits) and LOX-1, formation of reactive oxygen species, and collagen synthesis, concomitant with an increase in the activation of p38 and p44/42 mitogen-activated protein kinases . <more data available...>","18566433:6, 19292057:5, 18182394:3, 12874439:1080",2,4,null,"positive"]
["TGFB1 --+> TGM2","Expression","In Western blot analysis, TGF-beta1 (1 ng/ml) treatment was found to steadily up-regulate TGase 2 expression for up to 7 days., Transforming growth factor-beta and interleukin -1beta induced Factor XIIIa and tTGase expression in cartilage and meniscal organ cultures., This study suggests that in the isolated perfused rat kidney and in the absence of other exogenous growth factors, TGF-beta1 selectively increases the synthesis of extracellular matrix and tissue transglutaminase without changes that would result in the reduction of extracellular matrix degradation. <more data available...>","16044258:3, 11438463:3, 10505687:11, 17460246:6, 12874459:1070, 14555988:1123, 11686302:1246, 9582307:46, 9114053:189, 11689553:280 <more data available...>",2,18,null,"positive"]
["TGM2 --+> TGFB1","Expression","In addition, TG2 also activates transforming growth factor-beta (TGF-beta)., Particularly relevant is the finding that both TGF-beta and IL-12 regulations were significantly altered in the absence of TG2., Free Gd3+ ions may also activate tissue transglutaminase, which in turn activates transforming growth factor beta (TGF-beta) produced by dendritic cells., Increased TG2 expression in these fibroblasts led to NF-kappaB activation, resulting in the increased expression of transforming growth factor beta(1). <more data available...>","18688035:2, 15905580:8, 19886227:11, 19657147:2, 18558621:6, 12810961:2, 18523305:1259, 15199098:1330, 11686302:1320",2,9,null,"positive"]
["TGFB1 --+> NFATC1","Expression","Similarly, TNF-alpha activates osteoclastogenesis by stimulating translocation of TGF-beta-induced NFATc1., Addition of Transforming growth factor-ß during differentiation to either lineage inhibited NFATc activation., Using quantitative real-time PCR, we found that transforming growth factor-ß1 treatment results in a 4.5-fold increase in NFATc1 transcript levels in neural crest stem cells (Fig. 6).","18060870:6, 12810687:1296, 15148306:1175",2,3,null,"positive"]
["CD14 --+> CD83","Expression","In contrast, immature dendritic cells cultured in G4 plus human pancreatic RNase or eosinophil-derived neurotoxin for 48 h, although still CD14-, up-regulated the surface expression of CD83, CD86, and HLA-DR, indicating that human pancreatic RNase and eosinophil-derived neurotoxin treatment induced phenotypic maturation of DCs (Fig. 7A).","15528350:1252",2,1,null,"positive"]
["TGFB1 --+> CD14","Expression","At 2 hr, 50 ng/ml TGF-beta 1 significantly lowered CD14 expression (51%, P = 0.043)., TGF-beta and VD3 synergistically increased the expression of differentiation-associated markers such as the CD11b and CD14 antigens, whereas TGF-beta and dexamethasone did not., Furthermore, TGF-beta/D3 treatment (but not D3 alone) elicits the expression of membrane CD14, FcRI, FcRII, CD11a, CD11b, CD11c, ICAM-1, and PECAM-1 Ag at a level comparable to that observed on normal human monocytes., The same CCAAT/enhancer-binding protein site was also involved in the TGF-ß/Vit D3-dependent activation of CD14 expression (42). <more data available...>","7526045:5, 10547074:1, 8383719:5, 11698458:1270, 12821938:1143, 18497880:1254",2,6,null,"positive"]
["CD86 --+> TGFB1","Expression","Blockage of costimulatory signal CD(86) at early pregnancy can treat uncertain recurrent spontaneous abortion by stimulating the expression of TGF-beta(1), MMP-9 and PAI-1 and reducing the embryo resorption rate., Activation of T cells with PMA and ionomycin together with CTLA4-CD80/CD86 blockade results in decreased induction of CD25 and Bcl-X(L), reduced interleukin -2, and enhanced transforming growth factor-beta (TGF-beta) production., However, whether and how these B7-1 (CD80), B7-2 (CD86), and/or B7x ((3), (5), (15), (36)) molecules contribute to TGF-ß production by engaging CTLA-4 signaling remain to be determined. <more data available...>","17697576:14, 12429713:5, 9815262:1210, 10619862:1300",2,4,null,"positive"]
["TGFB1 --+> FCGR2B","Expression","Furthermore, TGF-beta/D3 treatment (but not D3 alone) elicits the expression of membrane CD14, FcRI, FcRII, CD11a, CD11b, CD11c, ICAM-1, and PECAM-1 Ag at a level comparable to that observed on normal human monocytes., IFN-a, IFN-?, TGF-ß, IL-10, and soluble IgG modulated CD32a and/or CD32b on circulating conventional DCs, which was similar to their effects on cytokine-induced monocyte-derived DCs.","8383719:5, 16167082:1141",2,2,null,"positive"]
["CD83 --+> CD86","Expression","However, the increase in surface expression of HLA-DR and CD86 after addition of LPS was significantly attenuated in cord DCs, with CD25 and CD83 expression also markedly reduced., Specifically, IRX-2-treated DC increased expression of CD83 and CCR7, markers for DC maturation and migration, respectively, and increased the expression of HLA-DR, CD54, and the costimulatory molecules CD86 and CD40, which are critical mediators of T cell activation., Correlating with CD83 expression, the basic as well as the lipopolysaccharide induced expression of the activation markers CD86 and MHC-II are significantly increased in CD83transgenic B cells and reciprocally decreased in CD83 mutant B cells. <more data available...>","11982599:2, 17667526:4, 17710154:3, 17056542:1160, 17878352:1075",2,5,null,"positive"]
["TGFB1 --+> GFAP","Expression","Cycloheximide did not block the effects of TGF-beta1 or FGF-2 on GFAP mRNA levels, but blocked the inhibitory effects of FGF-2 on the TGF-beta1-mediated increase in GFAP expression., Whereas untreated control cells expressed progressively the glial fibrillary acidic protein (GFAP) after arrest of multiplication, the addition of TGF beta 1 to proliferative cells prevented GFAP expression and accumulation of its mRNA., TGF-beta induced CysC and GFAP expression in AP-16 cells, an astrocyte progenitor-like cell line expressing GLAST (a glutamate transporter subtype specifically expressed in immature astrocytes). <more data available...>","9537840:5, 1397085:4, 15509901:2, 8170537:2, 8361632:2, 18419760:10, 19057972:3, 12118088:4, 10098836:1048, 11867550:1092 <more data available...>",2,14,null,"positive"]
["TGFB1 --+> ABCA1","Expression","TGF-beta1 significantly increased expressions of ABCA1, ABCG1 and SR-BI at both transcriptional and translational levels in a dose-dependent and time-dependent manner., transforming growth factor-ß increases ABC-1 expression and inhibits its down-regulation by interferon-?., TGF-ß1 also reduced foam cell formation by enhancing cholesterol efflux through increasing mRNA expression of ABCA1 and ABCG1., TGF-beta increases cholesterol efflux and ABC-1 expression in macrophage-derived foam cells: opposing the effects of IFN-gamma. <more data available...>","20057170:4, 11352993:1189, 11742878:1055, 15995168:2634, 20485864:4",2,5,null,"positive"]
["TGFB1 --+> CLU","Expression","At the same time, TGFbeta1 enhanced clusterin protein and mRNA expression., A single T to G base mutation in the AP-1 site (5'-TGAGGCA) abolishes TGFbeta-induced clusterin promoter transactivation., We hypothesize that activation of the TGF-beta signaling pathway, which often occurs after ionizing radiation exposure, can in turn activate the CLU promoter., Cytokines such as TGF beta 1 and interleukin 1 enhance the expression of clusterin, which may link clusterin to inflammatory mechanisms in Alzheimer disease. <more data available...>","10066375:3, 9334243:5, 15530543:10, 8892344:4, 9407436:5, 7730444:8, 8170537:2, 10406964:1149, 15671065:1426, 9334243:219 <more data available...>",2,33,null,"positive"]
["TGFB1 --+> SOCS3","Expression","TGF-beta inhibits IL-6-induced SOCS3 promoter activity in T cells., These data show that TGF-beta coordinately induces LIF and SOCS3 to promote prosurvival signaling., Furthermore, TGF-beta rapidly induces sustained SOCS-3 expression in macrophage/osteoclast precursors., In this study, we demonstrate that LPS-induced endogenous TGF-beta1 contributes to the inducible SOCS3 expression in macrophages., This suggests that TGF-beta-induced expression of SOCS3 may represent a crucial mechanism by which TGF-beta antagonizes specific anti-osteoclastic JAK/STAT signals, priming precursors for resorption rather than inflammatory functions. <more data available...>","19535626:4, 20181800:8, 12646633:7, 17920684:3, 13679037:8, 18031698:1059",2,6,null,"positive"]
["STAT1 --+> B2M","Expression","The same authors also show that transcription of the ß2-microglobulin gene is down-regulated in mouse Stat1-null T lymphocytes., A direct target of EOMES, IL2RB (CD122) (29), is also 7.4-fold up-regulated. ß-2 microglobulin , which is up-regulated by STAT1 and is part of MHC I, is fivefold up-regulated in L&H cells.","10921891:1271, 18794340:1113",2,2,null,"positive"]
["STAT3 --+> OSMR","Expression","STAT3 activation further enhances OSMR expression, thereby establishing a positive-feedback loop., We found that Stat3flx/flx/NIC tumors expressed lower levels of both cebpd and osmr, two genes that are induced by Stat3 (28, 29)., We show that OSMR expression is dependent on LIF-induced STAT3 and that the subsequent OSMR-mediated signal inhibits the phosphorylation of STAT5 and coordinately activates signal transducer and activator of transcription3-dependent apoptosis in the involuting mammary gland.","20348953:1139, 19690134:1181, 18927239:1084",2,3,null,"positive"]
["CSF1 --+> CCND1","Expression","Previously we showed that the macrophage-activating agent lipopolysaccharide blocks CSF-1-induced proliferation and cyclin D1 expression in macrophages., We further demonstrated that Cdc42 modulated M-CSF-stimulated cyclin D expression and phosphorylation of Rb and induced caspase 3 and Bim, thus contributing to osteoclast proliferation and apoptosis rates., In contrast to some other growth factor/cell systems, no evidence was obtained using the inhibitors for the involvement of PI3-kinase or p70s6k in CSF-1-mediated induction of c-fos mRNA expression or Erk-1 activity; in addition, no evidence was found for an involvement in the CSF-1-mediated increase in cyclin D1 expression or STAT activation. <more data available...>","9722538:2, 20501942:5, 9608681:6, 10602507:1124, 1483347:100, 9139801:1201, 10453356:1406, 17142780:1172, 11230342:1041, 9722538:50 <more data available...>",2,19,null,"positive"]
["NFE2L2 --+> FTL","Expression","The induction of GSTP1/2, GSTA4, and ferritin light chain mRNAs by butylated hydroxyanisole was decreased in the nrf2-null mouse liver, while the level of TXNRD1 was not changed much.","16135796:1104",2,1,null,"positive"]
["CD151 --+> CD9","Expression","Interestingly, cell surface expression of CD9 was significantly reduced on isolated CD151-null keratinocytes compared to wild-type cells when examined by quantitative immunofluorescence and flow cytometry (Fig. 5), possibly reflecting the requirement for CD151 for CD9 incorporation into these integrin complexes (40).","15199151:1325",2,1,null,"positive"]
["CD14 --+> ITGAX","Expression","Treatment of U937 cells with PMA markedly increased CD14, CD11a, CD11b and CD18 antigen expression, and slightly increased CD11c expression., In particular, those for CD11c and tumor necrosis factor a (TNFa) were markedly increased, and there were lesser, but significant, increases in Spp1, CD14, CD45, CCL9, Toll-like receptor 4 (TLR4), and interleukin-1B (IL-1ß) (Fig. 6G,H).","1689274:1, 18160655:1251",2,2,null,"positive"]
["RAPGEF3 --+> SOCS3","Expression","Conversely, down-regulation of protein kinase C activity with chemical inhibitors or small interfering RNA-mediated depletion of PKCalpha or -delta blocks EPAC-dependent SOCS-3 induction., Firstly, selective activation of EPAC in human umbilical vein endothelial cells increased C/EBP DNA binding activity and recruitment of C/EBPbeta to the SOCS-3 promoter., To determine whether the increase in SOCS-3 expression induced by Epac was functionally relevant, we also tested the ability of 8-pCPT to inhibit \"signal transducers and activators of transcription\" phosphorylation by sIL-6Ra/IL-6. <more data available...>","19423709:4, 18195020:4, 16914720:1228, 18195020:203, 19423709:274, 18195020:257, 18195020:233, 19423709:122, 19423709:290, 19423709:34 <more data available...>",2,19,null,"positive"]
["IRF8 --+> CSF1","Expression","Additionally, ICSBP expression in ICSBP-deficient cells rescues neurofibromin 1 expression, decreases ERK activation, and abolishes GM-CSF and M-CSF hypersensitivity (34).","16914719:1257",2,1,null,"positive"]
["STAT1 --+> ISG15","Expression","A single mutation (K161A) in the p48 contact region of Stat1 inhibited the Stat1-p48 interaction as well as the IFN-a-triggered ISG15 gene induction, whereas this mutation had no effect on either the Stat1-Stat2 interaction or the IFN-? response which is independent of p48 (Horvath et al., 1996).","10851063:1089",2,1,null,"positive"]
["STAT1 --+> CYBB","Expression","At the same time, STAT1 and IRF-1 together promote the interferon-?-induced transcription of the CYBB gene (26).","16162660:1069",2,1,null,"positive"]
["CSF1 --+> CD14","Expression","It has been demonstrated that the expression of CD16 and CD14 is regulated by macrophage colony stimulating factor (M-CSF) and GM-CSF., M-CSF was also shown by flowcytometric analysis to influence the expression of CD14, a receptor for LPS, which might render monocytes more sensitive to LPS., Daily administration of macrophage colony stimulating factor (M-CSF) to the mice resulted in increased levels of MSR-A expression and reduced levels of CD14 as well as several cytokine expressions, leading to shortening of the inflammatory process. <more data available...>","12153694:6, 8877404:9, 10594845:5, 9566797:4, 15256426:1265",2,5,null,"positive"]
["STAT3 --+> FLI1","Expression","A recent study showed that an enhanceosome responsible for activating SCL transcription was required for GATA-2, Fli-1, and Elf-1.37 As the expression of Fli-1 was induced via the STAT3 transcription factor,38 phosphorylation of STAT3 by the binding of HGF to c-met39 might activate Fli-1 or Elf-1.","14701703:1187",2,1,null,"positive"]
["STAT3 --+> CD9","Expression","Furthermore, activation of STAT3 induced the expression of CD9, indicating the LIF/STAT3 pathway is critical for maintaining CD9 expression., In a previous study, the addition of leukemia inhibitory factor or STAT3 activation induced CD9 expression in embryonic stem cells [13], which indicates that the leukemia inhibitory factor/STAT3 pathway is critical for maintaining CD9 expression.","11950938:5, 12954725:1222",2,2,null,"positive"]
["AQP4 --+> SLC14A1","Expression","In aging brain, UT-B1 abundance was increased twofold together with a fourfold increase in aquaporin-4 abundance.","12933359:8",2,1,null,"positive"]
["STAT3 --+> HPGD","Expression","Activation of signal transducer and activator of transcription3 may augment potently the androgen bound receptor signaling and contribute to synergistic induction of 15-PGDH expression by combined treatments with IL-6 and dihydrotestosterone.","14749354:1215",2,1,null,"positive"]
["SLC14A1 --+> GFAP","Expression","The abundance of GFAP, the usual marker of astrocytes and ependymal cells, was increased by 25% with age (data not shown), a variation much smaller than the doubling in UT-B1 or the fourfold increase in AQP-4.","12933359:1196",2,1,null,"positive"]
["AQP4 --+> GFAP","Expression","Likewise, AQP4 deficiency significantly downregulated expression of glial fibrillary acidic protein in perivascular processes of astrocytes., The abundance of GFAP, the usual marker of astrocytes and ependymal cells, was increased by 25% with age (data not shown), a variation much smaller than the doubling in UT-B1 or the fourfold increase in AQP-4.","18281883:2, 12933359:1196",2,2,null,"positive"]
["HLA-B --+> HLA-E","Expression","The only exceptions were HLA-B*1302 and HLA-B*2705, which induced a low level of HLA-E surface expression despite having the inappropriate sequence (Table 1); this is being fully investigated.","9427624:1189",2,1,null,"positive"]
["ITGB2 --+> TLR2","Expression","The anti-CD18 monoclonal antibody markedly reduced TLR2 expression in endothelial cells as induced by polymorphonuclear neutrophils.","14561708:1314",2,1,null,"positive"]
["TLR2 --+> ITGB2","Expression","Peptidoglycan (TLR2 ligand), flagellin (TLR5 ligand), and Imiquimod R837 (TLR7 ligand) could significantly upregulate cell surface expression of intercellular adhesion molecule (ICAM)-1 and CD18, and induce the release of IL-1beta, IL-6, IL-8, growth-related oncogene -alpha, and superoxides of eosinophils.","17332440:5",2,1,null,"positive"]
["TLR3 --+> TGFB1","Expression","Finally, the role of cytokines is difficult to associate with a given Toll-like receptor since Toll-like receptor-induced cytokine production, which was consistently observed, varied with each agonist: one should note however that TLR2, TLR3 and TLR7 agonists preferentially stimulated IL-10 and transforming growth factor-ß production which was not the case for the TLR4 agonist lipopolysaccharide.","20628601:1409",2,1,null,"positive"]
["NFE2L2 --+> SLCO2B1","Expression","As shown in Fig. 4, expression of Oatp2b1 was decreased by PXR and PPARa ligands, and increased by AhR and Nrf2 activators.","15919853:1172",2,1,null,"positive"]
["FLI1 --+> TGFBR2","Expression","Introduction of EWSR1-FLI1 into cells lacking the EWSR1-FLI1 fusion suppresses TGF-beta RII expression, whereas antisense to EWSR1-FLI1 in ES cell lines positive for this gene fusion restores TGF-beta RII expression., Regulation of the TGF-ß RII promoter by EWS-FLI1, FLI1, dnFLI1, EWS-ERG, ERG, dnERG, EWS-ETV1, ETV1, and dnETV1., The ERT (also called ESX/ESE-1) regulates the expression through the Z element (10) , whereas another ets family gene FLI1 fused with the EWSR1 gene down-regulates the Transforming growth factorßRII expression in Ewing sarcomas (11) .","10508522:7, 10749119:1136, 11719467:1050",2,3,null,"positive"]
["CD74 --+> CD86","Expression","In addition, overexpression of CD74 by mRNA electroporation in Dendritic cells increased the cell surface expression of CD80/CD86 and major histocompatibility complex class II.","18003616:1308",2,1,null,"positive"]
["PLEK --+> CCND1","Expression","The inability of the CKIP-1? pleckstrin homology mutant to promote either cyclin D1 or myogenin expression suggests that membrane association and probably phosphatidylinositol-3-phosphate binding are required for CKIP-1 action., Thus, our results suggest that proto-Dbl and Dbl homology/pleckstrin homology proteins may activate cyclin D1 through activation of JNK, which in turn may activate ATF-2 and Jun nuclear transcription factors to stimulate transcription from cyclin D1 promoter.","14729969:1317, 11907027:321",2,2,null,"positive"]
["STAT3 --+> CD14","Expression","STAT3 inhibitor pretreatment could also down-regulate high CD14 and CD16 expression by BxPC-3 conditioned medium treatment.","17545630:1248",2,1,null,"positive"]
["TGFB1 --+> GUSB","Expression","Beta-glucuronidase expression was increased by TGF-beta and decreased by IFN-gamma.","9712070:10",2,1,null,"positive"]
["NFATC1 --+> CCND1","Expression","Heit et al. showed that transgenic activation of NFATc1 in ß-cells induces proliferation by inducing Cyclin D and Cdk4 levels [23].","20689817:1266",2,1,null,"positive"]
["ANGPT1 --+> CCND1","Expression","angiopoietin1 up-regulated the expression of cyclin D1 in both of these cells.","16061664:5",2,1,null,"positive"]
["TGFB1 --+> MCL1","Expression","The increased levels of the cytokines, IL-4, IL-10, prostaglandin E2, and TGF-ß enhance the expressions of c-FLIP, Bcl-xL, and Mcl-1, which are involved in the resistance to apoptosis (32-34).","16740684:1107",2,1,null,"positive"]
["TGFB1 --+> AIF1","Expression","Furthermore, functional studies showed specific allograft inflammatory factor-1 isoform expression stimulation by transforming growth factor-beta., Stimulation of peripheral blood mononuclear cells with TGFbeta caused a specific and significant increase in the expression of AIF-1 isoform 2 transcripts (P < 0.005), which was due to stabilization of AIF-1 isoform 2 messenger RNA., Ten percent FCS, IFN-?, and interleukin-1ß are capable of inducing this protein, whereas AIF-1 is not expressed in unstimulated cells. basic fibroblast growth factor, platelet-derived growth factor, and transforming growth factor-ß can induce AIF-1 protein expression to a small degree.","17053503:3, 16868985:9, 10894811:1159",2,3,null,"positive"]
["LGALS1 --+> CD83","Expression","Furthermore, galectin-1 induced both CD83 and CD86 expression in a dose-dependent manner (Fig. 1D).","16785517:1209",2,1,null,"positive"]
["NFE2L2 --+> GFAP","Expression","Although the Nrf2 knockout mice lacked severe astrogliosis in more than 80% of cases, there was consistent neuronal damage, although it should be noted that we cannot rule out the possibility that the loss of Nrf2 may directly interfere with GFAP expression in astrocytes.","16945104:1253",2,1,null,"positive"]
["NFATC1 --+> ID3","Expression","Accordingly, we propose a model whereby early growth response1-NF-ATc1 cooperatively induces inhibitor of DNA binding 3 expression, which in turn promotes traversal of the ß-selection checkpoint by suppressing the activity of E proteins (54, 56, 68).","17878368:1298",2,1,null,"positive"]
["GFAP --+> VIM","Expression","As for GFAP, increased lesion-induced up-regulation of vimentin expression is also already apparent at 1 dpl, with knock-out animals showing higher expression than wild-type animals (Fig. 5b).","12843240:1209",2,1,null,"positive"]
["CEBPD --+> TF","Expression","In the non-transferrin-expressing HeLa cells, the transferrin promoter could be activated by C/EBP-delta., Suire et al. (12) showed, in cotransfection assays, that overexpression of C/EBP alpha (C/EBP) and C/EBP delta (NF-IL6beta, CRP3) in Sertoli cells stimulated transcription from the cAMP-regulated transferrin promoter containing a C/EBP binding site.","8226864:7, 9927313:1054",2,2,null,"positive"]
["TLR2 --+> CEBPD","Expression","TLR2 signaling by LpqH induced expression of liver inhibitory protein and C/EBPd and enhanced expression of LAP at time points that correlated kinetically with the onset of inhibition of IFN-?-induced CIITA expression., Toll-like receptor2 stimulation also induces C/EBPd expression and binding to the CIITA promoter [31].","17982082:1080, 19629181:349",2,2,null,"positive"]
["OAS1 --+> IRF9","Expression","Similar to expression of 2',5'-oligoadenylate synthetase, Mx, and IFN-stimulated gene17 [15, 17, 22], expression of Stat 1, Stat 2, IRF-9, and IRF-1 in the ovine endometrial S and glandular epithelium during early pregnancy was coordinate with temporal production of Interferon tau by the conceptus [2, 3].","11566724:1278",2,1,null,"positive"]
["PSMB9 --+> CCND1","Expression","Furthermore, analysis by real-time reverse transcription-PCR of the endogenous expression of cyclin D1 and pS2 indicated that the expression level of endogenous cyclin D1 and pS2 was also elevated with overexpression of LMP2 and decreased with LMP2 knockdown (Figure 2C).","16957778:1097",2,1,null,"positive"]
["CSF1 --+> CYBB","Expression","Consistent with this, we find that expression of gp91phox and p67phox protein is also increased by M-CSF differentiation in Western blots of cell lysate proteins (Fig. 1C)., Of interest to the current studies, HoxA9 overexpression in murine myeloid cells does not impair granulocyte-colony stimulating factor- or macrophage-colony stimulating factor-induced expression of gp91Phox, a phagocyte respiratory burst oxidase protein (4).","16210632:1196, 15681849:71",2,2,null,"positive"]
["CSF1 --+> TREM2","Expression","Addition of macrophage colony stimulating factor (M-CSF) to LN cell culture allowed the proliferation and expression of TREM2 in LN cells, and the addition of neutralizing anti-M-CSF antibodies suppressed the proliferation of LN cells despite the expression of TREM2., Whereas Humphery et al. recently reported that TREM-2 expression is induced during in vitro osteoclastogenesis induced by culture bone marrow-derived macrophages with macrophage CSF (MCSF) and the receptor activator of NF-?B ligand (4), we find that differentiation of macrophages in MCSF alone leads to expression of TREM-2. [Figure 3] View larger version (33K): [in this window] [in a new window] .","20345919:4, 16951310:1159",2,2,null,"positive"]
["STAT3 --+> SYNPO","Expression","Stat3-DN inhibited nef-containing vector-induced cyclin E expression and significantly increased synaptopodin expression (Figure 5C).","15343382:1157",2,1,null,"positive"]
["TGFB1 --+> SYNPO","Expression","Anti-TGF-ß antibody 2G7 blocked synaptopodin expression and inhibited the redistribution of zona occludens-1 (Figure 1D).","16207831:1114",2,1,null,"positive"]
["IRF8 --+> CTSC","Expression","Consistent with the Interferon regulatory factor-8-dependent induction of these genes, expression of cystatin C, cathepsin C, and prosaposin transcripts was lower in Irf-8-/- cells than that in wild-type cells (data not shown).","15947094:1145",2,1,null,"positive"]
["TGFB1 --+> PTGS1","Expression","Release of histamine, cysteinyl-leukotrienes, and tumour necrosis factor alpha was strongly reduced whereas prostaglandin D2 generation and cyclooxygenase 1 and 2 expression were upregulated by TGF-beta1., Prostaglandin E2, transforming growth factor-beta, and interleukin-1 beta variably regulate the expression of cyclooxygenase 1, cyclooxygenase 2, and lysyl oxidase in IMR90, human embryo lung fibroblasts., In a few experiments in MC3T3-E1 cells, TGFbeta stimulated PGHS-1 messenger RNA levels up to 5-fold at 4 h, with little change in glyceraldehyde 3-phosphate dehydrogenase (Fig. 1).","15951536:7, 8872612:0, 9348193:1158",2,3,null,"positive"]
["LGALS1 --+> CD86","Expression","Furthermore, galectin-1 induced both CD83 and CD86 expression in a dose-dependent manner (Fig. 1D)., Compared with eGFP-Dendritic cells, Galectin-1-Dendritic cells had enhanced levels of IAd, H2Kd, CD40, CD54, CD80, and CD86 expression (Fig. 4A)., Incubation of nontransduced Dendritic cells for 18 h with medium supplemented with 10 µM soluble human Galectin-1 induced an increase of IAd and CD86 expression similar to that triggered by recombinant adenovirus-Galectin-1 infection at a MOI of 50 (Fig. 4B).","16785517:1209, 16751364:260, 16751364:264",2,3,null,"positive"]
["ANGPT1 --+> APLN","Expression","angiopoietin 1 induces apelin expression on ECs .","18200044:1080",2,1,null,"positive"]
["SOX9 --+> CLU","Expression","Mutant Kras blocks acinar regeneration in favor of a persistently dedifferentiated state. (A-H) Clusterin and Sox9 (I-P) expression during regeneration and Kras-induced acinar-to-ductal metaplasia. (A and I) Clusterin expression is limited to some normal ducts in PBS-treated Pdx1-CreEarly mice, while Sox9 is restricted to ducts and centroacinar cells (arrowheads). (E and M) Acini in PBS-treated Pdx1-CreEarly;LSL-KrasG12D mice are negative for Clusterin and Sox9, while normal ducts and spontaneous pancreatic intraepithelial neoplasias are positive (asterisks). (B, F, J, and N) Damaged duct-like cells of both genotypes display clusterin- and Sox9-positive cells (insets). (C, D, K, and L) Clusterin and Sox9 are mainly restricted to duct cells (arrowheads) following regeneration in Pdx1-CreEarly pancreata.","20071774:1134",2,1,null,"positive"]
["TLR2 --+> LCN2","Expression","LCN2 expression is increased in response to activation of TLR2 and TLR4 signaling by bacterial peptides (42).","18317594:1267",2,1,null,"positive"]
["STAT3 --+> SBNO2","Expression","IL-10-mediated induction of ETV3 and SBNO2 expression was dependent upon both STAT3 and a stimulus through the TLR pathway.","18025162:2",2,1,null,"positive"]
["TGFB1 --+> IL13RA1","Expression","Transforming growth factor-ß can enhance the effects of IL-13 on activation and survival of eosinophils, and on the surface expression of IL-13Ra1 on eosinophils (Myrtek et al., 2004[Go]).","16888081:1218",2,1,null,"positive"]
["TGM2 --+> CYBB","Expression","Inhibition of cross-linking activity of TG2 by monodansylcadaverin in these cells led to diminished nitroblue tetrazolium positivity, production of less superoxide anion, and decreased expression of GP91PHOX, the membrane-associated subunit of NADPH oxidase.","16763214:3",2,1,null,"positive"]
["PTPN6 --+> ITGB2","Expression","Surface expression of ß2 integrins is increased on motheaten polymorphonuclear leukocytes .","11067945:1301",2,1,null,"positive"]
["P2RY6 --+> TGFB1","Expression","Furthermore, a P2Y6 receptor antagonist MRS2578 suppressed the stress-induced expression of periostin and transforming growth factor-ß messenger ribonucleic acids in vitro and in vivo.","19008857:1266",2,1,null,"positive"]
["STAT3 --+> VIM","Expression","Specific inhibition of STAT3 activation by Janus kinase2-specific inhibitor AG490 blocked STAT3 phosphorylation, cell motility, induction of N-cadherin and vimentin expression and IL6 production., Stat3 can enhance transcription of the vimentin gene.","19088723:9, 14712222:1097",2,2,null,"positive"]
["STAT1 --+> HLA-E","Expression","STAT-1 and GATA-1 bind to the IRR and upstream IFN response region, respectively, to stimulate transcription from the HLA-E promoter (73)., The transcription factors Stat-1 and GATA-1 bind to the IFN response region and upstream IFN response region, respectively, to stimulate transcription from the HLA-E promoter (26, 27).","18566411:1611, 17142760:1073",2,2,null,"positive"]
["CD44 --+> VIM","Expression","Serial transplantation of elongated epithelial cells results in progressive loss of tumorigenic potential; tumor heterogeneity; CD44, E-cadherin, and epithelial cytokeratin expression and increased alpha-smooth muscle actin I and vimentin expression.","18957543:2",2,1,null,"positive"]
["CSF1 --+> SERPING1","Expression","Interferon-gamma and alpha , colony stimulating factor-1, interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) all induce C1-INH synthesis in a variety of cell types.","9777421:6",2,1,null,"positive"]
["TGFB1 --+> CSF1R","Expression","In contrast, TGF-beta 1 down-modulated IL-3 and CSF-1 receptor expression by 54 and 55%, respectively, by 24 h., Cell surface expression of the monocyte/macrophage-specific marker c-fms was increased 3.1-fold following TGF-beta 1 treatment., Antagonists of TGF-beta1 signaling significantly inhibited both the induction of c-fms expression and cellular invasiveness, suggesting that additional studies are warranted to assess the therapeutic potential of TGF-beta antagonists in endometriosis., TGF-ß1 induces the expression of c-fms. <more data available...>","8409417:3, 8930403:10, 19505996:8, 17332318:234, 17332318:219, 17332318:248, 17332318:223, 17332318:289, 17332318:84, 17332318:235 <more data available...>",2,13,null,"positive"]
["ITGAX --+> CD86","Expression","We found that the expression level of co-stimulatory molecules, CD40, CD54, CD80, CD86 and CD11b, were elevated evidently, except CD11c, I-A(d) and H-2K(d)., As reported previously (24), bone marrow-derived macrophage-derived dendritic cells expressed high levels of CD11c, CD86, and I-Ab, and LPS up-regulated the expression of CD86 and I-Ab.","20499643:4, 19336404:170",2,2,null,"positive"]
["AIF1 --+> GFAP","Expression","Following paw incision and at spinal L5 segment GFAP expression was increased in laminae I-II and Iba1 in deep laminae on day 1, in the entire dorsal horn on day 4 and dissipated on day 7 after paw incision in parallel with the allodynia.","18538310:6",2,1,null,"positive"]
["APLN --+> CCND1","Expression","Apelin-13 also increased the levels of cyclin D1, cyclin E and pERK1/2., The Akt inhibitor 1701-1 significantly diminished the expression of phospho-Akt, phospho-ERK1/2, and cyclin D1 stimulated by apelin-13.","18508473:6, 20539939:4",2,2,null,"positive"]
["CSF1 --+> TLR2","Expression","CSF-1 also down-regulated expression of TLR1, TLR2, and TLR6, but not the LPS receptor, TLR4, or TLR5., TLR-2 expression on monocytes was enhanced by macrophage colony-stimulating factor (M-CSF) and interleukin-10 (IL-10), but was reduced by transforming growth factor beta1, while CD16 expression was inducible by these cytokines., Toll-like receptor 2 and 4 surface expressions on human monocytes are modulated by interferon-gamma and macrophage colony-stimulating factor.","11751985:7, 15146415:10, 11672593:100",2,3,null,"positive"]
["FCGR2A --+> CD14","Expression","We found 1) increased FMLP receptor and decreased C5a receptor expression, 2) a normal expression of intracellular FMLP receptors after incubation with PMA, 3) increased loss and decreased re-expression of FMLP receptors after incubation with this peptide, 4) normal expression of adhesion glycoproteins CR3 (CD11b/CD18) and LFA1 (CD11a/CD18), 5) further signs of in vivo preactivation: high expression of Fc gamma-RI (CD64) and Fc gamma-RII (CD32), decreased expression of Fc gamma-RIII (CD16), increased expression of CD14, and low expression of HLA-DR.","1370419:3",2,1,null,"positive"]
["CXCL10 --+> ISG15","Expression","Consistent with this finding, Respiratory syncytial virus-induced beta interferon (IFN-beta), interferon-inducible protein 10 (IP-10), chemokine ligand 5 (CCL-5), and IFN-stimulated gene 15 (ISG15) expression levels were decreased in RIG-I-silenced cells during the early phase of infection but not at later times (18 h postinfection).","17108032:5",2,1,null,"positive"]
["NFATC1 --+> PDPN","Expression","In vitro, endogenous and VEGF-A-induced VEGFR-3 and podoplanin expression by human microvascular endothelial cells was reduced by siRNA to NFATc1, to levels comparable to reductions seen with siRNA to Prox-1.","19233265:8",2,1,null,"positive"]
["TGFB1 --+> SRGN","Expression","Metabolic labeling experiments reveal that TGF-beta induces selectively the expression of proteoglycan-I, whereas the level of proteoglycan-II remains unaltered.","1863601:2",2,1,null,"positive"]
["STAT3 --+> TF","Expression","proteolysis-inducing factor activates both the transcription factors NF-kB and STAT3, which result in the increased production of IL-8, IL-6, and C-reactive protein and the decreased production of transferrin.","11259367:4",2,1,null,"positive"]
["B2M --+> TGFB1","Expression","AGE-beta2m also induced TGF-beta1 production by macrophages in a dose-dependent manner (410 +/- 80 pg/mL at 12.5 microg/mL, 621 +/- 62 pg/mL at 25 microg/mL, and 776 +/- 62 pg/mL at 50 microg/mL of AGE-beta2m).","10652049:6",2,1,null,"positive"]
["CSF1 --+> C3","Expression","Macrophage colony-stimulating factor (M-CSF) enhances complement component C3 production by human monocytes/macrophages.","8477063:100",2,1,null,"positive"]
["STAT3 --+> CXCL10","Expression","Inhibitors of p38 mitogen-activated protein kinase, c-Jun N-terminal kinase (JNK), phosphatidylinositol-3-OH kinase and signal transducer and activator of transcription 3 decreased OSM-induced CXCL10 production.","19616927:6",2,1,null,"positive"]
["TGFB1 --+> CX3CR1","Expression","TGF-beta1 upregulates CX3CR1 expression and inhibits fractalkine-stimulated signaling in rat microglia., These results showed that TGFß enhanced CX(3)CR1 expression and attenuated the LPS-induced increase in IL-1ß expression.","12446007:100, 20570721:11",2,2,null,"positive"]
["CEBPA --+> PROS1","Expression","Reporter gene analysis suggests that members of the CCAAT/enhancer binding protein (C/EBP) family of transcription factors are potent activators of protein S gene transcription in HepG2 cells.","17061980:6",2,1,null,"positive"]
["CSF1 --+> ITGB2","Expression","The levels of CD11a and CD18 expression on granulocytes were significantly enhanced by administration of M-CSF.","11789672:6",2,1,null,"positive"]
["CSF1 --+> LGALS3","Expression","Macrophage colony-stimulating factor (M-CSF), which is present at increased levels in MRL/lpr mice, but not in MRL/Mp- +/+ mice, induced the expression of Mac-2 antigen and Fas antigen on spleen adherent cells of MRL/Mp- +/+ mice.","8870694:4",2,1,null,"positive"]
["CSF1 --+> TNFRSF1A","Expression","Cell surface expression of TNFR1/2 expression on monocytes was induced by IL-10, and more efficiently in combination with M-CSF.","16859503:4",2,1,null,"positive"]
["GFAP --+> APOD","Expression","ApoD levels increased by 35% in the peri-infarct area after 10 and 30 days after pMCAO, mainly in neuron-specific nuclear protein (NeuN) positive neurons and glial fibrillary acidic protein (GFAP) positive astrocytes.","20083089:4",2,1,null,"positive"]
["NFE2L2 --+> PRDX6","Expression","Cotransfection with Nrf2 stimulated the Prdx6 promoter in an antioxidant-response element-dependent manner, whereas it was negatively regulated by Nrf3. siRNA targeting Nrf2 down-regulated reporter gene expression, whereas siRNA targeting the Nrf2 repressor, Keap1, up-regulated it.","18973804:4",2,1,null,"positive"]
["TGFB1 --+> ALOX5AP","Expression","The addition of anti-TGF-beta1 antibody reduced hydroxynonenal-induced 5-LOX and FLAP expression by 40%, indicating the partial involvement of a TGF-beta1-dependent mechanism., The expression of FLAP in Osteoarthritis osteoblasts is also modulated differently by 1,25(OH)2D3 and TGF-beta depending on their endogenous low and high prostaglandin E2 levels., TGFbeta1 and/or 1,25(OH)(2)D(3) induced a rapid and marked enhancement ( approximately 4-13-fold) in FLAP messenger RNA levels, which was associated with a subsequent and late increase in leukotriene B(4) production and prostaglandin E(2) synthesis. <more data available...>","20144213:12, 17156456:12, 15593193:4, 11090070:5",2,4,null,"positive"]
["AIF1 --+> CCND1","Expression","In contrast, the down-regulation of daintain/AIF-1 expression decreased cyclin D1 expression and inhibited the transcriptional activity of nuclear factor-kappa B.","18341653:7",2,1,null,"positive"]
["B2M --+> CCND1","Expression","Cyclin D1 and cyclin D2 transcripts are strongly induced by epidermal growth factor, and beta 2-microglobulin transcripts are strongly induced by TGF-beta in BALB keratinocytes released from quiescence by addition of epidermal growth factor.","8845303:4",2,1,null,"positive"]
["TGFB1 --+> TF","Expression","However, in quiescent, well-differentiated cells, TGF-beta repressed the mitogenic responses to both nutrients alone (by 90%) and to nutrients plus the exogenous stimulatory factors epidermal growth factor (E), insulin (I), and transferrin (T) (by 55-65%)., TGF-beta(1) and bFGF upregulate transferrin gene expression of cultured lens epithelial cells remarkably, can reduce lenticular oxidative damaging process in which transferrin participates and play an important role in the pathological mechanism of cataract formation after extracapsular cataract extraction.","1701348:3, 11835825:8",2,2,null,"positive"]
["HLA-C --+> CD86","Expression","We found that the expression level of co-stimulatory molecules, CD40, CD54, CD80, CD86 and CD11b, were elevated evidently, except CD11c, I-A(d) and H-2K(d).","20499643:4",2,1,null,"positive"]
["STAT1 --+> HSPB1","Expression","STAT-1 was required for transcriptional activation of the HSP27 gene, but not for the HSP70 gene, and cDNA transfection of STAT-1 in mumps virus-infected cells restored thermotolerance.","12917439:6",2,1,null,"positive"]
["CEBPA --+> CASP8","Expression","These findings indicate that C/EBPalpha or its oncoproteins activate the bcl-2 and FLICE inhibitory protein genes by tethering to their promoters through bound NF-kappaB p50.","18987666:8",2,1,null,"positive"]
["CHI3L1 --+> SOX9","Expression","HC-gp39 induced both SOX9 and type II collagen synthesis.","16949314:5",2,1,null,"positive"]
["TGFB1 --+> HPGD","Expression","Induction of 15-PGDH expression by TGF-beta1 was synergistically stimulated by the addition of Wnt3A which was inactive by itself., A number of anti-cancer agents, such as transforming growth factor-beta1 (TGF-beta1), glucocorticoids and some histone deacetylase inhibitors were found to induce 15-PGDH expression.","16844092:6, 17481556:12",2,2,null,"positive"]
["CD14 --+> CD68","Expression","human microglia cell line clone 3 cells are typical microglia, as suggested by the constitutive expression of Iba-1 and CD14, and IFN-gamma-induced expression of CD11b, CD68 and MHCII.","20375612:3",2,1,null,"positive"]
["GFAP --+> MET","Expression","Both Nf1(GFAP)CKO and wild-type astrocytes induced MET expression in neurites of wild-type hippocampal neurons in vitro, suggesting that astrocyte-derived signals may induce MET in Nf1 mutant mice.","17348023:5",2,1,null,"positive"]
["SOX9 --+> LXN","Expression","BMP-2 treatment upregulated Sox9 expression, and Sox9 stimulated the promoter activity of latexin.","19059214:7",2,1,null,"positive"]
["CEBPD --+> CCND1","Expression","Silencing of C/EBPdelta, Cdc27, or the anaphase promoting complex/cyclosome coactivator Cdh1 (FZR1) in MCF-10A breast epithelial cells increased cyclin D1 protein expression.","20439707:3",2,1,null,"positive"]
["STAT1 --+> IFIT3","Expression","Our results suggest that the induction of IFIT4 transcription by IFN-alpha depends upon sequential activation of PKCdelta, JNK and STAT1, and that the influence of PKCdelta or JNK on interferon-alpha-mediated induction of IFIT4 is dependent upon the phosphorylation of STAT1 at Ser-727.","17933493:6",2,1,null,"positive"]
["CSF1 --+> P2RX7","Expression","Furthermore, lipopolysaccharide and M-CSF could up-regulate P2X7 receptor expression in monocytes, while IFN-gamma, TNF-alpha and GM-CSF had weak effects, but pretreatment with these inducers could not further enhance lipopolysaccharide-stimulated P2X7 receptor expression in monocytes.","15830104:6",2,1,null,"positive"]
["AXL --+> SOCS3","Expression","In this issue, Rothlin et al. (2007) uncover a complex negative feedback mechanism to limit Toll-like receptor signaling involving the Tyro3/Axl/Mer family of receptor tyrosine kinases, which induce expression of the inhibitory proteins SOCS1 and SOCS3.","18083093:1",2,1,null,"positive"]
["TGFB1 --+> ITGAX","Expression","Furthermore, TGF-beta/D3 treatment (but not D3 alone) elicits the expression of membrane CD14, FcRI, FcRII, CD11a, CD11b, CD11c, ICAM-1, and PECAM-1 Ag at a level comparable to that observed on normal human monocytes.","8383719:5",2,1,null,"positive"]
["C1QA --+> C3","Expression","Production of complement C3 by Mphi is stimulated by C1q strongly, while the effect of mannan-binding lectin is much weaker.","10898508:6",2,1,null,"positive"]
["AIF1 --+> CD68","Expression","human microglia cell line clone 3 cells are typical microglia, as suggested by the constitutive expression of Iba-1 and CD14, and IFN-gamma-induced expression of CD11b, CD68 and MHCII.","20375612:3",2,1,null,"positive"]
["CSF1 --+> CSF1R","Expression","However, after 48 h, M-CSF significantly stimulated c-Fms expression., IL-10 together with M-CSF increased the expression of M-CSF receptors., This treatment completely prevented M-CSF-induced c-Fms expression in a dose-dependent manner but had little effect on TNFa-induced c-Fms up-regulation (Fig. 5D)., Incubation with CSF-1 down-regulated CSF-1R expression and was associated with proliferation of mononuclear cells with decreased CSF-1R binding., We demonstrated that one mechanism by which this occurs is PU.1 down-regulation by the negative control of NFI-A on M-CSFR levels (Fig. 7) because M-CSF induces PU.1 expression through M-CSFR in the hematopoietic myeloid-osteoclast lineage (1-3). <more data available...>","16461346:213, 8978307:46, 16461346:221, 19819976:310, 19059913:261, 19628784:169",2,6,null,"positive"]
["STAT1 --+> CASP1","Expression","Activation of caspase-1 gene expression requires IRF-1 and Stat-1 (24, 32)., In addition, overexpression of STAT-1 together with interferon-? treatment further enhanced the activity of the caspase-1 promoter., Recently, interferon-? and STAT-1 have been shown to modulate the level of caspase-1 expression in non-cardiac cells (28)., Moreover, transfection of antisense STAT-1 inhibited both the interferon-?/STAT-1- and ischemia-induced activation of the caspase-1 promoter (Fig. 5)., Down-regulation of EGFR is also postulated to induce apoptosis, and activation of Stat-1 has been reported to induce p21/WAF-1 or caspase 1 that may result in cell cycle arrest or apoptosis, respectively. <more data available...>","16135520:78, 10744676:204, 10744676:201, 10744676:206, 12714587:265, 17339457:351, 10744676:212, 10640742:219, 10744676:264, 9694822:49",2,10,null,"positive"]
["TGFB1 --+> CCND1","Expression","The expression of cyclin D1 in MCF10A cells is regulated by TGF-ß treatment., In addition, Sox17 counteracted repression of the cyclin D1 promoter by TGF-ß1 and Smad3., These results strongly suggest that TGF-ß regulates cyclin D1 expression in a ß-catenin-dependent manner., TGF-ß stimulates cyclin A expression without affecting cyclin D-cdk4/6 activity in suspended NRK cells., TGF-ß stimulated cyclin D1 expression in Ad-GFP-infected but not Ad-Cre-infected chondrocytes (Fig. 7a)., Although TGF-ß stimulated cyclin D1 expression in chondrocytes, this effect was abolished by inhibition of ß-catenin signaling. <more data available...>","18715870:116, 19479035:326, 16690606:242, 10702223:90, 16690606:239, 16690606:67, 19479035:260, 16517699:263, 15811853:143, 19479035:288 <more data available...>",2,19,null,"positive"]
["GRN --+> CCND1","Expression","In these cells, PCDGF/GP88 was shown to mediate the mitogenic activity of estrogen by stimulating cyclin D1 expression (20) ., granulin/epithelin precursor leads to activation of the mitogen-activated protein kinase pathway and to stimulation of cyclin D1 protein expression., Effect of PCDGF on cyclinD1 and c-myc expression in MCF-7 cells. (A) Stimulation of cyclin D1 expression by PCDGF., PCDGF in a time-dependent fashion stimulated cyclin D1 expression in MCF-7 cells, reaching a maximum of 4-fold over untreated controls after 5 h (Fig. 5 A). <more data available...>","14996734:66, 15653695:83, 11134521:212, 11134521:207, 11134521:254, 11134521:228, 11134521:220, 11134521:263",2,8,null,"positive"]
["CSF1R --+> PTPN6","Expression","Traumatic injury to the central nervous system activates microglia and strongly increases expression of SHP-1, which physically associates with and is activated by c-Fms in these cells (17).","12361947:312",2,1,null,"positive"]
["PTPN6 --+> CYBB","Expression","Consistent with this, SHP1 inhibition increases gp91PHOX and p67PHOXmRNA in undifferentiated U937 cells., In undifferentiated U937 cells, we found that overexpression of CS453-SHP1 increases gp91PHOX and p67PHOX mRNA abundance relative to control vector transfectants (Fig.2 C).","11483597:208, 11483597:223",2,2,null,"positive"]
["TLR2 --+> CD86","Expression","TLR2 is essential for neisserial porin up-regulation of B7-2 and class II MHC in B cells ., Anti-TLR2 blocked increases in the CD86 median fluorescence intensity, but not the percentage of cells positive for CD86., There may be some differences in the Toll-like receptor2-mediated signaling pathway between cytokine production and CD83/CD86 expression., This indicates that the up-regulation of B7-2 and class II MHC surface expression was dependent on the normal expression of TLR2 on the B cell., They also showed that, in human Immature dendritic cells, cytokine production and CD83/CD86 expression were independently induced by M161Ag through TLR2. <more data available...>","11823477:142, 11160304:195, 11160323:247, 11823477:146, 11160323:191, 19109203:128, 11316801:237, 19109203:149, 11160304:179, 11823477:182",2,10,null,"positive"]
["LCN2 --+> GFAP","Expression","Third, the LCN2-induced GFAP expression was blocked by a nitric oxide synthase inhibitor NG-monomethyl-L-arginine (Fig. 8F,G)., Because LCN2 also induced GFAP expression in astrocytes in our study (Fig. 6), we next attempted to determine whether NO is involved in the LCN2 actions in astrocytes., Rho/ROCK pathway appeared to play a pivotal role in regard to LCN2 actions on astrocyte morphology, based on the following results: (1) a ROCK inhibitor, Y27632, partly blocked LCN2-induced morphological changes (Fig. 9A,B); (2) Y27632 also inhibited the LCN2-induced GFAP expression (Fig. 9C,D); and (3) LCN2 induced Rho activation in astrocytes (Fig. 9E). <more data available...>","19129400:366, 19129400:358, 19129400:384, 19129400:439",2,4,null,"positive"]
["TGFB1 --+> Ctla2a","Expression","This suggests that TGF-ß promotes the up-regulation of the CTLA-2a expression on responding T cells.","19801522:182",2,1,null,"positive"]
["TREM2 --+> CD86","Expression","Ligation of triggering receptor expressed on myeloid cells-2 induced increased cell surface expression of CD40, CD86, and MHC class II but Ag-capturing mechanisms were not down-regulated (53)., KARAP/DAP12-TREM2 triggering on human Dendritic cells promotes incomplete maturation process, i.e., Dendritic cells up-regulation of CCR7, CD40, CD86, and MHC class II molecules, but not TNF-alpha nor IL-12 production (32).","14978127:315, 15128777:291",2,2,null,"positive"]
["STAT3 --+> MET","Expression","U-STAT3 induces the expression of well-known oncogenes, such as MRAS and MET, which are late-phase genes induced by IL-6.","19478064:203",2,1,null,"positive"]
["TLR2 --+> ITGAX","Expression","The TLR2 agonist Pam3Cys significantly stimulated the maturation of DCs by enhancing the surface expression of CD11c, MHC class I, MHC class II, CD40, CD80, and CD86.","19109203:128",2,1,null,"positive"]
["LGALS1 --+> TGFB1","Expression","We demonstrate here that Recombinant galectin-1 treatment induces the production of substantial amounts of TGF-ß1 and IL-10, which in turn may be responsible for counterregulating the uveitogenic Th1 response.","16670344:282",2,1,null,"positive"]
["CX3CR1 --+> TGFB1","Expression","CX3CR1 promotes TGF-ß1 expression and myofibroblast accumulation in wounded skin ., CX3CR1 promotes TGF-ß1 expression and activated fibroblast accumulation in wounded skin., These results suggest that CX3CR1 activity in vivo promotes TGF-ß1 production, which promotes accumulation of a-smooth muscle actin+-activated fibroblasts, which are the direct source of collagen, a key constituent of granulation tissue in skin wound repair. [Figure 10] View larger version (76K): [in this window] [in a new window] .","18097059:296, 18097059:303, 18097059:301",2,3,null,"positive"]
["STAT1 --+> IFI27","Expression","From results presented here, it is reasonable to propose that up-regulated STAT1 may enhance IFI27 and OAS1 expression in breast tumors.","19478064:183",2,1,null,"positive"]
["TGFB1 --+> ADAMTS1","Expression","Expression of ADAMTS1 is induced by transforming growth factor-ß in keratinocytes.","15843381:262",2,1,null,"positive"]
["CXCL14 --+> CD86","Expression","Fig. 5 shows that the addition of 200 ng/ml CXCL14 to dendritic cell markedly up-regulated expression of CD83, HLA-DR, CD86, and CD80 molecules when compare with CXCL14-untreated dendritic cell.","15843547:292",2,1,null,"positive"]
["CXCL14 --+> CD83","Expression","Fig. 5 shows that the addition of 200 ng/ml CXCL14 to dendritic cell markedly up-regulated expression of CD83, HLA-DR, CD86, and CD80 molecules when compare with CXCL14-untreated dendritic cell.","15843547:292",2,1,null,"positive"]
["CLEC5A --+> NFATC1","Expression","We also demonstrate that MDL-1 activation increases the expression of NFATc1 and ATPV0D2, which control cell fusion (Lee et al., 2006), as well as regulating bone resorption via TRAP and cathepsin K in osteoclasts (Takayanagi, 2005a).","20212065:226",2,1,null,"positive"]
["TLR2 --+> HSPB1","Expression","TLR1/2 ligand palmitoyl-3-cysteine-serine-lysine-4 (Pam3CSK4) induces activation of PKDs via a PKC-independent manner, and Pam3CSK4-induced expression of heat shock protein 27 and MCP-1, as well as activation of PKDs, is inhibited by Gö6976, but not by broad-spectrum PKC inhibitors, in mouse bone marrow-derived mast cells (26).","19414785:65",2,1,null,"positive"]
["TLR2 --+> STAT3","Expression","TLR2 activation triggers STAT3 and Smad3 activation., TLR2 activation sequentially stimulates NF-?B, STAT3 and Smad3 activation., In addition, blockade of TLR2 abrogated peptidoglycan-SA-induced STAT3 and Smad3 activation. [thumbnail] ., Secondly, HSP60 activation of TLR2 mediates the expression and phosphorylation of Stat3 in tumor cells., These finding indicated that peptidoglycan-SA-stimulated TLR2 activation increased NF-?B, STAT3 and Smad3 activities depending on a time pattern., Moreover, targeting TLR2 in the host or in the melanoma cells markedly inhibited the B16 cell-induced phosphorylation of Stat3 (Fig. 3F). <more data available...>","20520770:250, 20520770:260, 20520770:255, 19654875:266, 20520770:318, 19654875:200, 20520770:319, 19654875:159, 19654875:164",2,9,null,"positive"]
["CEBPD --+> SOCS3","Expression","The doxycycline-dependent expression of C/EBP-d neither increased Spi-2 and Socs3 transcripts nor interfered with their induction by IL6RIL6 (Fig. 5B).","14600146:227",2,1,null,"positive"]
["TGFBR1 --+> TGFB1","Expression","This persistence was because of autocrine synthesis of TGF-beta1, which was inhibited by both anti-TGF-beta1 antibody and the ALK5 inhibitor SB431542., Based on these findings, we hypothesize that the interaction between c-Ski and TßRI might interfere with nuclear translocation of the R-Smad/Smad4 complex, thereby attenuating TGF-ß signaling., These results show that constitutively reduced Tgfbr1-mediated TGF-beta signaling significantly enhances colorectal cancer development and results in increased tumor cell proliferation. <more data available...>","19193641:6, 20959473:4, 19147584:4, 19535626:7, 19432813:7",2,5,null,"positive"]
["CYBA --+> CYBB","Expression","Small interference RNA for p22(phox) prevented glycated low-density lipoprotein-induced expression of NOX2, HSF1, and PAI-1 in endothelial cells.","20630999:9",2,1,null,"positive"]
["PLAT --+> CCND1","Expression","Ectopic overexpression of an uninhibitable GSK3ß mutant eliminated tPA-induced cyclin D1 expression., Blockade of Erk1/2 activation or knockdown of p90RSK suppressed tPA-induced GSK3ß phosphorylation, cyclin D1 expression, and fibroblast proliferation.","20724593:6, 20724593:4",2,2,null,"positive"]
["LYN --+> MCL1","Expression","Inhibition of Lyn or rescue of miR181b expression reduced Mcl-1 expression in the MYL-R cells., Finally, stimulation of Lyn expression by 1,25-dihydroxyvitamin D(3) treatment in HL-60 cells, a cell model of acute myelogenous leukemia, decreased miR181b expression and increased Mcl-1 expression.","20693279:7, 20693279:10",2,2,null,"positive"]
["P2RX7 --+> CASP1","Expression","We recently reported that P2X7 receptor (P2X7R)-induced activation of caspase-1 inflammasomes is accompanied by release of MHC class II protein into extracellular compartments during brief stimulation of murine macrophages with ATP., Furthermore, the production of IL-18 and IL-1beta and caspase-1 activation were induced independently of a P2X7 purinergic receptor, and the inability of Delta\"region of difference 1\" in caspase-1 activation was compensated for by nigericin, an agent inducing the potassium ion efflux.","19342685:0, 19596775:7",2,2,null,"positive"]
["TLR3 --+> CLU","Expression","Conclusively, TLR3 activation induces expression of cytoprotective and anti-inflammatory CLU by vascular smooth muscle cells and mice, to potentially counteract atherosclerotic pathology., Toll-like receptor 3 mediates expression of clusterin/apolipoprotein J in vascular smooth muscle cells stimulated with RNA released from necrotic cells.","20692254:10, 20692254:100",2,2,null,"positive"]
["STAT1 --+> CXCL10","Expression","STAT1 was critical for IFN-gamma induction of both the Cxcl9 and Cxcl10 genes in microglia and in microglia and astrocytes, respectively.","20585034:7",2,1,null,"positive"]
["TGFB1 --+> STAT1","Expression","IFN-gamma down-regulates TGF-beta1-induced IgA expression through Stat1 and p300 signaling.","20016942:100",2,1,null,"positive"]
["ITGB2 ---| TGFB1","Expression","Having demonstrated the role of CD18-ICAM-dependent binding in monocyte-stimulated TGF-ß1 generation after TNF-a stimulation, we next examined the role of cell surface hyaluronan in these experiments., Collectively, our results indicate that CD18 at wild-type expression levels leads to effective DC-Treg contacts for the induction of sufficient TGF-ß1 expression by Tregs, while decreased CD18 expression promotes the psoriasiform skin disease in the Cd18 hypomorphic PL/J mouse model.","15574511:1201, 18521187:1264",2,2,null,"negative"]
["APLN ---| CSF1","Expression","IL-6, M-CSF, and macrophage inflammatory protein-1a expression levels were also decreased by apelin, although these differences did not reach statistical significance.. [Figure 5] View larger version (11K): [in this window] [in a new window] .","19304942:1182",2,1,null,"negative"]
["TGFB1 ---| PLAT","Expression","In contrast, TGF-beta1 triggered a large decrease of uPA and tPA, as well as a decrease of uPA and uPAR mRNAs., Thrombin increased t-PA activity and TGF-beta decreased it in parallel with t-PA antigen level, although these agents did not affect the synthesis of PAI-1., These data indicate that TGF-beta mediates astrocyte regulation of brain capillary endothelial expression of tPA and thrombomodulin., TGF-alpha enhanced the expression of the tissue type plasminogen activator (t-PA) gene, whereas TGF-beta increased the expression of the PA inhibitor-1 (PAI-1) gene and inhibited that of the t-PA gene. <more data available...>","14597403:7, 9807022:5, 10436120:11, 7947924:1, 12147618:13, 18037995:1239, 9716558:1287",2,7,null,"negative"]
["MAFB ---| NFATC1","Expression","Furthermore, reduced expression of MafB by RNAi enhances osteoclastogenesis and increases expression of NFATc1 and osteoclast-associated receptor.","17158225:6",2,1,null,"negative"]
["TGFB1 ---| TNFRSF1A","Expression","However, TGF-beta treatment of Burkitt's lymphoma41 cells was found not to affect the cell surface expression of Fas, TNF-R1, DR3, DR4, or DR5, or the steady-state expression levels of Fas ligand, TNF-R1, DR3, DR4, and DR5., However, we found that TGF-ß treatment significantly down-regulated expression of the TNF-a death receptor, TNFRSF1a, on 4T1 cells in vitro at the mRNA and protein level (Fig. 5A )., While transforming growth factorß attenuated the increase in tnfr1 compared to T20+FBS, transforming growth factora treatment further increased levels of the tnfr1 transcript (1.5 ± 0.2-fold versus T20 FBS; P < 0.05). <more data available...>","10946276:9, 18483268:1250, 11514335:1180, 18832695:1060, 11591746:1078",2,5,null,"negative"]
["NFE2L2 ---| TGFB1","Expression","Furthermore, activation or overexpression of Nrf2 inhibited the promoter activity of TGF-beta1 in a dose-dependent manner, whereas knockdown of Nrf2 by siRNA enhanced TGF-beta1 transcription and fibronectin production.","20103708:9",2,1,null,"negative"]
["TGFB1 ---| ADAMTS1","Expression","IL-1beta and TGF-beta1 differentially regulate ADAMTS-1 expression in human decidual stromal cells., In stromal cells, TGFbeta1 decreased ADAMTS-1, -5, -9, and -15 transcripts and increased ADAMTS-4, versican, and TIMP-3., Members of the ADAMTS family have previously been shown to be induced by inflammatory cytokines and TGFbeta1 [76], [77]., interleukin-1ß was found to have a stimulatory effect on ADAMTS-5 messenger RNA and protein levels, whereas transforming growth factor-ß1 decreases the expression of this ADAMTS subtype in these primary cultures.","16675485:8, 15599946:8, 20706631:1348, 17067994:1180",2,4,null,"negative"]
["SOX9 ---| CCND1","Expression","The arrows indicate Cyclin D1-positive proliferating chondrocytes. (C) Activation of the Cyclin D1 promoter by st ß-catenin is inhibited by Sox9 in 293 cells., Our in vitro and in vivo results indicate that Sox9 down-regulates the transcriptional activity of the ß-catenin-Tcf4 complex on endogenous target promoters, such as the c-Myc and cyclin D1 gene promoters.","15132997:1157, 17698607:1266",2,2,null,"negative"]
["CD14 ---| ITGB2","Expression","Collectively, results indicate that recombinant bovine Soluble CD14 inhibit lipopolysaccharide-induced increase in CD18 expression and TNF-alpha mRNA., These studies suggest that CD14 affects CD11b/CD18 function by inducing the synthesis of a lipid such as IMF-1, and that this lipid affects only the binding activity, not the phagocytosis-promoting capacity of CD11b/CD18., However, upregulation of CD14 activates CD11b/CD18, increasing the potential importance of CD11b/ ICAM-1 interactions (54).","12911858:9, 7519640:10, 9649567:1327",2,3,null,"negative"]
["ANGPT1 ---| TGFB1","Expression","Treatment with COMP-angiopoietin-1 also decreased the Cyclosporine A-induced increases in TGF-beta1 and Smad 2/3 levels while increasing Smad 7 levels., COMP-angiopoietin-1 treatment decreased monocyte/macrophage infiltration, tissue levels of TGF-beta1, and Smad 2/3 phosphorylation and increased Smad 7 in the obstructed kidney., They found that when angiopoietin 1* was administered a few days before the nephrotoxin, although the severity of acute renal failure was not affected, the strategy did improve the chronic fallout of cortical peritubular capillaries that occurred in the weeks after recovery from acute tubular necrosis; however, at the same time, the use of angiopoietin 1* was associated with worsened fibrotic response, upregulated TGF-ß expression, and increased renal inflammatory cells.","18463324:9, 16885409:9, 18799719:1132",2,3,null,"negative"]
["CCND1 ---| CEBPA","Expression","Moreover, isorhamnetin reduced the mRNA expression levels of C/EBPalpha and PPARgamma, which are known to be inhibited by c-myc or by cyclin D1 and PPARdelta, respectively., Cyclin D1 inhibits PPAR? ligand-induced gene expression without affecting C/EBPa or C/EBPß.","20097210:10, 12917338:1222",2,2,null,"negative"]
["TGFB1 ---| CD86","Expression","TGFbeta1 treatment significantly reduced the expression of CD54 and CD86., This resulted in secretion of high levels of IL-10 and TGF-beta together with increased surface expression of CD86., The results showed that TGF-beta1 and IL-10 could down-regulate the expressions of costimulatory molecules, including CD80, CD86 and CD40., IL-4, transforming growth factor-beta1, and nerve growth factor (NGF) repress GM-CSF-induced B7-2 and CD40, but not B7-1., Phosphorylated Smad-2 was undetectable and expression of surface co-stimulatory molecules (CD80/CD86) were upregulated in TbetaRIIDN DCs after antigen and TGF-beta1 stimulation. <more data available...>","17029006:3, 16246624:5, 18426675:7, 10229111:4, 17473921:4, 15499832:5, 17275522:5, 15528343:1311, 16293609:1226, 16123803:1127",2,10,null,"negative"]
["TLR2 ---| CXCL10","Expression","However, we found that TLR-2, TLR-3, TLR-4, and TLR-9 stimulation induced interferon-beta (IFN-beta), which is able to exert auto- and paracrine signaling, leading to the activation of secondary genes like IP-10., The bacterial TLR4 and TLR2 ligands, LPS and peptidoglycan , inhibit IFN-gamma- or dsRNA-dependent IP-10/CXCL10 production in Peripheral blood mononuclear cells, whereas IL-8/CXCL8 production was enhanced., Concomitant TLR2 stimulation blocks IP-10 and IL-12p35 induction by TLR3 and TLR4 agonists. <more data available...>","15491991:7, 14579283:3, 15585882:1190, 18057004:1179, 18025224:1222, 17170125:1102, 18188453:1255",2,7,null,"negative"]
["TGFB1 ---| CEBPA","Expression","Dexamethasone increased C/EBPalpha and PPARgamma expression in the absence of TGF-beta and also recovered the TGF-beta-mediated suppression of C/EBPalpha expression in preadipocytes., Also at the mRNA level, TGF-beta1 counteracted at one point or another the decrease in C/EBPalpha, C/EBPbeta, HNF1beta, and HNF4 expression; HNF1alpha and COUP-TF showed similar responses and, additionally, were downregulated by TGF-beta1 at 24 h (Northern blot)., Transforming growth factor-beta inhibits CCAAT/enhancer-binding protein expression and PPARgamma activity in unloaded bone marrow stromal cells. <more data available...>","12753899:6, 10425225:5, 15572034:100, 18310014:1073, 14605006:1333",2,5,null,"negative"]
["IRF8 ---| OAS1","Expression","Ectopic expression of TEL and ICSBP represses interferon-?-inducible 2', 5'-OAS gene expression., Furthermore, cooperation between IRF-2 and ICSBP is needed to repress the transcriptional activity of some promoters, such as those for MHC class I and 2'-5'oligoadenylate synthetase (11) (12) (13) (14)., This contrasts with earlier studies that concluded that ICSBP is a negative regulator of several IFN-responsive genes, including MHC class I, IFN-ß, ISG-54, ISG-15, 2'-5' oligoadenylate synthetase, and the Ig ? enhancer (5, 7).","12370291:1262, 10934221:1050, 10453013:1052",2,3,null,"negative"]
["ABCA1 ---| CLU","Expression","Notably, because 2-fold overexpression of ABCA1 was sufficient to reduce amyloid ß-peptide levels in PDAPP/Abca1 line D mice (Figure 5, A and C) without significant alterations in either apoE or apoJ levels, the beneficial effects of excess ABCA1 function in amyloid ß-peptide reduction appear to be largely independent of the absolute levels of apoE and apoJ., In addition to apoA-I, several other HDL-associated proteins have been reported to affect cholesterol efflux: PON1 enhances HDL-induced cholesterol efflux by increasing the binding affinity of HDL to macrophages and by stimulating ABCA1-mediated cholesterol transport (9), and apoJ, which is associated with lipid-poor HDL, stimulates reverse cholesterol transport by an unknown mechanism (10).","18202749:1242, 16682745:1064",2,2,null,"negative"]
["TGFB1 ---| TLR2","Expression","TGF-beta1 inhibited TLR2 and TLR4 expression and attenuated odontoblast responses., TLR2 promoter activity and nuclear factor -kappaB activation by IL-1alpha were inhibited by TGF-beta treatment., TLR-2 expression on monocytes was enhanced by macrophage colony-stimulating factor (M-CSF) and interleukin-10 (IL-10), but was reduced by transforming growth factor beta1, while CD16 expression was inducible by these cytokines., TGF-ß1 induces cathelicidin, CD14, and TLR2 by CYP27B1-dependent activation of 1,25OH vitamin D3.","19407153:6, 15039464:4, 15146415:10, 17290304:1129",2,4,null,"negative"]
["SOCS3 ---| TGFB1","Expression","In both AR42J cells and rat pancreas, cerulein induced expression of IL-6 and TGF-beta1, which is enhanced by transfection or injection of SOCS 3 antisense oligonucleotide (AS ODN)., Loss of SOCS3 in the liver promotes fibrosis by enhancing STAT3-mediated TGF-beta1 production., These data suggest that SOCS3 probably regulates the production of transforming growth factor-ß1 through appropriate tuning of STAT3 activation in CD4+ T cells., In nonneural cell systems, it has recently been shown that STAT3 upregulates transforming growth factor ß1 expression in hepatocytes and T cells, which is downregulated by SOCS3 (12, 24).","18035585:5, 16474852:100, 16606674:1203, 17452461:1196",2,4,null,"negative"]
["CCND1 ---| TGFBR2","Expression","Overexpression of Cyclin D1 was shown to attenuate the responsiveness of cells to TGF-ß through down-regulation of TGF-ß RII expression (Okamoto et al., 1994)., A previous study (Okamoto et al., 1994) determined that the overexpression of cyclin D1 in a human esophogeal cancer cell line resulted in the downregulation of the TGF-ß type II receptor.","10773876:1145, 10645011:1120",2,2,null,"negative"]
["TNFRSF1A ---| SOCS3","Expression","In addition to its proinflammatory role, TNF receptor signaling induces expression of SOCS3, a negative regulator of IL-6 and OSMR signaling and Nfkbie, and a negative regulator of TNF receptor signal transduction., We also showed that interplay between TLRs, TNF receptors, and IFNgamma signaling induces the expression of suppressor of cytokine signaling 1 (SOCS-1) and SOCS-3 and reduces IFNgamma-dependent STAT-1 phosphorylation, which might explain this inhibition., Herein we found that a deficiency of TNFR1 increased myocardial SOCS3 protein expression, which is in line with our previous result of an ischemia-reperfusion-induced increased expression of SOCS3 that is increased in TNFR1 knockout hearts (39).","19155971:5, 17907168:7, 17114246:1191",2,3,null,"negative"]
["PTGS1 ---| HPGD","Expression","Fig. 6 Inhibition of 15-PGDH expression by 15-PGDH-silencing RNA on the expression of cyclooxygenase-1 and COX-2 in A549 cells.","16632868:1231",2,1,null,"negative"]
["TLR3 ---| CLEC7A","Expression","Furthermore, activation of monocyte-derived dendritic cells with toll-like receptor 3 (TLR3) ligand but not with TLR2 ligand or TLR7 ligand resulted in down-regulation of hDectin-1 expression and reduced phagocytosis of apoptotic tumor cells as well as presentation of pp65-derived T-cell epitopes upon engulfment of cytomegalovirus -infected human foreskin fibroblasts.","17698636:2",2,1,null,"negative"]
["TGFB1 ---| CD83","Expression","The blockade of IL-10/TGFß clearly enhanced the expression of CD40, CD86, CD83, and CCR7 on DCs., Treatment of DCs with transforming growth factorß inhibited their expression of CD80, CD83, and CD86, and it up-regulated the expression of B7-H1.","15528343:1311, 16293609:1226",2,2,null,"negative"]
["IFI30 ---| TGFB1","Expression","The finding of increased expression of the IFN-?-induced IFI30 and of Eta-1 in lupus glomeruli together with decreased expression of TGF-ß point to an environment that would favor Th1 cell differentiation.","15199407:1258",2,1,null,"negative"]
["TGFB1 ---| C3","Expression","Transforming growth factor-beta1 acts as a potent inhibitor of complement C3 biosynthesis in human pancreatic cancer cell lines., Regulation of complement C3 synthesis by interleukin-1 and transforming growth factor-beta in rat non-transformed intestinal epithelial cell line, IEC-6., This may be associated with inhibition of complement C3 synthesis by TGF-ß in response to inflammatory cytokines18,19 and may be also associated with suppression of complement activation locally by blocking renal inflammation in response to high levels of latent TGF-ß1.","10707928:100, 8887027:100, 18216320:1156",2,3,null,"negative"]
["KLK6 ---| CCND1","Expression","The expression of both Cyclin D1 and KLK6 was seen to be reduced by SSE without (P < 0.05 and P < 0.01 for Cyclin D1 and KLK6, respectively) or with 17ß-estradiol supplementation (P < 0.01 for both Cyclin D1 and KLK6), where the effect was more consistent in the degree of inhibition.","16400187:1161",2,1,null,"negative"]
["CCND1 ---| KLK6","Expression","The expression of both Cyclin D1 and KLK6 was seen to be reduced by SSE without (P < 0.05 and P < 0.01 for Cyclin D1 and KLK6, respectively) or with 17ß-estradiol supplementation (P < 0.01 for both Cyclin D1 and KLK6), where the effect was more consistent in the degree of inhibition.","16400187:1161",2,1,null,"negative"]
["SOCS3 ---| GFAP","Expression","In addition, overexpression of SOCS3 in Neuroepithelial cells completely suppressed GFAP promoter activation by LIF, whereas SOCS3 did not have such a suppressive effect on BMP2-induced activation (see Fig. S1B in the supplemental material).","17452461:1124",2,1,null,"negative"]
["CSF1 ---| PTPRC","Expression","CD45 gene expression was reduced following exposure to M-CSF, PTN, or the combination of both cytokines (Figure 4A)., Secreted CSF-1 appears to cause monocyte recruitment and activation, thereby modulating immune functions and potentially the expression of the CD45RO phenotype in T cells.","19060246:1167, 8271294:15",2,2,null,"negative"]
["TGM2 ---| ABCA1","Expression","retinoic acid-stimulated expression of ABCA1 was attenuated in TG2-/- bone marrow macrophages in vitro.","16410462:1175",2,1,null,"negative"]
["TLR3 ---| ABCA1","Expression","TLR3 and TLR4 inhibit cholesterol efflux by reducing the expression of ABCA1 and several other genes.25 This is attributable to an inhibition of the transcription factor, lipid-X receptor ., TLR3/4 Ligands Inhibit ABCA1 Protein Expression and Macrophage Cholesterol Efflux . (A) Lipid A inhibits ABCA1 protein expression in murine macrophages.","15923538:1080, 14580333:1191",2,2,null,"negative"]
["SOCS3 ---| SERPINA3","Expression","Co-transfection studies revealed that constitutive expression of SOCS-1 and SOCS-3, but not SOCS-2 or CIS, blocked growth hormone-induced transactivation of the growth hormone-responsive serine protease inhibitor 2.1 gene promoter., Both SOCS-1 and SOCS-3 were found to inhibit GH-induced transcription of the Spi 2.1 promoter., This suggests that the induction of SOCS-3 by IL-6 cannot by itself block the GH action on IGF-I and Spi2.1 genes., Indeed, GH was recently reported to induce SOCS3, which can inhibit GH-induced trans-activation of the Spi 2.1 promoter in transfection assays (48). <more data available...>","9430658:6, 10551777:1193, 11014223:1212, 9892011:1322, 10433229:1053, 11606470:1061, 9430658:32",2,7,null,"negative"]
["PTPN6 ---| CCND1","Expression","Along this line goes the observation that the protein tyrosine phosphatase SHP-1, as mentioned above, decreases the transcriptional activity from TCF-sensitive dihydrofolate reductase, c-myc, and cyclin D1 promoters by about 50% (9).","16648485:1502",2,1,null,"negative"]
["IRF8 ---| CASP1","Expression","These results suggest that overexpression of ICSBP in U937 cells may affect apoptosis by enhancing expression of the proapoptotic genes of caspase-1 and -7., On the contrary, ectopic expression of ICSBP repressed the transcription of caspase-1 in both IFN-?-treated SW480 cells (Fig. 6, lane 6 vs 2 or 4) and SW620 cells (Fig. 6, lane 12 vs 8 or 10).","10430629:1178, 12794166:1264",2,2,null,"negative"]
["TGFB1 ---| Ccl9","Expression","Consistently, we found that expression of CCL9 in mouse colon cancer cell line CT26 was suppressed by TGF-ß family ligands, such as TGF-ß, activin, bone morphogenetic protein 4, and BMP7.","17974948:1088",2,1,null,"negative"]
["CCND1 ---| TGFBR1","Expression","Our findings suggest that in some cell types cyclin D1 expression may be important for TGF-beta1-mediated signaling and that cyclin D1 may be involved in the transcriptional regulation of TbetaRI., However, in this study it did not appear that cyclin D1 was affecting the different cyclin/cdk/inhibitor complexes, but rather caused the downregulation of the expression of the type II TGFß-1 receptor.","10471535:7, 10645011:1083",2,2,null,"negative"]
["LYN ---| SOCS3","Expression","Lyn suppresses constitutive SOCS-1 and SOCS-3 expression.","12761492:1096",2,1,null,"negative"]
["CLU ---| CD14","Expression","Enforced stable over-expression of CLU in K562 cells inhibited the expression of the CD14 differentiation marker and blocked differentiation to either monocytes/megacaryoblasts or to erythrocytes.","16955214:7",2,1,null,"negative"]
["IRF8 ---| CD68","Expression","However, our data show that PU.1/IRF-4 and IRF-8 heterocomplexes down-regulate CD68 promoter activity in macrophages and repression is dependent on the integrity of both the interferon regulatory factor family and PU.1 half-sites of this composite element., Repression of CD68 proximal promoter by IRF-4 and IRF-8 requires DNA contact., However, our data demonstrate that IRF-4 and IRF-8 can repress CD68 activity in a dose-dependent manner in THP-1 cells (Fig. 6, B and C)., In contrast, our results provide evidence that PU.1/IRF-4 and PU.1/IRF-8 complexes can repress CD68 promoter activity in human monocytic cells. <more data available...>","12676954:7, 12676954:320, 12676954:410, 12676954:378, 12676954:331, 12676954:421, 12676954:33",2,7,null,"negative"]
["MSN ---| CCND1","Expression","The expression of cell cycle mediators such as p16, cyclin D1 and cdk4, which can be the markers of ageing, was compared by RNA and was shown to be suppressed in moesin overexpressed endothelial cells.","19555429:3",2,1,null,"negative"]
["TGFB1 ---| B2M","Expression","TGF-beta 1 inhibits HLA-DR and beta 2-microglobulin expression in HeLa cells induced with r-IFN.","10455994:100",2,1,null,"negative"]
["TGFB1 ---| FLI1","Expression","We first showed that TGF-beta induces Fli1 phosphorylation on a threonine residue(s)., TGF-beta stimulation resulted in displacement of Fli1 from the CCN2 promoter and a transient inhibition of Fli1 synthesis., Thus, transforming growth factor-ß1 is a potent mediator of Fli1 acetylation., We demonstrated that transforming growth factor-ß elicits acetylation of Fli1 and the dissociation of Fli1 from the COL1A2 promoter., transforming growth factor-ß stimulation resulted in displacement of Fli1 from the CCN2 promoter and a transient inhibition of Fli1 synthesis. <more data available...>","19158279:2, 16829517:8, 17884818:176, 17884818:352, 16829517:57, 16829517:349, 16829517:269, 17884818:179",2,8,null,"negative"]
["CSF1R ---| CCND1","Expression","Substitution of phenylalanine for tyrosine at codon 809 (Y809F) of the human colony-stimulating factor 1 (CSF-1) receptor (CSF-1R) impairs ligand-stimulated tyrosine kinase activity, prevents induction of c-MYC and cyclin D1 genes, and blocks CSF-1-dependent progression through the G1 phase of the cell cycle.","9372970:0",2,1,null,"negative"]
["TGFB1 ---| C1QB","Expression","Interactions of transforming growth factor-beta1 with complement system gene expression are also indicated, because transforming growth factor-beta1 decreased C1qB messenger RNA in the cortex and hippocampus, after intraventricular infusion, and in cultured glia.","11074155:7",2,1,null,"negative"]
["SOCS3 ---| MCL1","Expression","Enforced expression of SOCS-3 also reduced IL-6 induction of phospho-STAT-3 and Mcl-1.","17241887:7",2,1,null,"negative"]
["TGFB1 ---| HLA-DQA1","Expression","Both constitutive and interferon-gamma (IFN-gamma), interleukin-4 (IL-4), IL-6 and tumour necrosis factor-alpha (TNF-alpha)-induced human leucocyte antigen -DR, human leucocyte antigen-DP and HLA-DQ antigens expression on monocytes was significantly down-regulated by calcitriol, IL-10 and transforming growth factor-beta (TGF-beta).","9135559:1",2,1,null,"negative"]
["HSPB1 ---| CASP8","Expression","Similarly, downregulation of Hsp27 caused a significantly enhanced the expression of apoptotic factors (caspase 8, caspase 3) and cytokines (bmp 15 and gdf 9).","20465849:11",2,1,null,"negative"]
["SOCS3 ---| OAS1","Expression","Our results demonstrate that SOCS-1 and SOCS-3 proteins inhibit IFN-alpha-induced activation of the Jak-STAT pathway and expression of the antiviral proteins 2',5'-OAS and MxA.","15240148:8",2,1,null,"negative"]
["ANGPT1 ---| CASP8","Expression","Angiopoietin-1 could decrease the expression of Bax, caspase3 and 8, and increase that of Bcl-2.","16701012:9",2,1,null,"negative"]
["DBI ---| CCND1","Expression","At the molecular level, ACBP induced p16Ink4, p21Waf1, p27Kip1, and bax tumor suppressor and apoptotic gene expression, as well as inhibited cyclin D1, c-myc, and bcl-2 gene expression that promote tumorigenesis.","19956858:4",2,1,null,"negative"]
["PTPRC ---| PTGS1","Expression","Anti-CD45 IgG F(ab')(2) up-regulated LTA(4) hydrolase mRNA expression and LTB(4) production, but down-regulated cyclooxygenase type 1 and COX-2 mRNA expression and PGE2 production, of naïve mononuclear cells compared to non-specific IgG F(ab')(2).","16673151:6",2,1,null,"negative"]
["HSPB1 ---| CCND1","Expression","We previously reported that overexpression of HSP25 delayed cell growth, increased the level of p21(waf), reduced the levels of cyclin D1, cyclin A and cdc2, and induced radioresistance in L929 cells.","11965498:0",2,1,null,"negative"]
["HSPB1 ---| CD86","Expression","However, HSP-27 treatment during monocyte differentiation to DC increased programmed cell death ligand 1 coinhibitor and depressed CD86 costimulator expression in parallel to decreased immature DC MLR activity.","17823891:5",2,1,null,"negative"]
["CEBPD ---| CCND1","Expression","CCAAT/enhancer-binding proteind may influence cyclin D1 levels by acting as a transcriptional repressor of cyclin D1 in G0 growth-arrested mammary epithelial cells.","10347224:341",2,1,null,"negative"]
["TGFB1 ---| HSPB1","Expression","Analysis of CAT activity showed that TGF-beta1 strongly suppressed promoter activity of Hsp27 and alphaB-crystallin (Fig. 9A)., The TGF-beta1-induced down-regulation of LEDGF, Hsp27, and alphaB-crystallin promoters activity was reversed by cotransfection with a plasmid expressing LEDGF., Surprisingly, TGF-beta1 treatment for 48 h markedly decreased the LEDGF, Hsp27, and alphaB-crystallin promoter activities with the decrease of abundance of LEDGF mRNA and protein., To determine that platelet-derived growth factor, IL-1ß, and TGFß induce phosphorylation of HSP27 in vivo through the p38mitogen-activated protein kinase pathway in migrating cells, we labeled cells using H3[32P]O4. <more data available...>","12649267:301, 12649267:50, 12649267:46, 10446196:195, 10446196:271, 15247230:211",2,6,null,"negative"]
["STAT1 ---| Iigp1","Expression","Together these studies indicate that although basal expression of IGTP, LRG47, TGTP, and IRG47 is independent of STAT1, the ability of IFN-gamma to up-regulate IGTP, IIGP, and TGTP is completely dependent on the activation of STAT1., Additionally, in the absence of STAT1, the infection-induced expression of the IFN-gamma-inducible GTPases, TGTP and IIGP, was not observed, whereas the expression of IGTP, IRG47, and LRG47 was shown to be partially independent of STAT1.","14688355:197, 14688355:65",2,2,null,"negative"]
["TGFBR2 ---| TLR2","Expression","Moreover, overexpression of a dominant negative mutant of TßRII also inhibited nontypeable Hemophilus influenzae-induced TLR2 up-regulation, whereas overexpression of a wild-type TßRII enhanced it (Fig. 1B)., Furthermore, overexpression of a dominant negative mutant of either TßRI or TßRII inhibited TGF-ß1-induced SBE activity (Fig. 1F, top) and nontypeable Hemophilus influenzae-induced TLR2 transcription in wild-type Mv1Lu cells (Fig. 1F, bottom), respectively, whereas overexpressing wild-type TßRI and TßRII rescued their responsiveness to either TGF-ß1 (Fig. 1F, top) or nontypeable Hemophilus influenzae (Fig. 1F, bottom) in R1B and DR26 cells, respectively.","16754688:151, 16754688:163",2,2,null,"negative"]
["CSF1 ---| CD14","Expression","As expected, CD14 expression was reduced upon neutralization of either IL-6 or M-CSF, implying Mesenchymal stem cells could retain the monocyte or macrophage immunophenotype (CD14) via M-CSF or/and IL-6, but the soluble factors through which Mesenchymal stem cells offset CD1a+ dendritic cell commitment driven by GM-CSF/IL-4 may need further evaluation.","15692068:242",2,1,null,"negative"]
["CD9 ---| CD14","Expression","CD14 expression and its association with TLR4 are enhanced in CD9 knockout macrophages ., The expression of CD14, complex formation of CD14 and TLR4, and their localization into the lipid raft are enhanced in CD9 knockout bone marrow-derived macrophages.","19414803:207, 19414803:213",2,2,null,"negative"]
["C3 ---| SOX9","Expression","Here, we show that SOX9 is up-regulated by a-MSH but is down-regulated by ASP in human melanocytes., SOX9 protein expression was decreased significantly in normal human epidermal melanocytes after treatment with ASP., RNAs then were extracted, and with RT-PCR, we showed that the expression level of SOX9 was decreased 4 h after ASP treatment compared with nontreated cells (Fig. 5 A)., SOX9 is down-regulated by ASP. (A) Expression levels of SOX9 gene using RT-PCR in neonatal moderately pigmented normal human epidermal melanocytes untreated (basal) or treated with ASP (10 nM) for 4 h. ß-actin expression served as a control.","17702866:255, 17702866:132, 17702866:120, 17702866:126",2,4,null,"negative"]
["KLK6 ---| TGFB1","Expression","Construction of the KLK6 interactome revealed that KLK6 might act via the transforming growth factor-ß1 pathway to reduce transforming growth factor-ß1 levels by degrading the extracellular protein fibronectin ( 40).","19383923:296",2,1,null,"negative"]
["STAT3 ---| CD86","Expression","The SOCS3 knock down macrophages have enhanced STAT3 activity that is associated with an increase in the M2a activation associated molecules mannose receptor, arginase and indeed SOCS1; decreased expression of the proinflammatory mediators IL-6 and NO and the costimulatory molecule CD86; and restored responsiveness of these cells to the anti-inflammatory effects of IL-4.","18424750:277",2,1,null,"negative"]
["STAT1 ---| CD86","Expression","Although STAT1 inhibits CD86 expression in cells at the precursor DC stage, its inhibitory effects are overridden in mature DCs, presumably by maturation signals, such as LPS (Fig. 5B).","14764699:258",2,1,null,"negative"]
["CSF1 ---| TLR2","Expression","CSF-1 also down-regulated expression of TLR1, TLR2, and TLR6, but not the LPS receptor, TLR4, or TLR5., The effect of CSF-1 was most pronounced on TLR9 expression (20-fold or greater reduction), but the moderate suppression of TLR2 and TLR6 mRNA levels by CSF-1 (4- to 5-fold) implies that responses to bacterial lipopeptides, peptidoglycan, and other TLR2 agonists might also be modulated by CSF-1.","11751985:57, 11751985:221",2,2,null,"negative"]
["SERPINA3 ---| GFAP","Expression","However, the down-regulation of other NFI isoforms did not effect expression of either a1-antichymotrypsin or GFAP, with the exception of the knock down of NFI-C, which down-regulated GFAP expression by 40%.","16565071:217",2,1,null,"negative"]
["FCGR2B ---| CD86","Expression","Thus, the absence of Fc?RIIB enhanced the expression of B7-1, B7-2, and MHC class II in the lungs of mice with tuberculosis as well as amplified the IL-12p40 response of M. tuberculosis-infected macrophages.","18292558:152",2,1,null,"negative"]
["TGFB1 ---| RAPGEF3","Expression","The ability of transforming growth factorß1 to inhibit expression of Epac1 provides an example of cross-talk between tyrosine kinase receptors and G protein-coupled receptor that occurs at a more distal site in the G protein-coupled receptor signaling pathway that is different than previously noted (30)., Our results, which show that transforming growth factorß1 decreases Epac1 expression in fibroblasts from multiple tissues, are akin to data indicating a similar decrease in Epac1 mRNA expression in U937 monocytic cells (18): transforming growth factorß-mediated inhibition of Epac expression may thus be a widespread mechanism for controlling responses to mitogens.","18434542:160, 18434542:142",2,2,null,"negative"]
["TGFB1 ---| CEBPD","Expression","Transforming growth factor-ß1 inhibits CCAAT/enhancer-binding protein-d expression and Smad3 interacts with CCAAT/enhancer-binding protein-ß., Interestingly, although Transforming growth factor-ß1 can inhibit interleukin-1ß-induced expression of CCAAT/enhancer-binding protein-d, there is minimal effect on CCAAT/enhancer-binding protein-ß.","14754879:200, 14754879:235",2,2,null,"negative"]
["TGFB1 ---| CASP8","Expression","Rather, TGF-ß down-regulated caspase-8 expression., TGF-ß down-regulates the expression of surface Fas and caspase-8 ., We demonstrated that TGF-ß exerts a strong anti apoptotic effect by inhibiting surface Fas as well as caspase-8 expression in HK cells., In this study, we report that TGF-ß inhibits Fas-mediated apoptosis of HK cells by down-regulating the expression of surface Fas and caspase-8., In fact, a recent report has shown that in human dermal fibroblasts, TGF-ß inhibits Fas-mediated apoptosis partly by decreasing the caspase-8 level (29).","15879113:241, 15879113:140, 15879113:233, 15879113:41, 15879113:245",2,5,null,"negative"]
["NFATC1 ---| CEBPA","Expression","Taken together, these data suggest that sustained activation of the NFATc1 signaling pathway inhibits the differentiation of 3T3-L1 cells into mature adipocytes by preventing the expression of the critical proadipogenic transcription factors PPARgamma and C/EBPalpha., This notion is further supported by our observation that ectopic expression of a constitutively active NFATc1 mutant also inhibits the MDI-induced differentiation of 3T3-L1 cells by preventing the expression of PPARgamma and C/EBPalpha, although this may be secondary to a transforming effect of NFATc1 in these cells.2 Experiments are currently under way to further delineate the role of calcineurin in the regulation of adipocyte differentiation.","12598522:131, 12351639:197",2,2,null,"negative"]
["TGFBR1 ---| CEBPA","Expression","Incubation with the Alk5 inhibitor decreased phospho-Smad3 (Fig. 4A), increased PPAR?, C/EBPa, and aP2 expression, and blocked the inhibitory effects of myostatin on each of these adipocyte markers (Fig. 4B).","18203713:190",2,1,null,"negative"]
["SOCS3 ---| A2M","Expression","SOCS1 and SOCS3 are potent inhibitors of a2-macroglobulin gene promoter activation.Human hepatoma cells (HepG2) were transfected with expression vectors coding for the EpoR/gp130 chimeric receptor protein (pRcCMV-EG(YYYYYY)) (2 µg), for the indicated suppressors of cytokine signaling/CIS proteins (4 µg), and an a2-macroglobulin promoter-luciferase reporter gene construct (pGL3a2M-215Luc) (2 µg).","10777583:135",2,1,null,"negative"]
["IFIH1 ---| CXCL10","Expression","Indeed, silencing of RIG-I, of its signaling adapter Cardif, and of both RIG-I and MDA-5 abolished IP10 production after stimulation with in vitro transcription 2.2 RNAs and clone 1 highlighting the requirement of RIG-I for recognition (Fig. 2F).","19470479:100",2,1,null,"negative"]
["LGALS1 ---| CCND1","Expression","Furthermore, we did not detect a significant galectin-1-dependent reduction of cyclin D1 or Cdk4 expression (Fig. 5A).","16105842:202",2,1,null,"negative"]
["TGFB1 ---| FCER1G","Expression","Recently, Tridandapani et al. (24) demonstrated that TGF-ß1 could inhibit FcR ?-chain expression on myeloid cells and monocytes.","15879091:258",2,1,null,"negative"]
["TRIM5 ---| CASP1","Expression","Similarly with ATP, knockdown of TRIM30 increased caspase-1 activation and IL-1ß production triggered by other NLRP3 inflammasome agonists, including nigericin, monosodium urate, and silica.","21048113:4",2,1,null,"negative"]
["TGFB1 ---| SOCS3","Expression","TGF-beta inhibits IL-6-induced SOCS3 promoter activity in T cells., In this report, we demonstrate that TGF-beta inhibits IL-6- and IL-21-induced SOCS3 expression, thus enhancing as well as prolonging STAT3 activation in naive CD4(+)CD25(-) T cells., These data suggest that the therapeutic effect of Flt3-L in reversing the hallmarks of allergic asthma in a mouse model is mediated by decreasing IL-6 and transforming growth factor-ß levels in the bronchoalveolar lavage fluid, which, in turn, decrease CD4(+)IL-17(+)IL-23R(+)receptor-?t(+)CD25(-) T cells and the expression of SOCS-1 and SOCS-3 in the lung of house dust mite-sensitized and -challenged mice.","19535626:4, 19535626:3, 19933379:10",2,3,null,"negative"]
["ISG15 ---| CCND1","Expression","The UBE1L-ISG15 pathway was proposed previously to target lung carcinogenesis by inhibiting cyclin D1 expression., Thus, a mechanism for UBE1L-mediated growth suppression was found by UBE1L-ISG15 preferentially inhibiting cyclin D1.","19074853:1, 19074853:13",2,2,null,"negative"]
["LGALS3 ---| CCND1","Expression","Finally, we demonstrated that silencing of galectin-3 enhanced apoptosis induction with chemotherapeutic agents by further reducing the expression of anti-apoptotic and/or cell survival molecules such as survivin, cyclin D1, and XIAP, and increasing the expression of pro-apoptotic XAF-1.","19843071:10",2,1,null,"negative"]
["TGFBR2 ---| TGFBR1","Expression","However, promoter activity of TGF-beta RI is decreased to a greater extent than TGF-beta RII as HKc/human papillomavirus type 16 progress to HKc/DR.","19344999:5",2,1,null,"negative"]
["LGALS1 ---| TGFB1","Expression","We demonstrated that overexpression of galectin-1 reduces type I collagen (COL1) expression and transcription in human renal epithelial cells under high glucose conditions and transforming growth factor-ß1 (TGF-ß1) stimulation.","20828557:2",2,1,null,"negative"]
["SELPLG --+> ITGB2","Expression","The overexpression of PSGL-1-enhanced beta2-integrin expression on endothelial progenitor cells surface, and this effect was Syk dependent., These data demonstrate that the PSGL-1 cytoplasmic domain is dispensable for leukocyte rolling on P-selectin but is essential to activate beta2 integrins to slow rolling on ICAM-1., The engagement of PSGL-1 increased the expression of beta(2)-integrin on the surface of neutrophils and enhanced the adhesion of neutrophils to the recombinant ICAM-1. monoclonal antibodies against CD18 impaired the adhesion of PSGL-1-engaged neutrophils to ICAM-1. <more data available...>","20705591:5, 18550846:8, 16626518:6, 17442598:1326, 15217824:1064, 17204662:1067",2,6,null,"positive"]
["SELPLG --+> CSF1","Expression","Our present work showed antibody engagement of PSGL-1 upregulated the transcriptional activity of CSF-1 promotor and increased the endogenous expression of CSF-1 mRNA in Jurkat cell.","16289055:2",2,1,null,"positive"]
["SELPLG --+> LYN","Expression","P-selectin-P-selectin-P-selectin glycoprotein ligand-1-induced tissue factor and IL8 expression through Lyn phosphorylation, and part of the inhibitory effect of IL10 depends on reduced phosphorylation.","18363812:11",2,1,null,"positive"]
["SELPLG --+> FCGR2A","Expression","In addition, anti-P-selectin glycoprotein ligand-1 antibody reduced the expression of CD11b, CD32, and CD33 in THP-1 after Platelet-derived microparticle stimulation.","11583705:11",2,1,null,"positive"]

{"sheet":"Global network","index":1,"n_rows":169,"n_cols":8,"rows_kept":169,"flags":["formulas_cached_only"]}
["AIF1 --+> GFAP","Expression","Following paw incision and at spinal L5 segment GFAP expression was increased in laminae I-II and Iba1 in deep laminae on day 1, in the entire dorsal horn on day 4 and dissipated on day 7 after paw incision in parallel with the allodynia.","18538310:6",2,1,null,"positive"]
["AIF1 --+> CCND1","Expression","In contrast, the down-regulation of daintain/AIF-1 expression decreased cyclin D1 expression and inhibited the transcriptional activity of nuclear factor-kappa B.","18341653:7",2,1,null,"positive"]
["AIF1 --+> CD68","Expression","human microglia cell line clone 3 cells are typical microglia, as suggested by the constitutive expression of Iba-1 and CD14, and IFN-gamma-induced expression of CD11b, CD68 and MHCII.","20375612:3",2,1,null,"positive"]
["ANGPT1 --+> CCND1","Expression","angiopoietin1 up-regulated the expression of cyclin D1 in both of these cells.","16061664:5",2,1,null,"positive"]
["ANGPT1 --+> APLN","Expression","angiopoietin 1 induces apelin expression on ECs .","18200044:1080",2,1,null,"positive"]
["APLN --+> CCND1","Expression","Apelin-13 also increased the levels of cyclin D1, cyclin E and pERK1/2., The Akt inhibitor 1701-1 significantly diminished the expression of phospho-Akt, phospho-ERK1/2, and cyclin D1 stimulated by apelin-13.","18508473:6, 20539939:4",2,2,null,"positive"]
["AQP4 --+> SLC14A1","Expression","In aging brain, UT-B1 abundance was increased twofold together with a fourfold increase in aquaporin-4 abundance.","12933359:8",2,1,null,"positive"]
["AQP4 --+> GFAP","Expression","Likewise, AQP4 deficiency significantly downregulated expression of glial fibrillary acidic protein in perivascular processes of astrocytes., The abundance of GFAP, the usual marker of astrocytes and ependymal cells, was increased by 25% with age (data not shown), a variation much smaller than the doubling in UT-B1 or the fourfold increase in AQP-4.","18281883:2, 12933359:1196",2,2,null,"positive"]
["AXL --+> SOCS3","Expression","In this issue, Rothlin et al. (2007) uncover a complex negative feedback mechanism to limit Toll-like receptor signaling involving the Tyro3/Axl/Mer family of receptor tyrosine kinases, which induce expression of the inhibitory proteins SOCS1 and SOCS3.","18083093:1",2,1,null,"positive"]
["B2M --+> TGFB1","Expression","AGE-beta2m also induced TGF-beta1 production by macrophages in a dose-dependent manner (410 +/- 80 pg/mL at 12.5 microg/mL, 621 +/- 62 pg/mL at 25 microg/mL, and 776 +/- 62 pg/mL at 50 microg/mL of AGE-beta2m).","10652049:6",2,1,null,"positive"]
["B2M --+> CCND1","Expression","Cyclin D1 and cyclin D2 transcripts are strongly induced by epidermal growth factor, and beta 2-microglobulin transcripts are strongly induced by TGF-beta in BALB keratinocytes released from quiescence by addition of epidermal growth factor.","8845303:4",2,1,null,"positive"]
["C1QA --+> C3","Expression","Production of complement C3 by Mphi is stimulated by C1q strongly, while the effect of mannan-binding lectin is much weaker.","10898508:6",2,1,null,"positive"]
["CCND1 --+> HSPB8","Expression","The transient transfection with cyclin D1 increased HSPB8 levels ~2-fold when these blots were quantified in image analysis; the HSPB8 knockdown was ~8-fold in each case.","18006821:1234",2,1,null,"positive"]
["CD14 --+> CD86","Expression","In contrast, immature dendritic cells cultured in G4 plus human pancreatic RNase or eosinophil-derived neurotoxin for 48 h, although still CD14-, up-regulated the surface expression of CD83, CD86, and HLA-DR, indicating that human pancreatic RNase and eosinophil-derived neurotoxin treatment induced phenotypic maturation of DCs (Fig. 7A).","15528350:1252",2,1,null,"positive"]
["CD14 --+> CD83","Expression","In contrast, immature dendritic cells cultured in G4 plus human pancreatic RNase or eosinophil-derived neurotoxin for 48 h, although still CD14-, up-regulated the surface expression of CD83, CD86, and HLA-DR, indicating that human pancreatic RNase and eosinophil-derived neurotoxin treatment induced phenotypic maturation of DCs (Fig. 7A).","15528350:1252",2,1,null,"positive"]
["CD14 --+> ITGAX","Expression","Treatment of U937 cells with PMA markedly increased CD14, CD11a, CD11b and CD18 antigen expression, and slightly increased CD11c expression., In particular, those for CD11c and tumor necrosis factor a (TNFa) were markedly increased, and there were lesser, but significant, increases in Spp1, CD14, CD45, CCL9, Toll-like receptor 4 (TLR4), and interleukin-1B (IL-1ß) (Fig. 6G,H).","1689274:1, 18160655:1251",2,2,null,"positive"]
["CD14 --+> CD68","Expression","human microglia cell line clone 3 cells are typical microglia, as suggested by the constitutive expression of Iba-1 and CD14, and IFN-gamma-induced expression of CD11b, CD68 and MHCII.","20375612:3",2,1,null,"positive"]
["CD151 --+> CD9","Expression","Interestingly, cell surface expression of CD9 was significantly reduced on isolated CD151-null keratinocytes compared to wild-type cells when examined by quantitative immunofluorescence and flow cytometry (Fig. 5), possibly reflecting the requirement for CD151 for CD9 incorporation into these integrin complexes (40).","15199151:1325",2,1,null,"positive"]
["CD44 --+> MET","Expression","CD44 isoforms bearing heparin sulfate chains can bind to HGF/SF and facilitate its presentation to c-Met., A blocking antibody to CD44v6 decreased HGF-induced c-Met phosphorylation as well as enhanced random- and site-directed migration., In this paper, we demonstrate that the activation of c-Met induced by InlB is dependent on CD44v6, a member of the CD44 family of transmembrane glycoproteins., In several types of cells, the activation of the receptor tyrosine kinase c-Met by its ligand hepatocyte growth factor (HGF) requires the coreceptor CD44v6. <more data available...>","12670907:1, 20357818:6, 19432801:3, 17065554:0, 17923692:2, 12183053:4, 10485493:1212",2,7,null,"positive"]
["CD44 --+> TGFB1","Expression","CD44 costimulation increased production of IL-10 in a partially IL-2-dependent manner and also promoted cell surface TGF-beta expression., Mechanistically, we demonstrate that CD44WT cells generated more active TGFbeta than CD44KO cells and that CD44 promotes the activation of TGFbeta via an MMP-dependent mechanism., We previously demonstrated in renal proximal tubular cells that the engagement of the extracellular polysaccharide hyaluronan with its receptor CD44 attenuated TGF-beta1 signaling., Gelatine zymography and immunofluorescent stain evidenced that elevated MMP-2 and MMP-9 activity and serum-dependent CD44 expression and its membranous localization may contribute to TGF-beta1 activation. <more data available...>","19635906:4, 18397995:3, 15084590:1, 19457680:7, 15574511:12, 15387373:2",2,6,null,"positive"]
["CD44 --+> VIM","Expression","Serial transplantation of elongated epithelial cells results in progressive loss of tumorigenic potential; tumor heterogeneity; CD44, E-cadherin, and epithelial cytokeratin expression and increased alpha-smooth muscle actin I and vimentin expression.","18957543:2",2,1,null,"positive"]
["CD74 --+> CCND1","Expression","CD74 up-regulates expression of cyclin D and cyclin E in HEK293 cells (Fig. 5C)., Our studies document that inhibition of the MIF and/or CD74 decreases cyclin D1 gene expression.","18941249:1274, 17142775:1398",2,2,null,"positive"]
["CD74 --+> CD86","Expression","In addition, overexpression of CD74 by mRNA electroporation in Dendritic cells increased the cell surface expression of CD80/CD86 and major histocompatibility complex class II.","18003616:1308",2,1,null,"positive"]
["CD83 --+> CD86","Expression","However, the increase in surface expression of HLA-DR and CD86 after addition of LPS was significantly attenuated in cord DCs, with CD25 and CD83 expression also markedly reduced., Specifically, IRX-2-treated DC increased expression of CD83 and CCR7, markers for DC maturation and migration, respectively, and increased the expression of HLA-DR, CD54, and the costimulatory molecules CD86 and CD40, which are critical mediators of T cell activation., Correlating with CD83 expression, the basic as well as the lipopolysaccharide induced expression of the activation markers CD86 and MHC-II are significantly increased in CD83transgenic B cells and reciprocally decreased in CD83 mutant B cells. <more data available...>","11982599:2, 17667526:4, 17710154:3, 17056542:1160, 17878352:1075",2,5,null,"positive"]
["CD86 --+> TGFB1","Expression","Blockage of costimulatory signal CD(86) at early pregnancy can treat uncertain recurrent spontaneous abortion by stimulating the expression of TGF-beta(1), MMP-9 and PAI-1 and reducing the embryo resorption rate., Activation of T cells with PMA and ionomycin together with CTLA4-CD80/CD86 blockade results in decreased induction of CD25 and Bcl-X(L), reduced interleukin -2, and enhanced transforming growth factor-beta (TGF-beta) production., However, whether and how these B7-1 (CD80), B7-2 (CD86), and/or B7x ((3), (5), (15), (36)) molecules contribute to TGF-ß production by engaging CTLA-4 signaling remain to be determined. <more data available...>","17697576:14, 12429713:5, 9815262:1210, 10619862:1300",2,4,null,"positive"]
["CEBPA --+> CSF1","Expression","For example, when expressed alone, RUNX1, C/EBPa, and PU.1 are poor activators of the M-CSF promoter.","15988004:1056",2,1,null,"positive"]
["CEBPA --+> PROS1","Expression","Reporter gene analysis suggests that members of the CCAAT/enhancer binding protein (C/EBP) family of transcription factors are potent activators of protein S gene transcription in HepG2 cells.","17061980:6",2,1,null,"positive"]
["CEBPA --+> CASP8","Expression","These findings indicate that C/EBPalpha or its oncoproteins activate the bcl-2 and FLICE inhibitory protein genes by tethering to their promoters through bound NF-kappaB p50.","18987666:8",2,1,null,"positive"]
["CEBPD --+> CEBPA","Expression","Previous investigations indicated that transcription of the C/EBPalpha gene is sequentially activated during differentiation, initially by C/EBPbeta and C/EBPdelta and later by C/EBPalpha (autoactivation)., Nuclear expression of the 36-kilodalton C/EBP delta protein increases immediately after birth, followed first by increases in the 38-kilodalton C/EBP beta protein expression and then by increases in the 42-kilodalton C/EBP alpha protein expression., These data demonstrate that Myc specifically inhibits the terminal stages of the adipogenic program and suggest that Myc may act by blocking C/EBPbeta- and C/EBPdelta-directed activation of C/EBPalpha and PPARgamma2 expression, although the precise molecular mechanism is not understood. <more data available...>","10373535:1, 7910803:4, 10623469:4, 18703634:1194, 18930917:1043, 18653467:1203, 12138207:1046, 12186946:1140, 16154099:1059, 17273556:1253 <more data available...>",2,43,null,"positive"]
["CEBPD --+> TF","Expression","In the non-transferrin-expressing HeLa cells, the transferrin promoter could be activated by C/EBP-delta., Suire et al. (12) showed, in cotransfection assays, that overexpression of C/EBP alpha (C/EBP) and C/EBP delta (NF-IL6beta, CRP3) in Sertoli cells stimulated transcription from the cAMP-regulated transferrin promoter containing a C/EBP binding site.","8226864:7, 9927313:1054",2,2,null,"positive"]
["CEBPD --+> CCND1","Expression","Silencing of C/EBPdelta, Cdc27, or the anaphase promoting complex/cyclosome coactivator Cdh1 (FZR1) in MCF-10A breast epithelial cells increased cyclin D1 protein expression.","20439707:3",2,1,null,"positive"]
["CEBPD --+> SOCS3","Expression","The doxycycline-dependent expression of C/EBP-d neither increased Spi-2 and Socs3 transcripts nor interfered with their induction by IL6RIL6 (Fig. 5B).","14600146:227",2,1,null,"positive"]
["CHI3L1 --+> SOX9","Expression","HC-gp39 induced both SOX9 and type II collagen synthesis.","16949314:5",2,1,null,"positive"]
["CLEC5A --+> NFATC1","Expression","We also demonstrate that MDL-1 activation increases the expression of NFATc1 and ATPV0D2, which control cell fusion (Lee et al., 2006), as well as regulating bone resorption via TRAP and cathepsin K in osteoclasts (Takayanagi, 2005a).","20212065:226",2,1,null,"positive"]
["CSF1 --+> NFATC1","Expression","Furthermore, anti-CD11b antibodies inhibited NFATc1 expression induced by M-CSF and RANKL in BMMs., S3 shows the normal osteoclast differentiation and expression of NFATc1 in NFATc2-/- monocyte/macrophage precursor cells that were stimulated with RANKL/M-CSF., Inhibition of c-Fos and NFATc1 expression induced by RANKL and M-CSF in RAGE-deficient prefusion osteoclasts To further understand how RAGE regulates osteoclast maturation and function, we examined expression of transcriptional factors essential for osteoclastogenesis, including c-Fos and NFATc1 (39, 40). <more data available...>","18775427:4, 16275763:1202, 16606672:1165, 17403683:264",2,4,null,"positive"]
["CSF1 --+> CEBPA","Expression","Ectopic expression of THOC5 mimicked M-CSF mediated cell maturation and enhanced protein expression of the myeloid transcription factors C/EBPbeta, C/EBPalpha, Pu-1 and also GAB2 (a PI-3 Kinase and macrophage development regulator)., M-CSF and G-CSF use separate pathways to activate ERK and modify C/EBPa .","19015024:4, 19587381:1161",2,2,null,"positive"]
["CSF1 --+> CCND1","Expression","Previously we showed that the macrophage-activating agent lipopolysaccharide blocks CSF-1-induced proliferation and cyclin D1 expression in macrophages., We further demonstrated that Cdc42 modulated M-CSF-stimulated cyclin D expression and phosphorylation of Rb and induced caspase 3 and Bim, thus contributing to osteoclast proliferation and apoptosis rates., In contrast to some other growth factor/cell systems, no evidence was obtained using the inhibitors for the involvement of PI3-kinase or p70s6k in CSF-1-mediated induction of c-fos mRNA expression or Erk-1 activity; in addition, no evidence was found for an involvement in the CSF-1-mediated increase in cyclin D1 expression or STAT activation. <more data available...>","9722538:2, 20501942:5, 9608681:6, 10602507:1124, 1483347:100, 9139801:1201, 10453356:1406, 17142780:1172, 11230342:1041, 9722538:50 <more data available...>",2,19,null,"positive"]
["CSF1 --+> CD14","Expression","It has been demonstrated that the expression of CD16 and CD14 is regulated by macrophage colony stimulating factor (M-CSF) and GM-CSF., M-CSF was also shown by flowcytometric analysis to influence the expression of CD14, a receptor for LPS, which might render monocytes more sensitive to LPS., Daily administration of macrophage colony stimulating factor (M-CSF) to the mice resulted in increased levels of MSR-A expression and reduced levels of CD14 as well as several cytokine expressions, leading to shortening of the inflammatory process. <more data available...>","12153694:6, 8877404:9, 10594845:5, 9566797:4, 15256426:1265",2,5,null,"positive"]
["CSF1 --+> CYBB","Expression","Consistent with this, we find that expression of gp91phox and p67phox protein is also increased by M-CSF differentiation in Western blots of cell lysate proteins (Fig. 1C)., Of interest to the current studies, HoxA9 overexpression in murine myeloid cells does not impair granulocyte-colony stimulating factor- or macrophage-colony stimulating factor-induced expression of gp91Phox, a phagocyte respiratory burst oxidase protein (4).","16210632:1196, 15681849:71",2,2,null,"positive"]
["CSF1 --+> TREM2","Expression","Addition of macrophage colony stimulating factor (M-CSF) to LN cell culture allowed the proliferation and expression of TREM2 in LN cells, and the addition of neutralizing anti-M-CSF antibodies suppressed the proliferation of LN cells despite the expression of TREM2., Whereas Humphery et al. recently reported that TREM-2 expression is induced during in vitro osteoclastogenesis induced by culture bone marrow-derived macrophages with macrophage CSF (MCSF) and the receptor activator of NF-?B ligand (4), we find that differentiation of macrophages in MCSF alone leads to expression of TREM-2. [Figure 3] View larger version (33K): [in this window] [in a new window] .","20345919:4, 16951310:1159",2,2,null,"positive"]
["CSF1 --+> SERPING1","Expression","Interferon-gamma and alpha , colony stimulating factor-1, interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) all induce C1-INH synthesis in a variety of cell types.","9777421:6",2,1,null,"positive"]
["CSF1 --+> TLR2","Expression","CSF-1 also down-regulated expression of TLR1, TLR2, and TLR6, but not the LPS receptor, TLR4, or TLR5., TLR-2 expression on monocytes was enhanced by macrophage colony-stimulating factor (M-CSF) and interleukin-10 (IL-10), but was reduced by transforming growth factor beta1, while CD16 expression was inducible by these cytokines., Toll-like receptor 2 and 4 surface expressions on human monocytes are modulated by interferon-gamma and macrophage colony-stimulating factor.","11751985:7, 15146415:10, 11672593:100",2,3,null,"positive"]
["CSF1 --+> C3","Expression","Macrophage colony-stimulating factor (M-CSF) enhances complement component C3 production by human monocytes/macrophages.","8477063:100",2,1,null,"positive"]
["CSF1 --+> ITGB2","Expression","The levels of CD11a and CD18 expression on granulocytes were significantly enhanced by administration of M-CSF.","11789672:6",2,1,null,"positive"]
["CSF1 --+> LGALS3","Expression","Macrophage colony-stimulating factor (M-CSF), which is present at increased levels in MRL/lpr mice, but not in MRL/Mp- +/+ mice, induced the expression of Mac-2 antigen and Fas antigen on spleen adherent cells of MRL/Mp- +/+ mice.","8870694:4",2,1,null,"positive"]
["CSF1 --+> TNFRSF1A","Expression","Cell surface expression of TNFR1/2 expression on monocytes was induced by IL-10, and more efficiently in combination with M-CSF.","16859503:4",2,1,null,"positive"]
["CSF1 --+> P2RX7","Expression","Furthermore, lipopolysaccharide and M-CSF could up-regulate P2X7 receptor expression in monocytes, while IFN-gamma, TNF-alpha and GM-CSF had weak effects, but pretreatment with these inducers could not further enhance lipopolysaccharide-stimulated P2X7 receptor expression in monocytes.","15830104:6",2,1,null,"positive"]
["CSF1 --+> CSF1R","Expression","However, after 48 h, M-CSF significantly stimulated c-Fms expression., IL-10 together with M-CSF increased the expression of M-CSF receptors., This treatment completely prevented M-CSF-induced c-Fms expression in a dose-dependent manner but had little effect on TNFa-induced c-Fms up-regulation (Fig. 5D)., Incubation with CSF-1 down-regulated CSF-1R expression and was associated with proliferation of mononuclear cells with decreased CSF-1R binding., We demonstrated that one mechanism by which this occurs is PU.1 down-regulation by the negative control of NFI-A on M-CSFR levels (Fig. 7) because M-CSF induces PU.1 expression through M-CSFR in the hematopoietic myeloid-osteoclast lineage (1-3). <more data available...>","16461346:213, 8978307:46, 16461346:221, 19819976:310, 19059913:261, 19628784:169",2,6,null,"positive"]
["CSF1R --+> PTPN6","Expression","Traumatic injury to the central nervous system activates microglia and strongly increases expression of SHP-1, which physically associates with and is activated by c-Fms in these cells (17).","12361947:312",2,1,null,"positive"]
["CTSD --+> ABCA1","Expression","Conversely, expression of CTSD increased both ABCA1 mRNA expression and cellular ABCA1 protein.","17032648:6",2,1,null,"positive"]
["CX3CR1 --+> TGFB1","Expression","CX3CR1 promotes TGF-ß1 expression and myofibroblast accumulation in wounded skin ., CX3CR1 promotes TGF-ß1 expression and activated fibroblast accumulation in wounded skin., These results suggest that CX3CR1 activity in vivo promotes TGF-ß1 production, which promotes accumulation of a-smooth muscle actin+-activated fibroblasts, which are the direct source of collagen, a key constituent of granulation tissue in skin wound repair. [Figure 10] View larger version (76K): [in this window] [in a new window] .","18097059:296, 18097059:303, 18097059:301",2,3,null,"positive"]
["CXCL10 --+> ISG15","Expression","Consistent with this finding, Respiratory syncytial virus-induced beta interferon (IFN-beta), interferon-inducible protein 10 (IP-10), chemokine ligand 5 (CCL-5), and IFN-stimulated gene 15 (ISG15) expression levels were decreased in RIG-I-silenced cells during the early phase of infection but not at later times (18 h postinfection).","17108032:5",2,1,null,"positive"]
["CXCL14 --+> CD86","Expression","Fig. 5 shows that the addition of 200 ng/ml CXCL14 to dendritic cell markedly up-regulated expression of CD83, HLA-DR, CD86, and CD80 molecules when compare with CXCL14-untreated dendritic cell.","15843547:292",2,1,null,"positive"]
["CXCL14 --+> CD83","Expression","Fig. 5 shows that the addition of 200 ng/ml CXCL14 to dendritic cell markedly up-regulated expression of CD83, HLA-DR, CD86, and CD80 molecules when compare with CXCL14-untreated dendritic cell.","15843547:292",2,1,null,"positive"]
["CYBA --+> CYBB","Expression","Small interference RNA for p22(phox) prevented glycated low-density lipoprotein-induced expression of NOX2, HSF1, and PAI-1 in endothelial cells.","20630999:9",2,1,null,"positive"]
["FCGR2A --+> CD14","Expression","We found 1) increased FMLP receptor and decreased C5a receptor expression, 2) a normal expression of intracellular FMLP receptors after incubation with PMA, 3) increased loss and decreased re-expression of FMLP receptors after incubation with this peptide, 4) normal expression of adhesion glycoproteins CR3 (CD11b/CD18) and LFA1 (CD11a/CD18), 5) further signs of in vivo preactivation: high expression of Fc gamma-RI (CD64) and Fc gamma-RII (CD32), decreased expression of Fc gamma-RIII (CD16), increased expression of CD14, and low expression of HLA-DR.","1370419:3",2,1,null,"positive"]
["FLI1 --+> TGFBR2","Expression","Introduction of EWSR1-FLI1 into cells lacking the EWSR1-FLI1 fusion suppresses TGF-beta RII expression, whereas antisense to EWSR1-FLI1 in ES cell lines positive for this gene fusion restores TGF-beta RII expression., Regulation of the TGF-ß RII promoter by EWS-FLI1, FLI1, dnFLI1, EWS-ERG, ERG, dnERG, EWS-ETV1, ETV1, and dnETV1., The ERT (also called ESX/ESE-1) regulates the expression through the Z element (10) , whereas another ets family gene FLI1 fused with the EWSR1 gene down-regulates the Transforming growth factorßRII expression in Ewing sarcomas (11) .","10508522:7, 10749119:1136, 11719467:1050",2,3,null,"positive"]
["GFAP --+> VIM","Expression","As for GFAP, increased lesion-induced up-regulation of vimentin expression is also already apparent at 1 dpl, with knock-out animals showing higher expression than wild-type animals (Fig. 5b).","12843240:1209",2,1,null,"positive"]
["GFAP --+> APOD","Expression","ApoD levels increased by 35% in the peri-infarct area after 10 and 30 days after pMCAO, mainly in neuron-specific nuclear protein (NeuN) positive neurons and glial fibrillary acidic protein (GFAP) positive astrocytes.","20083089:4",2,1,null,"positive"]
["GFAP --+> MET","Expression","Both Nf1(GFAP)CKO and wild-type astrocytes induced MET expression in neurites of wild-type hippocampal neurons in vitro, suggesting that astrocyte-derived signals may induce MET in Nf1 mutant mice.","17348023:5",2,1,null,"positive"]
["GRN --+> CCND1","Expression","In these cells, PCDGF/GP88 was shown to mediate the mitogenic activity of estrogen by stimulating cyclin D1 expression (20) ., granulin/epithelin precursor leads to activation of the mitogen-activated protein kinase pathway and to stimulation of cyclin D1 protein expression., Effect of PCDGF on cyclinD1 and c-myc expression in MCF-7 cells. (A) Stimulation of cyclin D1 expression by PCDGF., PCDGF in a time-dependent fashion stimulated cyclin D1 expression in MCF-7 cells, reaching a maximum of 4-fold over untreated controls after 5 h (Fig. 5 A). <more data available...>","14996734:66, 15653695:83, 11134521:212, 11134521:207, 11134521:254, 11134521:228, 11134521:220, 11134521:263",2,8,null,"positive"]
["HLA-B --+> HLA-E","Expression","The only exceptions were HLA-B*1302 and HLA-B*2705, which induced a low level of HLA-E surface expression despite having the inappropriate sequence (Table 1); this is being fully investigated.","9427624:1189",2,1,null,"positive"]
["HLA-C --+> CD86","Expression","We found that the expression level of co-stimulatory molecules, CD40, CD54, CD80, CD86 and CD11b, were elevated evidently, except CD11c, I-A(d) and H-2K(d).","20499643:4",2,1,null,"positive"]
["IRF8 --+> CSF1","Expression","Additionally, ICSBP expression in ICSBP-deficient cells rescues neurofibromin 1 expression, decreases ERK activation, and abolishes GM-CSF and M-CSF hypersensitivity (34).","16914719:1257",2,1,null,"positive"]
["IRF8 --+> CTSC","Expression","Consistent with the Interferon regulatory factor-8-dependent induction of these genes, expression of cystatin C, cathepsin C, and prosaposin transcripts was lower in Irf-8-/- cells than that in wild-type cells (data not shown).","15947094:1145",2,1,null,"positive"]
["ITGAX --+> CD86","Expression","We found that the expression level of co-stimulatory molecules, CD40, CD54, CD80, CD86 and CD11b, were elevated evidently, except CD11c, I-A(d) and H-2K(d)., As reported previously (24), bone marrow-derived macrophage-derived dendritic cells expressed high levels of CD11c, CD86, and I-Ab, and LPS up-regulated the expression of CD86 and I-Ab.","20499643:4, 19336404:170",2,2,null,"positive"]
["ITGB2 --+> TLR2","Expression","The anti-CD18 monoclonal antibody markedly reduced TLR2 expression in endothelial cells as induced by polymorphonuclear neutrophils.","14561708:1314",2,1,null,"positive"]
["LCN2 --+> GFAP","Expression","Third, the LCN2-induced GFAP expression was blocked by a nitric oxide synthase inhibitor NG-monomethyl-L-arginine (Fig. 8F,G)., Because LCN2 also induced GFAP expression in astrocytes in our study (Fig. 6), we next attempted to determine whether NO is involved in the LCN2 actions in astrocytes., Rho/ROCK pathway appeared to play a pivotal role in regard to LCN2 actions on astrocyte morphology, based on the following results: (1) a ROCK inhibitor, Y27632, partly blocked LCN2-induced morphological changes (Fig. 9A,B); (2) Y27632 also inhibited the LCN2-induced GFAP expression (Fig. 9C,D); and (3) LCN2 induced Rho activation in astrocytes (Fig. 9E). <more data available...>","19129400:366, 19129400:358, 19129400:384, 19129400:439",2,4,null,"positive"]
["LGALS1 --+> CD83","Expression","Furthermore, galectin-1 induced both CD83 and CD86 expression in a dose-dependent manner (Fig. 1D).","16785517:1209",2,1,null,"positive"]
["LGALS1 --+> CD86","Expression","Furthermore, galectin-1 induced both CD83 and CD86 expression in a dose-dependent manner (Fig. 1D)., Compared with eGFP-Dendritic cells, Galectin-1-Dendritic cells had enhanced levels of IAd, H2Kd, CD40, CD54, CD80, and CD86 expression (Fig. 4A)., Incubation of nontransduced Dendritic cells for 18 h with medium supplemented with 10 µM soluble human Galectin-1 induced an increase of IAd and CD86 expression similar to that triggered by recombinant adenovirus-Galectin-1 infection at a MOI of 50 (Fig. 4B).","16785517:1209, 16751364:260, 16751364:264",2,3,null,"positive"]
["LGALS1 --+> TGFB1","Expression","We demonstrate here that Recombinant galectin-1 treatment induces the production of substantial amounts of TGF-ß1 and IL-10, which in turn may be responsible for counterregulating the uveitogenic Th1 response.","16670344:282",2,1,null,"positive"]
["LGALS3 --+> CCND1","Expression","Recombinant galectin-3 induced cardiac fibroblast proliferation, collagen production, and cyclin D1 expression., Interestingly, galectin-3 induces cyclin D1 expression (an early G1 cyclin) and its associated kinase activity in the absence of cell anchorage., We found that galectin-3 induces cyclin D(1) promoter activity in human breast epithelial cells independent of cell adhesion through multiple cis-elements, including the SP1 and CRE sites., Finally, we demonstrated that silencing of galectin-3 enhanced apoptosis induction with chemotherapeutic agents by further reducing the expression of anti-apoptotic and/or cell survival molecules such as survivin, cyclin D1, and XIAP, and increasing the expression of pro-apoptotic XAF-1. <more data available...>","15520318:6, 10463621:6, 12439750:3, 19843071:10, 17403142:1279, 11062152:1156, 11724777:1188, 19190323:249, 15867344:44",2,9,null,"positive"]
["LGALS3 --+> TGFB1","Expression","Gal-3 increased transforming growth factor-ß1, -ß2, and -ß3 expression in left ventricle compared with vehicle group; Ac-SDKP inhibited this effect., Thus disruption of the Galectin-3gene blocks fibrosis despite similar expression levels of TGF-ß.","19098114:1203, 16549783:134",2,2,null,"positive"]
["LYN --+> MCL1","Expression","Inhibition of Lyn or rescue of miR181b expression reduced Mcl-1 expression in the MYL-R cells., Finally, stimulation of Lyn expression by 1,25-dihydroxyvitamin D(3) treatment in HL-60 cells, a cell model of acute myelogenous leukemia, decreased miR181b expression and increased Mcl-1 expression.","20693279:7, 20693279:10",2,2,null,"positive"]
["NCF1 --+> TLR2","Expression","Small inhibitory RNA to p47Phox in THP-1 cells abrogated high-glucose-induced TLR2 and TLR4 expression.","18650365:10",2,1,null,"positive"]
["NFATC1 --+> CCND1","Expression","Heit et al. showed that transgenic activation of NFATc1 in ß-cells induces proliferation by inducing Cyclin D and Cdk4 levels [23].","20689817:1266",2,1,null,"positive"]
["NFATC1 --+> ID3","Expression","Accordingly, we propose a model whereby early growth response1-NF-ATc1 cooperatively induces inhibitor of DNA binding 3 expression, which in turn promotes traversal of the ß-selection checkpoint by suppressing the activity of E proteins (54, 56, 68).","17878368:1298",2,1,null,"positive"]
["NFATC1 --+> PDPN","Expression","In vitro, endogenous and VEGF-A-induced VEGFR-3 and podoplanin expression by human microvascular endothelial cells was reduced by siRNA to NFATc1, to levels comparable to reductions seen with siRNA to Prox-1.","19233265:8",2,1,null,"positive"]
["NFE2L2 --+> FTL","Expression","The induction of GSTP1/2, GSTA4, and ferritin light chain mRNAs by butylated hydroxyanisole was decreased in the nrf2-null mouse liver, while the level of TXNRD1 was not changed much.","16135796:1104",2,1,null,"positive"]
["NFE2L2 --+> SLCO2B1","Expression","As shown in Fig. 4, expression of Oatp2b1 was decreased by PXR and PPARa ligands, and increased by AhR and Nrf2 activators.","15919853:1172",2,1,null,"positive"]
["NFE2L2 --+> GFAP","Expression","Although the Nrf2 knockout mice lacked severe astrogliosis in more than 80% of cases, there was consistent neuronal damage, although it should be noted that we cannot rule out the possibility that the loss of Nrf2 may directly interfere with GFAP expression in astrocytes.","16945104:1253",2,1,null,"positive"]
["NFE2L2 --+> PRDX6","Expression","Cotransfection with Nrf2 stimulated the Prdx6 promoter in an antioxidant-response element-dependent manner, whereas it was negatively regulated by Nrf3. siRNA targeting Nrf2 down-regulated reporter gene expression, whereas siRNA targeting the Nrf2 repressor, Keap1, up-regulated it.","18973804:4",2,1,null,"positive"]
["OAS1 --+> IRF9","Expression","Similar to expression of 2',5'-oligoadenylate synthetase, Mx, and IFN-stimulated gene17 [15, 17, 22], expression of Stat 1, Stat 2, IRF-9, and IRF-1 in the ovine endometrial S and glandular epithelium during early pregnancy was coordinate with temporal production of Interferon tau by the conceptus [2, 3].","11566724:1278",2,1,null,"positive"]
["P2RX7 --+> CASP1","Expression","We recently reported that P2X7 receptor (P2X7R)-induced activation of caspase-1 inflammasomes is accompanied by release of MHC class II protein into extracellular compartments during brief stimulation of murine macrophages with ATP., Furthermore, the production of IL-18 and IL-1beta and caspase-1 activation were induced independently of a P2X7 purinergic receptor, and the inability of Delta\"region of difference 1\" in caspase-1 activation was compensated for by nigericin, an agent inducing the potassium ion efflux.","19342685:0, 19596775:7",2,2,null,"positive"]
["P2RY6 --+> TGFB1","Expression","Furthermore, a P2Y6 receptor antagonist MRS2578 suppressed the stress-induced expression of periostin and transforming growth factor-ß messenger ribonucleic acids in vitro and in vivo.","19008857:1266",2,1,null,"positive"]
["PLAT --+> CCND1","Expression","Ectopic overexpression of an uninhibitable GSK3ß mutant eliminated tPA-induced cyclin D1 expression., Blockade of Erk1/2 activation or knockdown of p90RSK suppressed tPA-induced GSK3ß phosphorylation, cyclin D1 expression, and fibroblast proliferation.","20724593:6, 20724593:4",2,2,null,"positive"]
["PLEK --+> CCND1","Expression","The inability of the CKIP-1? pleckstrin homology mutant to promote either cyclin D1 or myogenin expression suggests that membrane association and probably phosphatidylinositol-3-phosphate binding are required for CKIP-1 action., Thus, our results suggest that proto-Dbl and Dbl homology/pleckstrin homology proteins may activate cyclin D1 through activation of JNK, which in turn may activate ATF-2 and Jun nuclear transcription factors to stimulate transcription from cyclin D1 promoter.","14729969:1317, 11907027:321",2,2,null,"positive"]
["PSMB9 --+> CCND1","Expression","Furthermore, analysis by real-time reverse transcription-PCR of the endogenous expression of cyclin D1 and pS2 indicated that the expression level of endogenous cyclin D1 and pS2 was also elevated with overexpression of LMP2 and decreased with LMP2 knockdown (Figure 2C).","16957778:1097",2,1,null,"positive"]
["PTPN6 --+> ITGB2","Expression","Surface expression of ß2 integrins is increased on motheaten polymorphonuclear leukocytes .","11067945:1301",2,1,null,"positive"]
["PTPN6 --+> CYBB","Expression","Consistent with this, SHP1 inhibition increases gp91PHOX and p67PHOXmRNA in undifferentiated U937 cells., In undifferentiated U937 cells, we found that overexpression of CS453-SHP1 increases gp91PHOX and p67PHOX mRNA abundance relative to control vector transfectants (Fig.2 C).","11483597:208, 11483597:223",2,2,null,"positive"]
["RAPGEF3 --+> SOCS3","Expression","Conversely, down-regulation of protein kinase C activity with chemical inhibitors or small interfering RNA-mediated depletion of PKCalpha or -delta blocks EPAC-dependent SOCS-3 induction., Firstly, selective activation of EPAC in human umbilical vein endothelial cells increased C/EBP DNA binding activity and recruitment of C/EBPbeta to the SOCS-3 promoter., To determine whether the increase in SOCS-3 expression induced by Epac was functionally relevant, we also tested the ability of 8-pCPT to inhibit \"signal transducers and activators of transcription\" phosphorylation by sIL-6Ra/IL-6. <more data available...>","19423709:4, 18195020:4, 16914720:1228, 18195020:203, 19423709:274, 18195020:257, 18195020:233, 19423709:122, 19423709:290, 19423709:34 <more data available...>",2,19,null,"positive"]
["SLC14A1 --+> GFAP","Expression","The abundance of GFAP, the usual marker of astrocytes and ependymal cells, was increased by 25% with age (data not shown), a variation much smaller than the doubling in UT-B1 or the fourfold increase in AQP-4.","12933359:1196",2,1,null,"positive"]
["SOX9 --+> CLU","Expression","Mutant Kras blocks acinar regeneration in favor of a persistently dedifferentiated state. (A-H) Clusterin and Sox9 (I-P) expression during regeneration and Kras-induced acinar-to-ductal metaplasia. (A and I) Clusterin expression is limited to some normal ducts in PBS-treated Pdx1-CreEarly mice, while Sox9 is restricted to ducts and centroacinar cells (arrowheads). (E and M) Acini in PBS-treated Pdx1-CreEarly;LSL-KrasG12D mice are negative for Clusterin and Sox9, while normal ducts and spontaneous pancreatic intraepithelial neoplasias are positive (asterisks). (B, F, J, and N) Damaged duct-like cells of both genotypes display clusterin- and Sox9-positive cells (insets). (C, D, K, and L) Clusterin and Sox9 are mainly restricted to duct cells (arrowheads) following regeneration in Pdx1-CreEarly pancreata.","20071774:1134",2,1,null,"positive"]
["SOX9 --+> LXN","Expression","BMP-2 treatment upregulated Sox9 expression, and Sox9 stimulated the promoter activity of latexin.","19059214:7",2,1,null,"positive"]
["STAT1 --+> MCL1","Expression","Further, mutation of STAT1/STAT2 prevented the effect of both Abeta and SGK1 on Mcl-1 expression.","19609277:10",2,1,null,"positive"]
["STAT1 --+> B2M","Expression","The same authors also show that transcription of the ß2-microglobulin gene is down-regulated in mouse Stat1-null T lymphocytes., A direct target of EOMES, IL2RB (CD122) (29), is also 7.4-fold up-regulated. ß-2 microglobulin , which is up-regulated by STAT1 and is part of MHC I, is fivefold up-regulated in L&H cells.","10921891:1271, 18794340:1113",2,2,null,"positive"]
["STAT1 --+> ISG15","Expression","A single mutation (K161A) in the p48 contact region of Stat1 inhibited the Stat1-p48 interaction as well as the IFN-a-triggered ISG15 gene induction, whereas this mutation had no effect on either the Stat1-Stat2 interaction or the IFN-? response which is independent of p48 (Horvath et al., 1996).","10851063:1089",2,1,null,"positive"]
["STAT1 --+> CYBB","Expression","At the same time, STAT1 and IRF-1 together promote the interferon-?-induced transcription of the CYBB gene (26).","16162660:1069",2,1,null,"positive"]
["STAT1 --+> HLA-E","Expression","STAT-1 and GATA-1 bind to the IRR and upstream IFN response region, respectively, to stimulate transcription from the HLA-E promoter (73)., The transcription factors Stat-1 and GATA-1 bind to the IFN response region and upstream IFN response region, respectively, to stimulate transcription from the HLA-E promoter (26, 27).","18566411:1611, 17142760:1073",2,2,null,"positive"]
["STAT1 --+> HSPB1","Expression","STAT-1 was required for transcriptional activation of the HSP27 gene, but not for the HSP70 gene, and cDNA transfection of STAT-1 in mumps virus-infected cells restored thermotolerance.","12917439:6",2,1,null,"positive"]
["STAT1 --+> IFIT3","Expression","Our results suggest that the induction of IFIT4 transcription by IFN-alpha depends upon sequential activation of PKCdelta, JNK and STAT1, and that the influence of PKCdelta or JNK on interferon-alpha-mediated induction of IFIT4 is dependent upon the phosphorylation of STAT1 at Ser-727.","17933493:6",2,1,null,"positive"]
["STAT1 --+> CASP1","Expression","Activation of caspase-1 gene expression requires IRF-1 and Stat-1 (24, 32)., In addition, overexpression of STAT-1 together with interferon-? treatment further enhanced the activity of the caspase-1 promoter., Recently, interferon-? and STAT-1 have been shown to modulate the level of caspase-1 expression in non-cardiac cells (28)., Moreover, transfection of antisense STAT-1 inhibited both the interferon-?/STAT-1- and ischemia-induced activation of the caspase-1 promoter (Fig. 5)., Down-regulation of EGFR is also postulated to induce apoptosis, and activation of Stat-1 has been reported to induce p21/WAF-1 or caspase 1 that may result in cell cycle arrest or apoptosis, respectively. <more data available...>","16135520:78, 10744676:204, 10744676:201, 10744676:206, 12714587:265, 17339457:351, 10744676:212, 10640742:219, 10744676:264, 9694822:49",2,10,null,"positive"]
["STAT1 --+> IFI27","Expression","From results presented here, it is reasonable to propose that up-regulated STAT1 may enhance IFI27 and OAS1 expression in breast tumors.","19478064:183",2,1,null,"positive"]
["STAT1 --+> CXCL10","Expression","STAT1 was critical for IFN-gamma induction of both the Cxcl9 and Cxcl10 genes in microglia and in microglia and astrocytes, respectively.","20585034:7",2,1,null,"positive"]
["STAT3 --+> CEBPA","Expression","Gene expression profile and quantitative PCR analysis of G-CSF-stimulated cell lines revealed that the expression of C/EBPalpha was up-regulated by the activation of Stat3., Treatment of freshly isolated adult rat hepatocytes with 10-100 mM ethanol rapidly (< 3 min) inhibits interleukin-6 (IL-6)-induced STAT3 activation, tyrosine and serine phosphorylation and IL-6-induced CCAAT enhancer binding protein (C/EBP) alpha and beta mRNA expression., One is that activated Stat3 binds to the promoter region of C/EBPa and induces the transcription of C/EBPa. <more data available...>","15664994:3, 10486586:2, 15664994:261, 15664994:66, 15664994:47, 15664994:255, 15664994:266",2,7,null,"positive"]
["STAT3 --+> OSMR","Expression","STAT3 activation further enhances OSMR expression, thereby establishing a positive-feedback loop., We found that Stat3flx/flx/NIC tumors expressed lower levels of both cebpd and osmr, two genes that are induced by Stat3 (28, 29)., We show that OSMR expression is dependent on LIF-induced STAT3 and that the subsequent OSMR-mediated signal inhibits the phosphorylation of STAT5 and coordinately activates signal transducer and activator of transcription3-dependent apoptosis in the involuting mammary gland.","20348953:1139, 19690134:1181, 18927239:1084",2,3,null,"positive"]
["STAT3 --+> FLI1","Expression","A recent study showed that an enhanceosome responsible for activating SCL transcription was required for GATA-2, Fli-1, and Elf-1.37 As the expression of Fli-1 was induced via the STAT3 transcription factor,38 phosphorylation of STAT3 by the binding of HGF to c-met39 might activate Fli-1 or Elf-1.","14701703:1187",2,1,null,"positive"]
["STAT3 --+> CD9","Expression","Furthermore, activation of STAT3 induced the expression of CD9, indicating the LIF/STAT3 pathway is critical for maintaining CD9 expression., In a previous study, the addition of leukemia inhibitory factor or STAT3 activation induced CD9 expression in embryonic stem cells [13], which indicates that the leukemia inhibitory factor/STAT3 pathway is critical for maintaining CD9 expression.","11950938:5, 12954725:1222",2,2,null,"positive"]
["STAT3 --+> HPGD","Expression","Activation of signal transducer and activator of transcription3 may augment potently the androgen bound receptor signaling and contribute to synergistic induction of 15-PGDH expression by combined treatments with IL-6 and dihydrotestosterone.","14749354:1215",2,1,null,"positive"]
["STAT3 --+> CD14","Expression","STAT3 inhibitor pretreatment could also down-regulate high CD14 and CD16 expression by BxPC-3 conditioned medium treatment.","17545630:1248",2,1,null,"positive"]
["STAT3 --+> SYNPO","Expression","Stat3-DN inhibited nef-containing vector-induced cyclin E expression and significantly increased synaptopodin expression (Figure 5C).","15343382:1157",2,1,null,"positive"]
["STAT3 --+> SBNO2","Expression","IL-10-mediated induction of ETV3 and SBNO2 expression was dependent upon both STAT3 and a stimulus through the TLR pathway.","18025162:2",2,1,null,"positive"]
["STAT3 --+> VIM","Expression","Specific inhibition of STAT3 activation by Janus kinase2-specific inhibitor AG490 blocked STAT3 phosphorylation, cell motility, induction of N-cadherin and vimentin expression and IL6 production., Stat3 can enhance transcription of the vimentin gene.","19088723:9, 14712222:1097",2,2,null,"positive"]
["STAT3 --+> TF","Expression","proteolysis-inducing factor activates both the transcription factors NF-kB and STAT3, which result in the increased production of IL-8, IL-6, and C-reactive protein and the decreased production of transferrin.","11259367:4",2,1,null,"positive"]
["STAT3 --+> CXCL10","Expression","Inhibitors of p38 mitogen-activated protein kinase, c-Jun N-terminal kinase (JNK), phosphatidylinositol-3-OH kinase and signal transducer and activator of transcription 3 decreased OSM-induced CXCL10 production.","19616927:6",2,1,null,"positive"]
["STAT3 --+> MET","Expression","U-STAT3 induces the expression of well-known oncogenes, such as MRAS and MET, which are late-phase genes induced by IL-6.","19478064:203",2,1,null,"positive"]
["TGFB1 --+> TGFBR2","Expression","These data indicate that TGFB1-insensitivity in LbetaT2 cells results from a deficiency in Tgfbr2 expression., Expression of the transforming growth factor-beta type II receptor (TGF-beta RII) is highly regulated and is a critical determinant of the cellular response to TGF-beta., Dysregulated TGF-beta signalling may result from mutations in TGFBR1 and TGFBR2 genes, thus resulting in degenerative changes in the vessel wall., TGF-beta1 treatment increased the expression of TGF-beta1, TbetaR-I and TbetaR-II in mesenchymal cells in the cambium layer at 7 days in culture. <more data available...>","16384533:13, 11179682:0, 18550062:2, 12038632:8, 10861501:5, 9167190:2, 9516449:3, 11290556:6, 12198207:11, 19088080:4 <more data available...>",2,24,null,"positive"]
["TGFB1 --+> HSPB1","Expression","Retinoic acid enhanced the TGF-beta-induced increase of mRNA for HSP27., The TGF-beta-stimulated increase in the level of mRNA for HSP27 was also attenuated by T(3)., The TGF-beta1-induced down-regulation of LEDGF, Hsp27, and alphaB-crystallin promoters activity was reversed by cotransfection with a plasmid expressing LEDGF., SP600125, a specific inhibitor of stress-activated protein kinase /c-Jun N-terminal kinase (JNK), markedly reduced the HSP27 expression induced by TGF-beta., TGF-ß1 incubation resulted in increased expression of HSP-27 and decreased expression of HSP-72. <more data available...>","11909638:7, 12706291:3, 12649267:8, 18407296:5, 18577533:1198, 18596079:1181, 16055503:1191",2,7,null,"positive"]
["TGFB1 --+> TGFBR1","Expression","Interestingly, TGF-beta1 differentially stimulated or inhibited the expression of TbetaR-I and TbetaR-II mRNA in the gliomas., Dysregulated TGF-beta signalling may result from mutations in TGFBR1 and TGFBR2 genes, thus resulting in degenerative changes in the vessel wall., Furthermore, this truncated Smad4 functioned as a dominant negative form in TGF-beta1-mediated reporter activity and TGF-beta1 receptor expression., TGF-beta1 treatment increased the expression of TGF-beta1, TbetaR-I and TbetaR-II in mesenchymal cells in the cambium layer at 7 days in culture. <more data available...>","10048979:3, 18550062:2, 12860278:5, 12038632:8, 10861501:5, 9516449:3, 12198207:11, 19091788:9, 19038005:5, 15546867:6 <more data available...>",2,30,null,"positive"]
["TGFB1 --+> MET","Expression","In contrast, a combination of IL-6 and TGFbeta1 down-regulated c-met expression as well as Sp1 DNA binding activity., Real-time RT-PCR and Northern and Western blot analyses revealed that TGF-beta1 significantly induced c-met expression in HKC cells, which primarily took place at the gene transcriptional level., With respect to gene expression, fibrotic genes like transforming growth factor-beta (TGF-beta) and collagen Ialpha (Col-1alpha) were down-regulated by pirfenidone and increased expression of regenerative genes like hepatocyte growth factor (HGF) and c-met . <more data available...>","11469916:13, 15339794:3, 18652820:6, 15770602:6",2,4,null,"positive"]
["TGFB1 --+> A2M","Expression","It was blocked when bovine adrenocortical cells were exposed to 5,6-dichlorobenzimidazole riboside, a potent inhibitor of RNA polymerase II, suggesting that TGF-beta 1 acts as an activator of alpha 2-M gene expression at the transcriptional level., This is supported by the following observations: (i) Treatment of adrenocortical cells by FGF-2 resulted in a time-dependent and dose-dependent increase of alpha 2M synthesis, (ii) FGF-2 did not modify alpha 2M secretion rate; (iii) The induction of alpha 2M synthesis by FGF-2 was not observed in the presence of the transcription inhibitor DRB; (iv) The amount of alpha 2M mRNA was increased by 2 to 3 fold under either FGF-2 or TGF beta 1 treatment; (v) Optimal doses of TGF beta and FGF-2 synergistically increased alpha 2M synthesis. <more data available...>","1689294:5, 7524573:1, 9570034:1745, 15618353:1348",2,4,null,"positive"]
["TGFB1 --+> INPP5D","Expression","Activin/TGF-beta-induced expression of SHIP results in intracellular changes in the pool of phospholipids, as well as in inhibition of both Akt/PKB (protein kinase B) phosphorylation and cell survival., TGF-beta1 treatment does not increase IRAK-M or SHIP1 protein expression in shSMAD4 THP-1 cells, whereas it does so in shLUC THP1 cells, indicating that TGF-beta1 regulates IRAK-M and SHIP1 expression through a SMAD4-dependent pathway., lipopolysaccharide also upregulates the secretion and activation of TGFß, which, in turn, activates the transcription of the negative regulator SHIP. <more data available...>","12447389:5, 20404275:8, 15308103:1213, 15604218:1211, 17947710:1361, 16636301:1257, 19139077:265, 19139077:274, 19542365:220, 15778380:183 <more data available...>",2,16,null,"positive"]
["TGFB1 --+> THBS2","Expression","Using this assay, we observed that thrombospondin-1 and CISP/thrombospondin-2 syntheses were respectively stimulated threefold and twofold by a 24-h treatment with 2 ng/ml TGF beta 1., Further, p38 MAPK mediated induction of collagen I and TSP-2 expression by TGF-beta1 was still achieved in the presence of dexamethasone, showing that dexamethasone does not block p38 while it delays Smad2 phosphorylation and antagonizes stimulation of a Smad3/Smad4 dependent TGF-beta reporter construct., Further, the observation that TGFß can stimulate TSP-1 and -2 expression in bovine adrenal tissue [58] provides evidence to support further studies regarding the potential role of TGFß in regulating Thrombospondin expression in bovine follicles.","7698241:4, 15905080:5, 15616224:1300",2,3,null,"positive"]
["TGFB1 --+> VIM","Expression","Furthermore, induction of vimentin expression by TGF-beta1 and hypoxia was evaluated in gastric cancer cells., Here, we suggest a mechanism to explain how TGFbeta1 contributes to the up-regulation of vimentin expression while blocking myogenesis., Western blotting analysis showed that TGF-beta1 decreased cytokeratin and increased vimentin levels, while DMSO decreased both cytokeratin and vimentin., TGF-beta/IL-1beta treatment induced epithelial to mesenchymal-like phenotype transition (EMT), changing cell morphology and expression of vimentin and E-cadherin. <more data available...>","20358301:4, 17270292:2, 10580588:7, 20671927:3, 19213777:6, 1879463:2, 19116990:5, 19659836:8, 11752026:1166, 16382155:1202 <more data available...>",2,35,null,"positive"]
["TGFB1 --+> S100A4","Expression","TGF-beta1 increased S100A4 expression in cultured ileal fibroblasts., Furthermore, TGFbeta1 up-regulated epithelial markers CTNNB1 and CTNND1, but suppressed mesenchymal markers, such as S100A4, FGF1 and FGF2., Consistent with these observations, S100A4 increases cell invasion ability induced by TGF-beta in MCF10CA1a.cl1 cells, and depletion of the protein in MDA-MB-231 cells inhibits it., In vitro experiments using human dermal microvascular endothelial cells demonstrated that TGF-beta1 induced myofibroblastic features in human dermal microvascular endothelial cells, including spindle cell morphology, reduction of CD34 expression, and induction of S100A4, alpha-smooth muscle actin, and COL1A1 expression, as well as the increased nuclear expression of phospho-Smad2. <more data available...>","20489045:10, 20592463:9, 20070253:8, 19608867:2, 17974953:1193, 12163453:1072, 16889607:1246, 14747385:1161, 19487818:1150, 17562716:291 <more data available...>",2,11,null,"positive"]
["TGFB1 --+> CYBB","Expression","Transfection of wild-type mouse cardiac fibroblasts with AAV/TGFbeta (ACT)(1) markedly enhanced the expression of NADPH oxidases (p22(phox), p47(phox), and gp91(phox) subunits) and LOX-1, formation of reactive oxygen species, and collagen synthesis, concomitant with an increase in the activation of p38 and p44/42 mitogen-activated protein kinases ., TGF-ß1 upregulates the expression of p22phox, p47phox, p67phox, and gp91phox in rat mesangial cells (Figure 2B) and p22phox mRNA in tubular epithelial cells (Figure 2C), suggesting that TGF-ß1-induced reactive oxygen species may be NADPH oxidase dependent. <more data available...>","18182394:3, 12874439:1080, 12482831:1145",2,3,null,"positive"]
["TGFB1 --+> ITGB5","Expression","Thus, TGF-beta increases expression of the integrin beta(5) gene by mechanisms involving Sp1/Sp3 and Smad transcription factors., We investigated the effects of PPARalpha ligands on TGF-beta-induced beta3 and beta5 integrin expression and potential interaction between PPARalpha and TGF-beta signaling., In that scenario, however, Peroxisome proliferator-activated receptor-a activation antagonized transforming growth factor-ß-induced ß5-integrin transcription in vascular smooth muscle cells., Agonists of peroxisome proliferator-activated receptor-a inhibit TGFß-responsive ß5 integrin expression and disrupt formation of the Sp1-Smad4 complex, in parallel with induction of peroxisome proliferator-activated receptor-a/Smad4 interaction (43). <more data available...>","10964912:9, 12456495:3, 17098824:1241, 16249187:1329, 14684628:1206, 12130649:44",2,6,null,"positive"]
["TGFB1 --+> CSF1","Expression","Anti-TGF-beta 1 decreased (p < 0.05) M-CSF induced colonies in 5/6 donors., Transforming growth factor beta (TGF-beta) increased both the synthesis of CSF-1 and its accumulation in the matrix., The M-CSF activity in the conditioned medium of mouse osteoblast-like MC3T3-E1 cells was increased by TGF-beta as well as interleukin-1 treatment., Here we show that TGF-beta1 induces the expression of macrophage-CSF (M-CSF) in vascular endothelial cells via a signaling pathway(s) involving hydrogen peroxide (H2O2)., Other agents, including PTH (35), tumor necrosis factor-alpha (36), and transforming growth factor-beta (37), have been shown to increase MCSF expression at the level of gene transcription. <more data available...>","7804125:8, 8591991:10, 8048485:1, 9278333:1, 9492032:1246, 16707491:363, 17332318:77",2,7,null,"positive"]
["TGFB1 --+> RBP1","Expression","In both cell populations, transforming growth factor-beta 1 treatment increased CRBP-1 expression., We also demonstrate that CRBP-1 expression by fibroblasts is regulated in vitro by retinoic acid and transforming growth factor-beta1., The expression of CRBP-1 is regulated at the transcriptional level by TGF-beta and retinoic acid but not synergistically, suggesting a possible common pathway., TGF-ß1 should be capable of diffusing through the microporous membrane, subsequently modulating CRBP-1 transcription.","12004002:12, 9403724:10, 11319755:4, 12419830:1201",2,4,null,"positive"]
["TGFB1 --+> SOX9","Expression","Moreover, exogenous TGF-beta can induce Sox9 expression in the mandibular arch., In addition, up-regulation of Fibronectin and suppression of Sox9 expression by TGF-beta1 was also found to be mediated by CTGF., Transforming growth factor-beta treatment increased MAPK activity and Sox-9, aggrecan, and collagen type II gene expression., TGF-beta1 increased the Sox9 messenger ribonucleic acid expression to 180% compared to control group in intervertebral disc tissue., TGF-beta1-stimulated gene expression of chondrogenic regulators, Sox9, Runx2 and Ihh, was also affected by activity of PD98059 and SB203580, to different degrees. <more data available...>","18684439:6, 17111364:7, 15564911:11, 20157375:7, 20590658:6, 18496879:5, 16575901:3, 17525254:5, 18602912:6, 19321054:8 <more data available...>",2,15,null,"positive"]
["TGFB1 --+> TGM2","Expression","In Western blot analysis, TGF-beta1 (1 ng/ml) treatment was found to steadily up-regulate TGase 2 expression for up to 7 days., Transforming growth factor-beta and interleukin -1beta induced Factor XIIIa and tTGase expression in cartilage and meniscal organ cultures., This study suggests that in the isolated perfused rat kidney and in the absence of other exogenous growth factors, TGF-beta1 selectively increases the synthesis of extracellular matrix and tissue transglutaminase without changes that would result in the reduction of extracellular matrix degradation. <more data available...>","16044258:3, 11438463:3, 10505687:11, 17460246:6, 12874459:1070, 14555988:1123, 11686302:1246, 9582307:46, 9114053:189, 11689553:280 <more data available...>",2,18,null,"positive"]
["TGFB1 --+> NFATC1","Expression","Similarly, TNF-alpha activates osteoclastogenesis by stimulating translocation of TGF-beta-induced NFATc1., Addition of Transforming growth factor-ß during differentiation to either lineage inhibited NFATc activation., Using quantitative real-time PCR, we found that transforming growth factor-ß1 treatment results in a 4.5-fold increase in NFATc1 transcript levels in neural crest stem cells (Fig. 6).","18060870:6, 12810687:1296, 15148306:1175",2,3,null,"positive"]
["TGFB1 --+> CD14","Expression","At 2 hr, 50 ng/ml TGF-beta 1 significantly lowered CD14 expression (51%, P = 0.043)., TGF-beta and VD3 synergistically increased the expression of differentiation-associated markers such as the CD11b and CD14 antigens, whereas TGF-beta and dexamethasone did not., Furthermore, TGF-beta/D3 treatment (but not D3 alone) elicits the expression of membrane CD14, FcRI, FcRII, CD11a, CD11b, CD11c, ICAM-1, and PECAM-1 Ag at a level comparable to that observed on normal human monocytes., The same CCAAT/enhancer-binding protein site was also involved in the TGF-ß/Vit D3-dependent activation of CD14 expression (42). <more data available...>","7526045:5, 10547074:1, 8383719:5, 11698458:1270, 12821938:1143, 18497880:1254",2,6,null,"positive"]
["TGFB1 --+> FCGR2B","Expression","Furthermore, TGF-beta/D3 treatment (but not D3 alone) elicits the expression of membrane CD14, FcRI, FcRII, CD11a, CD11b, CD11c, ICAM-1, and PECAM-1 Ag at a level comparable to that observed on normal human monocytes., IFN-a, IFN-?, TGF-ß, IL-10, and soluble IgG modulated CD32a and/or CD32b on circulating conventional DCs, which was similar to their effects on cytokine-induced monocyte-derived DCs.","8383719:5, 16167082:1141",2,2,null,"positive"]
["TGFB1 --+> GFAP","Expression","Cycloheximide did not block the effects of TGF-beta1 or FGF-2 on GFAP mRNA levels, but blocked the inhibitory effects of FGF-2 on the TGF-beta1-mediated increase in GFAP expression., Whereas untreated control cells expressed progressively the glial fibrillary acidic protein (GFAP) after arrest of multiplication, the addition of TGF beta 1 to proliferative cells prevented GFAP expression and accumulation of its mRNA., TGF-beta induced CysC and GFAP expression in AP-16 cells, an astrocyte progenitor-like cell line expressing GLAST (a glutamate transporter subtype specifically expressed in immature astrocytes). <more data available...>","9537840:5, 1397085:4, 15509901:2, 8170537:2, 8361632:2, 18419760:10, 19057972:3, 12118088:4, 10098836:1048, 11867550:1092 <more data available...>",2,14,null,"positive"]
["TGFB1 --+> ABCA1","Expression","TGF-beta1 significantly increased expressions of ABCA1, ABCG1 and SR-BI at both transcriptional and translational levels in a dose-dependent and time-dependent manner., transforming growth factor-ß increases ABC-1 expression and inhibits its down-regulation by interferon-?., TGF-ß1 also reduced foam cell formation by enhancing cholesterol efflux through increasing mRNA expression of ABCA1 and ABCG1., TGF-beta increases cholesterol efflux and ABC-1 expression in macrophage-derived foam cells: opposing the effects of IFN-gamma. <more data available...>","20057170:4, 11352993:1189, 11742878:1055, 15995168:2634, 20485864:4",2,5,null,"positive"]
["TGFB1 --+> CLU","Expression","At the same time, TGFbeta1 enhanced clusterin protein and mRNA expression., A single T to G base mutation in the AP-1 site (5'-TGAGGCA) abolishes TGFbeta-induced clusterin promoter transactivation., We hypothesize that activation of the TGF-beta signaling pathway, which often occurs after ionizing radiation exposure, can in turn activate the CLU promoter., Cytokines such as TGF beta 1 and interleukin 1 enhance the expression of clusterin, which may link clusterin to inflammatory mechanisms in Alzheimer disease. <more data available...>","10066375:3, 9334243:5, 15530543:10, 8892344:4, 9407436:5, 7730444:8, 8170537:2, 10406964:1149, 15671065:1426, 9334243:219 <more data available...>",2,33,null,"positive"]
["TGFB1 --+> SOCS3","Expression","TGF-beta inhibits IL-6-induced SOCS3 promoter activity in T cells., These data show that TGF-beta coordinately induces LIF and SOCS3 to promote prosurvival signaling., Furthermore, TGF-beta rapidly induces sustained SOCS-3 expression in macrophage/osteoclast precursors., In this study, we demonstrate that LPS-induced endogenous TGF-beta1 contributes to the inducible SOCS3 expression in macrophages., This suggests that TGF-beta-induced expression of SOCS3 may represent a crucial mechanism by which TGF-beta antagonizes specific anti-osteoclastic JAK/STAT signals, priming precursors for resorption rather than inflammatory functions. <more data available...>","19535626:4, 20181800:8, 12646633:7, 17920684:3, 13679037:8, 18031698:1059",2,6,null,"positive"]
["TGFB1 --+> GUSB","Expression","Beta-glucuronidase expression was increased by TGF-beta and decreased by IFN-gamma.","9712070:10",2,1,null,"positive"]
["TGFB1 --+> MCL1","Expression","The increased levels of the cytokines, IL-4, IL-10, prostaglandin E2, and TGF-ß enhance the expressions of c-FLIP, Bcl-xL, and Mcl-1, which are involved in the resistance to apoptosis (32-34).","16740684:1107",2,1,null,"positive"]
["TGFB1 --+> AIF1","Expression","Furthermore, functional studies showed specific allograft inflammatory factor-1 isoform expression stimulation by transforming growth factor-beta., Stimulation of peripheral blood mononuclear cells with TGFbeta caused a specific and significant increase in the expression of AIF-1 isoform 2 transcripts (P < 0.005), which was due to stabilization of AIF-1 isoform 2 messenger RNA., Ten percent FCS, IFN-?, and interleukin-1ß are capable of inducing this protein, whereas AIF-1 is not expressed in unstimulated cells. basic fibroblast growth factor, platelet-derived growth factor, and transforming growth factor-ß can induce AIF-1 protein expression to a small degree.","17053503:3, 16868985:9, 10894811:1159",2,3,null,"positive"]
["TGFB1 --+> SYNPO","Expression","Anti-TGF-ß antibody 2G7 blocked synaptopodin expression and inhibited the redistribution of zona occludens-1 (Figure 1D).","16207831:1114",2,1,null,"positive"]
["TGFB1 --+> PTGS1","Expression","Release of histamine, cysteinyl-leukotrienes, and tumour necrosis factor alpha was strongly reduced whereas prostaglandin D2 generation and cyclooxygenase 1 and 2 expression were upregulated by TGF-beta1., Prostaglandin E2, transforming growth factor-beta, and interleukin-1 beta variably regulate the expression of cyclooxygenase 1, cyclooxygenase 2, and lysyl oxidase in IMR90, human embryo lung fibroblasts., In a few experiments in MC3T3-E1 cells, TGFbeta stimulated PGHS-1 messenger RNA levels up to 5-fold at 4 h, with little change in glyceraldehyde 3-phosphate dehydrogenase (Fig. 1).","15951536:7, 8872612:0, 9348193:1158",2,3,null,"positive"]
["TGFB1 --+> IL13RA1","Expression","Transforming growth factor-ß can enhance the effects of IL-13 on activation and survival of eosinophils, and on the surface expression of IL-13Ra1 on eosinophils (Myrtek et al., 2004[Go]).","16888081:1218",2,1,null,"positive"]
["TGFB1 --+> CSF1R","Expression","In contrast, TGF-beta 1 down-modulated IL-3 and CSF-1 receptor expression by 54 and 55%, respectively, by 24 h., Cell surface expression of the monocyte/macrophage-specific marker c-fms was increased 3.1-fold following TGF-beta 1 treatment., Antagonists of TGF-beta1 signaling significantly inhibited both the induction of c-fms expression and cellular invasiveness, suggesting that additional studies are warranted to assess the therapeutic potential of TGF-beta antagonists in endometriosis., TGF-ß1 induces the expression of c-fms. <more data available...>","8409417:3, 8930403:10, 19505996:8, 17332318:234, 17332318:219, 17332318:248, 17332318:223, 17332318:289, 17332318:84, 17332318:235 <more data available...>",2,13,null,"positive"]
["TGFB1 --+> SRGN","Expression","Metabolic labeling experiments reveal that TGF-beta induces selectively the expression of proteoglycan-I, whereas the level of proteoglycan-II remains unaltered.","1863601:2",2,1,null,"positive"]
["TGFB1 --+> CX3CR1","Expression","TGF-beta1 upregulates CX3CR1 expression and inhibits fractalkine-stimulated signaling in rat microglia., These results showed that TGFß enhanced CX(3)CR1 expression and attenuated the LPS-induced increase in IL-1ß expression.","12446007:100, 20570721:11",2,2,null,"positive"]
["TGFB1 --+> ALOX5AP","Expression","The addition of anti-TGF-beta1 antibody reduced hydroxynonenal-induced 5-LOX and FLAP expression by 40%, indicating the partial involvement of a TGF-beta1-dependent mechanism., The expression of FLAP in Osteoarthritis osteoblasts is also modulated differently by 1,25(OH)2D3 and TGF-beta depending on their endogenous low and high prostaglandin E2 levels., TGFbeta1 and/or 1,25(OH)(2)D(3) induced a rapid and marked enhancement ( approximately 4-13-fold) in FLAP messenger RNA levels, which was associated with a subsequent and late increase in leukotriene B(4) production and prostaglandin E(2) synthesis. <more data available...>","20144213:12, 17156456:12, 15593193:4, 11090070:5",2,4,null,"positive"]
["TGFB1 --+> TF","Expression","However, in quiescent, well-differentiated cells, TGF-beta repressed the mitogenic responses to both nutrients alone (by 90%) and to nutrients plus the exogenous stimulatory factors epidermal growth factor (E), insulin (I), and transferrin (T) (by 55-65%)., TGF-beta(1) and bFGF upregulate transferrin gene expression of cultured lens epithelial cells remarkably, can reduce lenticular oxidative damaging process in which transferrin participates and play an important role in the pathological mechanism of cataract formation after extracapsular cataract extraction.","1701348:3, 11835825:8",2,2,null,"positive"]
["TGFB1 --+> HPGD","Expression","Induction of 15-PGDH expression by TGF-beta1 was synergistically stimulated by the addition of Wnt3A which was inactive by itself., A number of anti-cancer agents, such as transforming growth factor-beta1 (TGF-beta1), glucocorticoids and some histone deacetylase inhibitors were found to induce 15-PGDH expression.","16844092:6, 17481556:12",2,2,null,"positive"]
["TGFB1 --+> ITGAX","Expression","Furthermore, TGF-beta/D3 treatment (but not D3 alone) elicits the expression of membrane CD14, FcRI, FcRII, CD11a, CD11b, CD11c, ICAM-1, and PECAM-1 Ag at a level comparable to that observed on normal human monocytes.","8383719:5",2,1,null,"positive"]
["TGFB1 --+> CCND1","Expression","The expression of cyclin D1 in MCF10A cells is regulated by TGF-ß treatment., In addition, Sox17 counteracted repression of the cyclin D1 promoter by TGF-ß1 and Smad3., These results strongly suggest that TGF-ß regulates cyclin D1 expression in a ß-catenin-dependent manner., TGF-ß stimulates cyclin A expression without affecting cyclin D-cdk4/6 activity in suspended NRK cells., TGF-ß stimulated cyclin D1 expression in Ad-GFP-infected but not Ad-Cre-infected chondrocytes (Fig. 7a)., Although TGF-ß stimulated cyclin D1 expression in chondrocytes, this effect was abolished by inhibition of ß-catenin signaling. <more data available...>","18715870:116, 19479035:326, 16690606:242, 10702223:90, 16690606:239, 16690606:67, 19479035:260, 16517699:263, 15811853:143, 19479035:288 <more data available...>",2,19,null,"positive"]
["TGFB1 --+> Ctla2a","Expression","This suggests that TGF-ß promotes the up-regulation of the CTLA-2a expression on responding T cells.","19801522:182",2,1,null,"positive"]
["TGFB1 --+> ADAMTS1","Expression","Expression of ADAMTS1 is induced by transforming growth factor-ß in keratinocytes.","15843381:262",2,1,null,"positive"]
["TGFB1 --+> STAT1","Expression","IFN-gamma down-regulates TGF-beta1-induced IgA expression through Stat1 and p300 signaling.","20016942:100",2,1,null,"positive"]
["TGFBR1 --+> TGFB1","Expression","This persistence was because of autocrine synthesis of TGF-beta1, which was inhibited by both anti-TGF-beta1 antibody and the ALK5 inhibitor SB431542., Based on these findings, we hypothesize that the interaction between c-Ski and TßRI might interfere with nuclear translocation of the R-Smad/Smad4 complex, thereby attenuating TGF-ß signaling., These results show that constitutively reduced Tgfbr1-mediated TGF-beta signaling significantly enhances colorectal cancer development and results in increased tumor cell proliferation. <more data available...>","19193641:6, 20959473:4, 19147584:4, 19535626:7, 19432813:7",2,5,null,"positive"]
["TGM2 --+> TGFB1","Expression","In addition, TG2 also activates transforming growth factor-beta (TGF-beta)., Particularly relevant is the finding that both TGF-beta and IL-12 regulations were significantly altered in the absence of TG2., Free Gd3+ ions may also activate tissue transglutaminase, which in turn activates transforming growth factor beta (TGF-beta) produced by dendritic cells., Increased TG2 expression in these fibroblasts led to NF-kappaB activation, resulting in the increased expression of transforming growth factor beta(1). <more data available...>","18688035:2, 15905580:8, 19886227:11, 19657147:2, 18558621:6, 12810961:2, 18523305:1259, 15199098:1330, 11686302:1320",2,9,null,"positive"]
["TGM2 --+> CYBB","Expression","Inhibition of cross-linking activity of TG2 by monodansylcadaverin in these cells led to diminished nitroblue tetrazolium positivity, production of less superoxide anion, and decreased expression of GP91PHOX, the membrane-associated subunit of NADPH oxidase.","16763214:3",2,1,null,"positive"]
["TLR2 --+> ITGB2","Expression","Peptidoglycan (TLR2 ligand), flagellin (TLR5 ligand), and Imiquimod R837 (TLR7 ligand) could significantly upregulate cell surface expression of intercellular adhesion molecule (ICAM)-1 and CD18, and induce the release of IL-1beta, IL-6, IL-8, growth-related oncogene -alpha, and superoxides of eosinophils.","17332440:5",2,1,null,"positive"]
["TLR2 --+> CEBPD","Expression","TLR2 signaling by LpqH induced expression of liver inhibitory protein and C/EBPd and enhanced expression of LAP at time points that correlated kinetically with the onset of inhibition of IFN-?-induced CIITA expression., Toll-like receptor2 stimulation also induces C/EBPd expression and binding to the CIITA promoter [31].","17982082:1080, 19629181:349",2,2,null,"positive"]
["TLR2 --+> LCN2","Expression","LCN2 expression is increased in response to activation of TLR2 and TLR4 signaling by bacterial peptides (42).","18317594:1267",2,1,null,"positive"]
["TLR2 --+> CD86","Expression","TLR2 is essential for neisserial porin up-regulation of B7-2 and class II MHC in B cells ., Anti-TLR2 blocked increases in the CD86 median fluorescence intensity, but not the percentage of cells positive for CD86., There may be some differences in the Toll-like receptor2-mediated signaling pathway between cytokine production and CD83/CD86 expression., This indicates that the up-regulation of B7-2 and class II MHC surface expression was dependent on the normal expression of TLR2 on the B cell., They also showed that, in human Immature dendritic cells, cytokine production and CD83/CD86 expression were independently induced by M161Ag through TLR2. <more data available...>","11823477:142, 11160304:195, 11160323:247, 11823477:146, 11160323:191, 19109203:128, 11316801:237, 19109203:149, 11160304:179, 11823477:182",2,10,null,"positive"]
["TLR2 --+> ITGAX","Expression","The TLR2 agonist Pam3Cys significantly stimulated the maturation of DCs by enhancing the surface expression of CD11c, MHC class I, MHC class II, CD40, CD80, and CD86.","19109203:128",2,1,null,"positive"]
["TLR2 --+> HSPB1","Expression","TLR1/2 ligand palmitoyl-3-cysteine-serine-lysine-4 (Pam3CSK4) induces activation of PKDs via a PKC-independent manner, and Pam3CSK4-induced expression of heat shock protein 27 and MCP-1, as well as activation of PKDs, is inhibited by Gö6976, but not by broad-spectrum PKC inhibitors, in mouse bone marrow-derived mast cells (26).","19414785:65",2,1,null,"positive"]
["TLR2 --+> STAT3","Expression","TLR2 activation triggers STAT3 and Smad3 activation., TLR2 activation sequentially stimulates NF-?B, STAT3 and Smad3 activation., In addition, blockade of TLR2 abrogated peptidoglycan-SA-induced STAT3 and Smad3 activation. [thumbnail] ., Secondly, HSP60 activation of TLR2 mediates the expression and phosphorylation of Stat3 in tumor cells., These finding indicated that peptidoglycan-SA-stimulated TLR2 activation increased NF-?B, STAT3 and Smad3 activities depending on a time pattern., Moreover, targeting TLR2 in the host or in the melanoma cells markedly inhibited the B16 cell-induced phosphorylation of Stat3 (Fig. 3F). <more data available...>","20520770:250, 20520770:260, 20520770:255, 19654875:266, 20520770:318, 19654875:200, 20520770:319, 19654875:159, 19654875:164",2,9,null,"positive"]
["TLR3 --+> CXCL10","Expression","Both TLR3 and RIG-I are required for CXCL10 expression., We established that stimulation of TLR3-positive cell lines and primary human endometrial epithelial cells with dsRNA leads to TLR3-dependent expression of interleukin -6, IL-8, interferon -inducible protein 10, RANTES, and IFN-beta., Furthermore, IRF-3 is thought to be required for Toll-like receptor3-induced type I IFN and IP-10 production., In addition to IFNß, activation of the TLR3/4 pathway also leads to the production of other mediators such as IP-10 and RANTES. <more data available...>","18258184:5, 15935884:5, 17660379:1240, 14580333:1257, 15315972:1197, 12453406:1108, 17785432:1346, 17170125:1102, 17332880:1148, 18188453:1255 <more data available...>",2,15,null,"positive"]
["TLR3 --+> TGFB1","Expression","Finally, the role of cytokines is difficult to associate with a given Toll-like receptor since Toll-like receptor-induced cytokine production, which was consistently observed, varied with each agonist: one should note however that TLR2, TLR3 and TLR7 agonists preferentially stimulated IL-10 and transforming growth factor-ß production which was not the case for the TLR4 agonist lipopolysaccharide.","20628601:1409",2,1,null,"positive"]
["TLR3 --+> CLU","Expression","Conclusively, TLR3 activation induces expression of cytoprotective and anti-inflammatory CLU by vascular smooth muscle cells and mice, to potentially counteract atherosclerotic pathology., Toll-like receptor 3 mediates expression of clusterin/apolipoprotein J in vascular smooth muscle cells stimulated with RNA released from necrotic cells.","20692254:10, 20692254:100",2,2,null,"positive"]
["TREM2 --+> CD86","Expression","Ligation of triggering receptor expressed on myeloid cells-2 induced increased cell surface expression of CD40, CD86, and MHC class II but Ag-capturing mechanisms were not down-regulated (53)., KARAP/DAP12-TREM2 triggering on human Dendritic cells promotes incomplete maturation process, i.e., Dendritic cells up-regulation of CCR7, CD40, CD86, and MHC class II molecules, but not TNF-alpha nor IL-12 production (32).","14978127:315, 15128777:291",2,2,null,"positive"]

{"sheet":"Core network","index":2,"n_rows":125,"n_cols":8,"rows_kept":125,"flags":["formulas_cached_only"]}
["TGFB1 --+> TGFBR2","Expression","These data indicate that TGFB1-insensitivity in LbetaT2 cells results from a deficiency in Tgfbr2 expression., Expression of the transforming growth factor-beta type II receptor (TGF-beta RII) is highly regulated and is a critical determinant of the cellular response to TGF-beta., Dysregulated TGF-beta signalling may result from mutations in TGFBR1 and TGFBR2 genes, thus resulting in degenerative changes in the vessel wall., TGF-beta1 treatment increased the expression of TGF-beta1, TbetaR-I and TbetaR-II in mesenchymal cells in the cambium layer at 7 days in culture. <more data available...>","16384533:13, 11179682:0, 18550062:2, 12038632:8, 10861501:5, 9167190:2, 9516449:3, 11290556:6, 12198207:11, 19088080:4 <more data available...>",2,24,null,"positive"]
["TGFB1 --+> HSPB1","Expression","Retinoic acid enhanced the TGF-beta-induced increase of mRNA for HSP27., The TGF-beta-stimulated increase in the level of mRNA for HSP27 was also attenuated by T(3)., The TGF-beta1-induced down-regulation of LEDGF, Hsp27, and alphaB-crystallin promoters activity was reversed by cotransfection with a plasmid expressing LEDGF., SP600125, a specific inhibitor of stress-activated protein kinase /c-Jun N-terminal kinase (JNK), markedly reduced the HSP27 expression induced by TGF-beta., TGF-ß1 incubation resulted in increased expression of HSP-27 and decreased expression of HSP-72. <more data available...>","11909638:7, 12706291:3, 12649267:8, 18407296:5, 18577533:1198, 18596079:1181, 16055503:1191",2,7,null,"positive"]
["TGFB1 --+> TGFBR1","Expression","Interestingly, TGF-beta1 differentially stimulated or inhibited the expression of TbetaR-I and TbetaR-II mRNA in the gliomas., Dysregulated TGF-beta signalling may result from mutations in TGFBR1 and TGFBR2 genes, thus resulting in degenerative changes in the vessel wall., Furthermore, this truncated Smad4 functioned as a dominant negative form in TGF-beta1-mediated reporter activity and TGF-beta1 receptor expression., TGF-beta1 treatment increased the expression of TGF-beta1, TbetaR-I and TbetaR-II in mesenchymal cells in the cambium layer at 7 days in culture. <more data available...>","10048979:3, 18550062:2, 12860278:5, 12038632:8, 10861501:5, 9516449:3, 12198207:11, 19091788:9, 19038005:5, 15546867:6 <more data available...>",2,30,null,"positive"]
["TGFB1 --+> MET","Expression","In contrast, a combination of IL-6 and TGFbeta1 down-regulated c-met expression as well as Sp1 DNA binding activity., Real-time RT-PCR and Northern and Western blot analyses revealed that TGF-beta1 significantly induced c-met expression in HKC cells, which primarily took place at the gene transcriptional level., With respect to gene expression, fibrotic genes like transforming growth factor-beta (TGF-beta) and collagen Ialpha (Col-1alpha) were down-regulated by pirfenidone and increased expression of regenerative genes like hepatocyte growth factor (HGF) and c-met . <more data available...>","11469916:13, 15339794:3, 18652820:6, 15770602:6",2,4,null,"positive"]
["TGFB1 --+> A2M","Expression","It was blocked when bovine adrenocortical cells were exposed to 5,6-dichlorobenzimidazole riboside, a potent inhibitor of RNA polymerase II, suggesting that TGF-beta 1 acts as an activator of alpha 2-M gene expression at the transcriptional level., This is supported by the following observations: (i) Treatment of adrenocortical cells by FGF-2 resulted in a time-dependent and dose-dependent increase of alpha 2M synthesis, (ii) FGF-2 did not modify alpha 2M secretion rate; (iii) The induction of alpha 2M synthesis by FGF-2 was not observed in the presence of the transcription inhibitor DRB; (iv) The amount of alpha 2M mRNA was increased by 2 to 3 fold under either FGF-2 or TGF beta 1 treatment; (v) Optimal doses of TGF beta and FGF-2 synergistically increased alpha 2M synthesis. <more data available...>","1689294:5, 7524573:1, 9570034:1745, 15618353:1348",2,4,null,"positive"]
["TGFB1 --+> INPP5D","Expression","Activin/TGF-beta-induced expression of SHIP results in intracellular changes in the pool of phospholipids, as well as in inhibition of both Akt/PKB (protein kinase B) phosphorylation and cell survival., TGF-beta1 treatment does not increase IRAK-M or SHIP1 protein expression in shSMAD4 THP-1 cells, whereas it does so in shLUC THP1 cells, indicating that TGF-beta1 regulates IRAK-M and SHIP1 expression through a SMAD4-dependent pathway., lipopolysaccharide also upregulates the secretion and activation of TGFß, which, in turn, activates the transcription of the negative regulator SHIP. <more data available...>","12447389:5, 20404275:8, 15308103:1213, 15604218:1211, 17947710:1361, 16636301:1257, 19139077:265, 19139077:274, 19542365:220, 15778380:183 <more data available...>",2,16,null,"positive"]
["TGFB1 --+> THBS2","Expression","Using this assay, we observed that thrombospondin-1 and CISP/thrombospondin-2 syntheses were respectively stimulated threefold and twofold by a 24-h treatment with 2 ng/ml TGF beta 1., Further, p38 MAPK mediated induction of collagen I and TSP-2 expression by TGF-beta1 was still achieved in the presence of dexamethasone, showing that dexamethasone does not block p38 while it delays Smad2 phosphorylation and antagonizes stimulation of a Smad3/Smad4 dependent TGF-beta reporter construct., Further, the observation that TGFß can stimulate TSP-1 and -2 expression in bovine adrenal tissue [58] provides evidence to support further studies regarding the potential role of TGFß in regulating Thrombospondin expression in bovine follicles.","7698241:4, 15905080:5, 15616224:1300",2,3,null,"positive"]
["TGFB1 --+> VIM","Expression","Furthermore, induction of vimentin expression by TGF-beta1 and hypoxia was evaluated in gastric cancer cells., Here, we suggest a mechanism to explain how TGFbeta1 contributes to the up-regulation of vimentin expression while blocking myogenesis., Western blotting analysis showed that TGF-beta1 decreased cytokeratin and increased vimentin levels, while DMSO decreased both cytokeratin and vimentin., TGF-beta/IL-1beta treatment induced epithelial to mesenchymal-like phenotype transition (EMT), changing cell morphology and expression of vimentin and E-cadherin. <more data available...>","20358301:4, 17270292:2, 10580588:7, 20671927:3, 19213777:6, 1879463:2, 19116990:5, 19659836:8, 11752026:1166, 16382155:1202 <more data available...>",2,35,null,"positive"]
["TGFB1 --+> S100A4","Expression","TGF-beta1 increased S100A4 expression in cultured ileal fibroblasts., Furthermore, TGFbeta1 up-regulated epithelial markers CTNNB1 and CTNND1, but suppressed mesenchymal markers, such as S100A4, FGF1 and FGF2., Consistent with these observations, S100A4 increases cell invasion ability induced by TGF-beta in MCF10CA1a.cl1 cells, and depletion of the protein in MDA-MB-231 cells inhibits it., In vitro experiments using human dermal microvascular endothelial cells demonstrated that TGF-beta1 induced myofibroblastic features in human dermal microvascular endothelial cells, including spindle cell morphology, reduction of CD34 expression, and induction of S100A4, alpha-smooth muscle actin, and COL1A1 expression, as well as the increased nuclear expression of phospho-Smad2. <more data available...>","20489045:10, 20592463:9, 20070253:8, 19608867:2, 17974953:1193, 12163453:1072, 16889607:1246, 14747385:1161, 19487818:1150, 17562716:291 <more data available...>",2,11,null,"positive"]
["TGFB1 --+> CYBB","Expression","Transfection of wild-type mouse cardiac fibroblasts with AAV/TGFbeta (ACT)(1) markedly enhanced the expression of NADPH oxidases (p22(phox), p47(phox), and gp91(phox) subunits) and LOX-1, formation of reactive oxygen species, and collagen synthesis, concomitant with an increase in the activation of p38 and p44/42 mitogen-activated protein kinases ., TGF-ß1 upregulates the expression of p22phox, p47phox, p67phox, and gp91phox in rat mesangial cells (Figure 2B) and p22phox mRNA in tubular epithelial cells (Figure 2C), suggesting that TGF-ß1-induced reactive oxygen species may be NADPH oxidase dependent. <more data available...>","18182394:3, 12874439:1080, 12482831:1145",2,3,null,"positive"]
["TGFB1 --+> ITGB5","Expression","Thus, TGF-beta increases expression of the integrin beta(5) gene by mechanisms involving Sp1/Sp3 and Smad transcription factors., We investigated the effects of PPARalpha ligands on TGF-beta-induced beta3 and beta5 integrin expression and potential interaction between PPARalpha and TGF-beta signaling., In that scenario, however, Peroxisome proliferator-activated receptor-a activation antagonized transforming growth factor-ß-induced ß5-integrin transcription in vascular smooth muscle cells., Agonists of peroxisome proliferator-activated receptor-a inhibit TGFß-responsive ß5 integrin expression and disrupt formation of the Sp1-Smad4 complex, in parallel with induction of peroxisome proliferator-activated receptor-a/Smad4 interaction (43). <more data available...>","10964912:9, 12456495:3, 17098824:1241, 16249187:1329, 14684628:1206, 12130649:44",2,6,null,"positive"]
["TGFB1 --+> CSF1","Expression","Anti-TGF-beta 1 decreased (p < 0.05) M-CSF induced colonies in 5/6 donors., Transforming growth factor beta (TGF-beta) increased both the synthesis of CSF-1 and its accumulation in the matrix., The M-CSF activity in the conditioned medium of mouse osteoblast-like MC3T3-E1 cells was increased by TGF-beta as well as interleukin-1 treatment., Here we show that TGF-beta1 induces the expression of macrophage-CSF (M-CSF) in vascular endothelial cells via a signaling pathway(s) involving hydrogen peroxide (H2O2)., Other agents, including PTH (35), tumor necrosis factor-alpha (36), and transforming growth factor-beta (37), have been shown to increase MCSF expression at the level of gene transcription. <more data available...>","7804125:8, 8591991:10, 8048485:1, 9278333:1, 9492032:1246, 16707491:363, 17332318:77",2,7,null,"positive"]
["TGFB1 --+> RBP1","Expression","In both cell populations, transforming growth factor-beta 1 treatment increased CRBP-1 expression., We also demonstrate that CRBP-1 expression by fibroblasts is regulated in vitro by retinoic acid and transforming growth factor-beta1., The expression of CRBP-1 is regulated at the transcriptional level by TGF-beta and retinoic acid but not synergistically, suggesting a possible common pathway., TGF-ß1 should be capable of diffusing through the microporous membrane, subsequently modulating CRBP-1 transcription.","12004002:12, 9403724:10, 11319755:4, 12419830:1201",2,4,null,"positive"]
["TGFB1 --+> SOX9","Expression","Moreover, exogenous TGF-beta can induce Sox9 expression in the mandibular arch., In addition, up-regulation of Fibronectin and suppression of Sox9 expression by TGF-beta1 was also found to be mediated by CTGF., Transforming growth factor-beta treatment increased MAPK activity and Sox-9, aggrecan, and collagen type II gene expression., TGF-beta1 increased the Sox9 messenger ribonucleic acid expression to 180% compared to control group in intervertebral disc tissue., TGF-beta1-stimulated gene expression of chondrogenic regulators, Sox9, Runx2 and Ihh, was also affected by activity of PD98059 and SB203580, to different degrees. <more data available...>","18684439:6, 17111364:7, 15564911:11, 20157375:7, 20590658:6, 18496879:5, 16575901:3, 17525254:5, 18602912:6, 19321054:8 <more data available...>",2,15,null,"positive"]
["TGFB1 --+> NCF1","Expression","In addition, LPS-induced ERK phosphorylation and subsequent Ser345 phosphorylation on p47phox were significantly inhibited by TGF-beta1 pretreatment., TGF-beta1 at 10 ng/mL significantly increased the intercellular reactive oxidative species production and p47phox expression (P < 0.05)., Transfection of wild-type mouse cardiac fibroblasts with AAV/TGFbeta (ACT)(1) markedly enhanced the expression of NADPH oxidases (p22(phox), p47(phox), and gp91(phox) subunits) and LOX-1, formation of reactive oxygen species, and collagen synthesis, concomitant with an increase in the activation of p38 and p44/42 mitogen-activated protein kinases . <more data available...>","18566433:6, 19292057:5, 18182394:3, 12874439:1080",2,4,null,"positive"]
["TGFB1 --+> TGM2","Expression","In Western blot analysis, TGF-beta1 (1 ng/ml) treatment was found to steadily up-regulate TGase 2 expression for up to 7 days., Transforming growth factor-beta and interleukin -1beta induced Factor XIIIa and tTGase expression in cartilage and meniscal organ cultures., This study suggests that in the isolated perfused rat kidney and in the absence of other exogenous growth factors, TGF-beta1 selectively increases the synthesis of extracellular matrix and tissue transglutaminase without changes that would result in the reduction of extracellular matrix degradation. <more data available...>","16044258:3, 11438463:3, 10505687:11, 17460246:6, 12874459:1070, 14555988:1123, 11686302:1246, 9582307:46, 9114053:189, 11689553:280 <more data available...>",2,18,null,"positive"]
["TGFB1 --+> NFATC1","Expression","Similarly, TNF-alpha activates osteoclastogenesis by stimulating translocation of TGF-beta-induced NFATc1., Addition of Transforming growth factor-ß during differentiation to either lineage inhibited NFATc activation., Using quantitative real-time PCR, we found that transforming growth factor-ß1 treatment results in a 4.5-fold increase in NFATc1 transcript levels in neural crest stem cells (Fig. 6).","18060870:6, 12810687:1296, 15148306:1175",2,3,null,"positive"]
["TGFB1 --+> CD14","Expression","At 2 hr, 50 ng/ml TGF-beta 1 significantly lowered CD14 expression (51%, P = 0.043)., TGF-beta and VD3 synergistically increased the expression of differentiation-associated markers such as the CD11b and CD14 antigens, whereas TGF-beta and dexamethasone did not., Furthermore, TGF-beta/D3 treatment (but not D3 alone) elicits the expression of membrane CD14, FcRI, FcRII, CD11a, CD11b, CD11c, ICAM-1, and PECAM-1 Ag at a level comparable to that observed on normal human monocytes., The same CCAAT/enhancer-binding protein site was also involved in the TGF-ß/Vit D3-dependent activation of CD14 expression (42). <more data available...>","7526045:5, 10547074:1, 8383719:5, 11698458:1270, 12821938:1143, 18497880:1254",2,6,null,"positive"]
["TGFB1 --+> FCGR2B","Expression","Furthermore, TGF-beta/D3 treatment (but not D3 alone) elicits the expression of membrane CD14, FcRI, FcRII, CD11a, CD11b, CD11c, ICAM-1, and PECAM-1 Ag at a level comparable to that observed on normal human monocytes., IFN-a, IFN-?, TGF-ß, IL-10, and soluble IgG modulated CD32a and/or CD32b on circulating conventional DCs, which was similar to their effects on cytokine-induced monocyte-derived DCs.","8383719:5, 16167082:1141",2,2,null,"positive"]
["TGFB1 --+> GFAP","Expression","Cycloheximide did not block the effects of TGF-beta1 or FGF-2 on GFAP mRNA levels, but blocked the inhibitory effects of FGF-2 on the TGF-beta1-mediated increase in GFAP expression., Whereas untreated control cells expressed progressively the glial fibrillary acidic protein (GFAP) after arrest of multiplication, the addition of TGF beta 1 to proliferative cells prevented GFAP expression and accumulation of its mRNA., TGF-beta induced CysC and GFAP expression in AP-16 cells, an astrocyte progenitor-like cell line expressing GLAST (a glutamate transporter subtype specifically expressed in immature astrocytes). <more data available...>","9537840:5, 1397085:4, 15509901:2, 8170537:2, 8361632:2, 18419760:10, 19057972:3, 12118088:4, 10098836:1048, 11867550:1092 <more data available...>",2,14,null,"positive"]
["TGFB1 --+> ABCA1","Expression","TGF-beta1 significantly increased expressions of ABCA1, ABCG1 and SR-BI at both transcriptional and translational levels in a dose-dependent and time-dependent manner., transforming growth factor-ß increases ABC-1 expression and inhibits its down-regulation by interferon-?., TGF-ß1 also reduced foam cell formation by enhancing cholesterol efflux through increasing mRNA expression of ABCA1 and ABCG1., TGF-beta increases cholesterol efflux and ABC-1 expression in macrophage-derived foam cells: opposing the effects of IFN-gamma. <more data available...>","20057170:4, 11352993:1189, 11742878:1055, 15995168:2634, 20485864:4",2,5,null,"positive"]
["TGFB1 --+> CLU","Expression","At the same time, TGFbeta1 enhanced clusterin protein and mRNA expression., A single T to G base mutation in the AP-1 site (5'-TGAGGCA) abolishes TGFbeta-induced clusterin promoter transactivation., We hypothesize that activation of the TGF-beta signaling pathway, which often occurs after ionizing radiation exposure, can in turn activate the CLU promoter., Cytokines such as TGF beta 1 and interleukin 1 enhance the expression of clusterin, which may link clusterin to inflammatory mechanisms in Alzheimer disease. <more data available...>","10066375:3, 9334243:5, 15530543:10, 8892344:4, 9407436:5, 7730444:8, 8170537:2, 10406964:1149, 15671065:1426, 9334243:219 <more data available...>",2,33,null,"positive"]
["TGFB1 --+> SOCS3","Expression","TGF-beta inhibits IL-6-induced SOCS3 promoter activity in T cells., These data show that TGF-beta coordinately induces LIF and SOCS3 to promote prosurvival signaling., Furthermore, TGF-beta rapidly induces sustained SOCS-3 expression in macrophage/osteoclast precursors., In this study, we demonstrate that LPS-induced endogenous TGF-beta1 contributes to the inducible SOCS3 expression in macrophages., This suggests that TGF-beta-induced expression of SOCS3 may represent a crucial mechanism by which TGF-beta antagonizes specific anti-osteoclastic JAK/STAT signals, priming precursors for resorption rather than inflammatory functions. <more data available...>","19535626:4, 20181800:8, 12646633:7, 17920684:3, 13679037:8, 18031698:1059",2,6,null,"positive"]
["TGFB1 --+> GUSB","Expression","Beta-glucuronidase expression was increased by TGF-beta and decreased by IFN-gamma.","9712070:10",2,1,null,"positive"]
["TGFB1 --+> MCL1","Expression","The increased levels of the cytokines, IL-4, IL-10, prostaglandin E2, and TGF-ß enhance the expressions of c-FLIP, Bcl-xL, and Mcl-1, which are involved in the resistance to apoptosis (32-34).","16740684:1107",2,1,null,"positive"]
["TGFB1 --+> AIF1","Expression","Furthermore, functional studies showed specific allograft inflammatory factor-1 isoform expression stimulation by transforming growth factor-beta., Stimulation of peripheral blood mononuclear cells with TGFbeta caused a specific and significant increase in the expression of AIF-1 isoform 2 transcripts (P < 0.005), which was due to stabilization of AIF-1 isoform 2 messenger RNA., Ten percent FCS, IFN-?, and interleukin-1ß are capable of inducing this protein, whereas AIF-1 is not expressed in unstimulated cells. basic fibroblast growth factor, platelet-derived growth factor, and transforming growth factor-ß can induce AIF-1 protein expression to a small degree.","17053503:3, 16868985:9, 10894811:1159",2,3,null,"positive"]
["TGFB1 --+> SYNPO","Expression","Anti-TGF-ß antibody 2G7 blocked synaptopodin expression and inhibited the redistribution of zona occludens-1 (Figure 1D).","16207831:1114",2,1,null,"positive"]
["TGFB1 --+> PTGS1","Expression","Release of histamine, cysteinyl-leukotrienes, and tumour necrosis factor alpha was strongly reduced whereas prostaglandin D2 generation and cyclooxygenase 1 and 2 expression were upregulated by TGF-beta1., Prostaglandin E2, transforming growth factor-beta, and interleukin-1 beta variably regulate the expression of cyclooxygenase 1, cyclooxygenase 2, and lysyl oxidase in IMR90, human embryo lung fibroblasts., In a few experiments in MC3T3-E1 cells, TGFbeta stimulated PGHS-1 messenger RNA levels up to 5-fold at 4 h, with little change in glyceraldehyde 3-phosphate dehydrogenase (Fig. 1).","15951536:7, 8872612:0, 9348193:1158",2,3,null,"positive"]
["TGFB1 --+> IL13RA1","Expression","Transforming growth factor-ß can enhance the effects of IL-13 on activation and survival of eosinophils, and on the surface expression of IL-13Ra1 on eosinophils (Myrtek et al., 2004[Go]).","16888081:1218",2,1,null,"positive"]
["TGFB1 --+> CSF1R","Expression","In contrast, TGF-beta 1 down-modulated IL-3 and CSF-1 receptor expression by 54 and 55%, respectively, by 24 h., Cell surface expression of the monocyte/macrophage-specific marker c-fms was increased 3.1-fold following TGF-beta 1 treatment., Antagonists of TGF-beta1 signaling significantly inhibited both the induction of c-fms expression and cellular invasiveness, suggesting that additional studies are warranted to assess the therapeutic potential of TGF-beta antagonists in endometriosis., TGF-ß1 induces the expression of c-fms. <more data available...>","8409417:3, 8930403:10, 19505996:8, 17332318:234, 17332318:219, 17332318:248, 17332318:223, 17332318:289, 17332318:84, 17332318:235 <more data available...>",2,13,null,"positive"]
["TGFB1 --+> SRGN","Expression","Metabolic labeling experiments reveal that TGF-beta induces selectively the expression of proteoglycan-I, whereas the level of proteoglycan-II remains unaltered.","1863601:2",2,1,null,"positive"]
["TGFB1 --+> CX3CR1","Expression","TGF-beta1 upregulates CX3CR1 expression and inhibits fractalkine-stimulated signaling in rat microglia., These results showed that TGFß enhanced CX(3)CR1 expression and attenuated the LPS-induced increase in IL-1ß expression.","12446007:100, 20570721:11",2,2,null,"positive"]
["TGFB1 --+> ALOX5AP","Expression","The addition of anti-TGF-beta1 antibody reduced hydroxynonenal-induced 5-LOX and FLAP expression by 40%, indicating the partial involvement of a TGF-beta1-dependent mechanism., The expression of FLAP in Osteoarthritis osteoblasts is also modulated differently by 1,25(OH)2D3 and TGF-beta depending on their endogenous low and high prostaglandin E2 levels., TGFbeta1 and/or 1,25(OH)(2)D(3) induced a rapid and marked enhancement ( approximately 4-13-fold) in FLAP messenger RNA levels, which was associated with a subsequent and late increase in leukotriene B(4) production and prostaglandin E(2) synthesis. <more data available...>","20144213:12, 17156456:12, 15593193:4, 11090070:5",2,4,null,"positive"]
["TGFB1 --+> TF","Expression","However, in quiescent, well-differentiated cells, TGF-beta repressed the mitogenic responses to both nutrients alone (by 90%) and to nutrients plus the exogenous stimulatory factors epidermal growth factor (E), insulin (I), and transferrin (T) (by 55-65%)., TGF-beta(1) and bFGF upregulate transferrin gene expression of cultured lens epithelial cells remarkably, can reduce lenticular oxidative damaging process in which transferrin participates and play an important role in the pathological mechanism of cataract formation after extracapsular cataract extraction.","1701348:3, 11835825:8",2,2,null,"positive"]
["TGFB1 --+> HPGD","Expression","Induction of 15-PGDH expression by TGF-beta1 was synergistically stimulated by the addition of Wnt3A which was inactive by itself., A number of anti-cancer agents, such as transforming growth factor-beta1 (TGF-beta1), glucocorticoids and some histone deacetylase inhibitors were found to induce 15-PGDH expression.","16844092:6, 17481556:12",2,2,null,"positive"]
["TGFB1 --+> ITGAX","Expression","Furthermore, TGF-beta/D3 treatment (but not D3 alone) elicits the expression of membrane CD14, FcRI, FcRII, CD11a, CD11b, CD11c, ICAM-1, and PECAM-1 Ag at a level comparable to that observed on normal human monocytes.","8383719:5",2,1,null,"positive"]
["TGFB1 --+> CCND1","Expression","The expression of cyclin D1 in MCF10A cells is regulated by TGF-ß treatment., In addition, Sox17 counteracted repression of the cyclin D1 promoter by TGF-ß1 and Smad3., These results strongly suggest that TGF-ß regulates cyclin D1 expression in a ß-catenin-dependent manner., TGF-ß stimulates cyclin A expression without affecting cyclin D-cdk4/6 activity in suspended NRK cells., TGF-ß stimulated cyclin D1 expression in Ad-GFP-infected but not Ad-Cre-infected chondrocytes (Fig. 7a)., Although TGF-ß stimulated cyclin D1 expression in chondrocytes, this effect was abolished by inhibition of ß-catenin signaling. <more data available...>","18715870:116, 19479035:326, 16690606:242, 10702223:90, 16690606:239, 16690606:67, 19479035:260, 16517699:263, 15811853:143, 19479035:288 <more data available...>",2,19,null,"positive"]
["TGFB1 --+> Ctla2a","Expression","This suggests that TGF-ß promotes the up-regulation of the CTLA-2a expression on responding T cells.","19801522:182",2,1,null,"positive"]
["TGFB1 --+> ADAMTS1","Expression","Expression of ADAMTS1 is induced by transforming growth factor-ß in keratinocytes.","15843381:262",2,1,null,"positive"]
["TGFB1 --+> STAT1","Expression","IFN-gamma down-regulates TGF-beta1-induced IgA expression through Stat1 and p300 signaling.","20016942:100",2,1,null,"positive"]
["TGFBR1 --+> TGFB1","Expression","This persistence was because of autocrine synthesis of TGF-beta1, which was inhibited by both anti-TGF-beta1 antibody and the ALK5 inhibitor SB431542., Based on these findings, we hypothesize that the interaction between c-Ski and TßRI might interfere with nuclear translocation of the R-Smad/Smad4 complex, thereby attenuating TGF-ß signaling., These results show that constitutively reduced Tgfbr1-mediated TGF-beta signaling significantly enhances colorectal cancer development and results in increased tumor cell proliferation. <more data available...>","19193641:6, 20959473:4, 19147584:4, 19535626:7, 19432813:7",2,5,null,"positive"]
["LGALS3 --+> CCND1","Expression","Recombinant galectin-3 induced cardiac fibroblast proliferation, collagen production, and cyclin D1 expression., Interestingly, galectin-3 induces cyclin D1 expression (an early G1 cyclin) and its associated kinase activity in the absence of cell anchorage., We found that galectin-3 induces cyclin D(1) promoter activity in human breast epithelial cells independent of cell adhesion through multiple cis-elements, including the SP1 and CRE sites., Finally, we demonstrated that silencing of galectin-3 enhanced apoptosis induction with chemotherapeutic agents by further reducing the expression of anti-apoptotic and/or cell survival molecules such as survivin, cyclin D1, and XIAP, and increasing the expression of pro-apoptotic XAF-1. <more data available...>","15520318:6, 10463621:6, 12439750:3, 19843071:10, 17403142:1279, 11062152:1156, 11724777:1188, 19190323:249, 15867344:44",2,9,null,"positive"]
["LGALS3 --+> TGFB1","Expression","Gal-3 increased transforming growth factor-ß1, -ß2, and -ß3 expression in left ventricle compared with vehicle group; Ac-SDKP inhibited this effect., Thus disruption of the Galectin-3gene blocks fibrosis despite similar expression levels of TGF-ß.","19098114:1203, 16549783:134",2,2,null,"positive"]
["CCND1 --+> HSPB8","Expression","The transient transfection with cyclin D1 increased HSPB8 levels ~2-fold when these blots were quantified in image analysis; the HSPB8 knockdown was ~8-fold in each case.","18006821:1234",2,1,null,"positive"]
["CXCL10 --+> ISG15","Expression","Consistent with this finding, Respiratory syncytial virus-induced beta interferon (IFN-beta), interferon-inducible protein 10 (IP-10), chemokine ligand 5 (CCL-5), and IFN-stimulated gene 15 (ISG15) expression levels were decreased in RIG-I-silenced cells during the early phase of infection but not at later times (18 h postinfection).","17108032:5",2,1,null,"positive"]
["CEBPD --+> CEBPA","Expression","Previous investigations indicated that transcription of the C/EBPalpha gene is sequentially activated during differentiation, initially by C/EBPbeta and C/EBPdelta and later by C/EBPalpha (autoactivation)., Nuclear expression of the 36-kilodalton C/EBP delta protein increases immediately after birth, followed first by increases in the 38-kilodalton C/EBP beta protein expression and then by increases in the 42-kilodalton C/EBP alpha protein expression., These data demonstrate that Myc specifically inhibits the terminal stages of the adipogenic program and suggest that Myc may act by blocking C/EBPbeta- and C/EBPdelta-directed activation of C/EBPalpha and PPARgamma2 expression, although the precise molecular mechanism is not understood. <more data available...>","10373535:1, 7910803:4, 10623469:4, 18703634:1194, 18930917:1043, 18653467:1203, 12138207:1046, 12186946:1140, 16154099:1059, 17273556:1253 <more data available...>",2,43,null,"positive"]
["CEBPD --+> TF","Expression","In the non-transferrin-expressing HeLa cells, the transferrin promoter could be activated by C/EBP-delta., Suire et al. (12) showed, in cotransfection assays, that overexpression of C/EBP alpha (C/EBP) and C/EBP delta (NF-IL6beta, CRP3) in Sertoli cells stimulated transcription from the cAMP-regulated transferrin promoter containing a C/EBP binding site.","8226864:7, 9927313:1054",2,2,null,"positive"]
["CEBPD --+> CCND1","Expression","Silencing of C/EBPdelta, Cdc27, or the anaphase promoting complex/cyclosome coactivator Cdh1 (FZR1) in MCF-10A breast epithelial cells increased cyclin D1 protein expression.","20439707:3",2,1,null,"positive"]
["CEBPD --+> SOCS3","Expression","The doxycycline-dependent expression of C/EBP-d neither increased Spi-2 and Socs3 transcripts nor interfered with their induction by IL6RIL6 (Fig. 5B).","14600146:227",2,1,null,"positive"]
["CEBPA --+> CSF1","Expression","For example, when expressed alone, RUNX1, C/EBPa, and PU.1 are poor activators of the M-CSF promoter.","15988004:1056",2,1,null,"positive"]
["CEBPA --+> PROS1","Expression","Reporter gene analysis suggests that members of the CCAAT/enhancer binding protein (C/EBP) family of transcription factors are potent activators of protein S gene transcription in HepG2 cells.","17061980:6",2,1,null,"positive"]
["STAT3 --+> CEBPA","Expression","Gene expression profile and quantitative PCR analysis of G-CSF-stimulated cell lines revealed that the expression of C/EBPalpha was up-regulated by the activation of Stat3., Treatment of freshly isolated adult rat hepatocytes with 10-100 mM ethanol rapidly (< 3 min) inhibits interleukin-6 (IL-6)-induced STAT3 activation, tyrosine and serine phosphorylation and IL-6-induced CCAAT enhancer binding protein (C/EBP) alpha and beta mRNA expression., One is that activated Stat3 binds to the promoter region of C/EBPa and induces the transcription of C/EBPa. <more data available...>","15664994:3, 10486586:2, 15664994:261, 15664994:66, 15664994:47, 15664994:255, 15664994:266",2,7,null,"positive"]
["STAT3 --+> OSMR","Expression","STAT3 activation further enhances OSMR expression, thereby establishing a positive-feedback loop., We found that Stat3flx/flx/NIC tumors expressed lower levels of both cebpd and osmr, two genes that are induced by Stat3 (28, 29)., We show that OSMR expression is dependent on LIF-induced STAT3 and that the subsequent OSMR-mediated signal inhibits the phosphorylation of STAT5 and coordinately activates signal transducer and activator of transcription3-dependent apoptosis in the involuting mammary gland.","20348953:1139, 19690134:1181, 18927239:1084",2,3,null,"positive"]
["STAT3 --+> FLI1","Expression","A recent study showed that an enhanceosome responsible for activating SCL transcription was required for GATA-2, Fli-1, and Elf-1.37 As the expression of Fli-1 was induced via the STAT3 transcription factor,38 phosphorylation of STAT3 by the binding of HGF to c-met39 might activate Fli-1 or Elf-1.","14701703:1187",2,1,null,"positive"]
["STAT3 --+> CD9","Expression","Furthermore, activation of STAT3 induced the expression of CD9, indicating the LIF/STAT3 pathway is critical for maintaining CD9 expression., In a previous study, the addition of leukemia inhibitory factor or STAT3 activation induced CD9 expression in embryonic stem cells [13], which indicates that the leukemia inhibitory factor/STAT3 pathway is critical for maintaining CD9 expression.","11950938:5, 12954725:1222",2,2,null,"positive"]
["STAT3 --+> HPGD","Expression","Activation of signal transducer and activator of transcription3 may augment potently the androgen bound receptor signaling and contribute to synergistic induction of 15-PGDH expression by combined treatments with IL-6 and dihydrotestosterone.","14749354:1215",2,1,null,"positive"]
["STAT3 --+> CD14","Expression","STAT3 inhibitor pretreatment could also down-regulate high CD14 and CD16 expression by BxPC-3 conditioned medium treatment.","17545630:1248",2,1,null,"positive"]
["STAT3 --+> SYNPO","Expression","Stat3-DN inhibited nef-containing vector-induced cyclin E expression and significantly increased synaptopodin expression (Figure 5C).","15343382:1157",2,1,null,"positive"]
["STAT3 --+> SBNO2","Expression","IL-10-mediated induction of ETV3 and SBNO2 expression was dependent upon both STAT3 and a stimulus through the TLR pathway.","18025162:2",2,1,null,"positive"]
["STAT3 --+> VIM","Expression","Specific inhibition of STAT3 activation by Janus kinase2-specific inhibitor AG490 blocked STAT3 phosphorylation, cell motility, induction of N-cadherin and vimentin expression and IL6 production., Stat3 can enhance transcription of the vimentin gene.","19088723:9, 14712222:1097",2,2,null,"positive"]
["STAT3 --+> TF","Expression","proteolysis-inducing factor activates both the transcription factors NF-kB and STAT3, which result in the increased production of IL-8, IL-6, and C-reactive protein and the decreased production of transferrin.","11259367:4",2,1,null,"positive"]
["STAT3 --+> CXCL10","Expression","Inhibitors of p38 mitogen-activated protein kinase, c-Jun N-terminal kinase (JNK), phosphatidylinositol-3-OH kinase and signal transducer and activator of transcription 3 decreased OSM-induced CXCL10 production.","19616927:6",2,1,null,"positive"]
["STAT3 --+> MET","Expression","U-STAT3 induces the expression of well-known oncogenes, such as MRAS and MET, which are late-phase genes induced by IL-6.","19478064:203",2,1,null,"positive"]
["STAT1 --+> MCL1","Expression","Further, mutation of STAT1/STAT2 prevented the effect of both Abeta and SGK1 on Mcl-1 expression.","19609277:10",2,1,null,"positive"]
["STAT1 --+> B2M","Expression","The same authors also show that transcription of the ß2-microglobulin gene is down-regulated in mouse Stat1-null T lymphocytes., A direct target of EOMES, IL2RB (CD122) (29), is also 7.4-fold up-regulated. ß-2 microglobulin , which is up-regulated by STAT1 and is part of MHC I, is fivefold up-regulated in L&H cells.","10921891:1271, 18794340:1113",2,2,null,"positive"]
["STAT1 --+> ISG15","Expression","A single mutation (K161A) in the p48 contact region of Stat1 inhibited the Stat1-p48 interaction as well as the IFN-a-triggered ISG15 gene induction, whereas this mutation had no effect on either the Stat1-Stat2 interaction or the IFN-? response which is independent of p48 (Horvath et al., 1996).","10851063:1089",2,1,null,"positive"]
["STAT1 --+> CYBB","Expression","At the same time, STAT1 and IRF-1 together promote the interferon-?-induced transcription of the CYBB gene (26).","16162660:1069",2,1,null,"positive"]
["STAT1 --+> HLA-E","Expression","STAT-1 and GATA-1 bind to the IRR and upstream IFN response region, respectively, to stimulate transcription from the HLA-E promoter (73)., The transcription factors Stat-1 and GATA-1 bind to the IFN response region and upstream IFN response region, respectively, to stimulate transcription from the HLA-E promoter (26, 27).","18566411:1611, 17142760:1073",2,2,null,"positive"]
["STAT1 --+> HSPB1","Expression","STAT-1 was required for transcriptional activation of the HSP27 gene, but not for the HSP70 gene, and cDNA transfection of STAT-1 in mumps virus-infected cells restored thermotolerance.","12917439:6",2,1,null,"positive"]
["STAT1 --+> IFIT3","Expression","Our results suggest that the induction of IFIT4 transcription by IFN-alpha depends upon sequential activation of PKCdelta, JNK and STAT1, and that the influence of PKCdelta or JNK on interferon-alpha-mediated induction of IFIT4 is dependent upon the phosphorylation of STAT1 at Ser-727.","17933493:6",2,1,null,"positive"]
["STAT1 --+> CASP1","Expression","Activation of caspase-1 gene expression requires IRF-1 and Stat-1 (24, 32)., In addition, overexpression of STAT-1 together with interferon-? treatment further enhanced the activity of the caspase-1 promoter., Recently, interferon-? and STAT-1 have been shown to modulate the level of caspase-1 expression in non-cardiac cells (28)., Moreover, transfection of antisense STAT-1 inhibited both the interferon-?/STAT-1- and ischemia-induced activation of the caspase-1 promoter (Fig. 5)., Down-regulation of EGFR is also postulated to induce apoptosis, and activation of Stat-1 has been reported to induce p21/WAF-1 or caspase 1 that may result in cell cycle arrest or apoptosis, respectively. <more data available...>","16135520:78, 10744676:204, 10744676:201, 10744676:206, 12714587:265, 17339457:351, 10744676:212, 10640742:219, 10744676:264, 9694822:49",2,10,null,"positive"]
["STAT1 --+> IFI27","Expression","From results presented here, it is reasonable to propose that up-regulated STAT1 may enhance IFI27 and OAS1 expression in breast tumors.","19478064:183",2,1,null,"positive"]
["STAT1 --+> CXCL10","Expression","STAT1 was critical for IFN-gamma induction of both the Cxcl9 and Cxcl10 genes in microglia and in microglia and astrocytes, respectively.","20585034:7",2,1,null,"positive"]
["CSF1 --+> NFATC1","Expression","Furthermore, anti-CD11b antibodies inhibited NFATc1 expression induced by M-CSF and RANKL in BMMs., S3 shows the normal osteoclast differentiation and expression of NFATc1 in NFATc2-/- monocyte/macrophage precursor cells that were stimulated with RANKL/M-CSF., Inhibition of c-Fos and NFATc1 expression induced by RANKL and M-CSF in RAGE-deficient prefusion osteoclasts To further understand how RAGE regulates osteoclast maturation and function, we examined expression of transcriptional factors essential for osteoclastogenesis, including c-Fos and NFATc1 (39, 40). <more data available...>","18775427:4, 16275763:1202, 16606672:1165, 17403683:264",2,4,null,"positive"]
["CSF1 --+> CEBPA","Expression","Ectopic expression of THOC5 mimicked M-CSF mediated cell maturation and enhanced protein expression of the myeloid transcription factors C/EBPbeta, C/EBPalpha, Pu-1 and also GAB2 (a PI-3 Kinase and macrophage development regulator)., M-CSF and G-CSF use separate pathways to activate ERK and modify C/EBPa .","19015024:4, 19587381:1161",2,2,null,"positive"]
["CSF1 --+> CCND1","Expression","Previously we showed that the macrophage-activating agent lipopolysaccharide blocks CSF-1-induced proliferation and cyclin D1 expression in macrophages., We further demonstrated that Cdc42 modulated M-CSF-stimulated cyclin D expression and phosphorylation of Rb and induced caspase 3 and Bim, thus contributing to osteoclast proliferation and apoptosis rates., In contrast to some other growth factor/cell systems, no evidence was obtained using the inhibitors for the involvement of PI3-kinase or p70s6k in CSF-1-mediated induction of c-fos mRNA expression or Erk-1 activity; in addition, no evidence was found for an involvement in the CSF-1-mediated increase in cyclin D1 expression or STAT activation. <more data available...>","9722538:2, 20501942:5, 9608681:6, 10602507:1124, 1483347:100, 9139801:1201, 10453356:1406, 17142780:1172, 11230342:1041, 9722538:50 <more data available...>",2,19,null,"positive"]
["CSF1 --+> CD14","Expression","It has been demonstrated that the expression of CD16 and CD14 is regulated by macrophage colony stimulating factor (M-CSF) and GM-CSF., M-CSF was also shown by flowcytometric analysis to influence the expression of CD14, a receptor for LPS, which might render monocytes more sensitive to LPS., Daily administration of macrophage colony stimulating factor (M-CSF) to the mice resulted in increased levels of MSR-A expression and reduced levels of CD14 as well as several cytokine expressions, leading to shortening of the inflammatory process. <more data available...>","12153694:6, 8877404:9, 10594845:5, 9566797:4, 15256426:1265",2,5,null,"positive"]
["CSF1 --+> CYBB","Expression","Consistent with this, we find that expression of gp91phox and p67phox protein is also increased by M-CSF differentiation in Western blots of cell lysate proteins (Fig. 1C)., Of interest to the current studies, HoxA9 overexpression in murine myeloid cells does not impair granulocyte-colony stimulating factor- or macrophage-colony stimulating factor-induced expression of gp91Phox, a phagocyte respiratory burst oxidase protein (4).","16210632:1196, 15681849:71",2,2,null,"positive"]
["CSF1 --+> TREM2","Expression","Addition of macrophage colony stimulating factor (M-CSF) to LN cell culture allowed the proliferation and expression of TREM2 in LN cells, and the addition of neutralizing anti-M-CSF antibodies suppressed the proliferation of LN cells despite the expression of TREM2., Whereas Humphery et al. recently reported that TREM-2 expression is induced during in vitro osteoclastogenesis induced by culture bone marrow-derived macrophages with macrophage CSF (MCSF) and the receptor activator of NF-?B ligand (4), we find that differentiation of macrophages in MCSF alone leads to expression of TREM-2. [Figure 3] View larger version (33K): [in this window] [in a new window] .","20345919:4, 16951310:1159",2,2,null,"positive"]
["CSF1 --+> SERPING1","Expression","Interferon-gamma and alpha , colony stimulating factor-1, interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) all induce C1-INH synthesis in a variety of cell types.","9777421:6",2,1,null,"positive"]
["CSF1 --+> TLR2","Expression","CSF-1 also down-regulated expression of TLR1, TLR2, and TLR6, but not the LPS receptor, TLR4, or TLR5., TLR-2 expression on monocytes was enhanced by macrophage colony-stimulating factor (M-CSF) and interleukin-10 (IL-10), but was reduced by transforming growth factor beta1, while CD16 expression was inducible by these cytokines., Toll-like receptor 2 and 4 surface expressions on human monocytes are modulated by interferon-gamma and macrophage colony-stimulating factor.","11751985:7, 15146415:10, 11672593:100",2,3,null,"positive"]
["CSF1 --+> C3","Expression","Macrophage colony-stimulating factor (M-CSF) enhances complement component C3 production by human monocytes/macrophages.","8477063:100",2,1,null,"positive"]
["CSF1 --+> ITGB2","Expression","The levels of CD11a and CD18 expression on granulocytes were significantly enhanced by administration of M-CSF.","11789672:6",2,1,null,"positive"]
["CSF1 --+> LGALS3","Expression","Macrophage colony-stimulating factor (M-CSF), which is present at increased levels in MRL/lpr mice, but not in MRL/Mp- +/+ mice, induced the expression of Mac-2 antigen and Fas antigen on spleen adherent cells of MRL/Mp- +/+ mice.","8870694:4",2,1,null,"positive"]
["CSF1 --+> TNFRSF1A","Expression","Cell surface expression of TNFR1/2 expression on monocytes was induced by IL-10, and more efficiently in combination with M-CSF.","16859503:4",2,1,null,"positive"]
["CSF1 --+> P2RX7","Expression","Furthermore, lipopolysaccharide and M-CSF could up-regulate P2X7 receptor expression in monocytes, while IFN-gamma, TNF-alpha and GM-CSF had weak effects, but pretreatment with these inducers could not further enhance lipopolysaccharide-stimulated P2X7 receptor expression in monocytes.","15830104:6",2,1,null,"positive"]
["CSF1 --+> CSF1R","Expression","However, after 48 h, M-CSF significantly stimulated c-Fms expression., IL-10 together with M-CSF increased the expression of M-CSF receptors., This treatment completely prevented M-CSF-induced c-Fms expression in a dose-dependent manner but had little effect on TNFa-induced c-Fms up-regulation (Fig. 5D)., Incubation with CSF-1 down-regulated CSF-1R expression and was associated with proliferation of mononuclear cells with decreased CSF-1R binding., We demonstrated that one mechanism by which this occurs is PU.1 down-regulation by the negative control of NFI-A on M-CSFR levels (Fig. 7) because M-CSF induces PU.1 expression through M-CSFR in the hematopoietic myeloid-osteoclast lineage (1-3). <more data available...>","16461346:213, 8978307:46, 16461346:221, 19819976:310, 19059913:261, 19628784:169",2,6,null,"positive"]
["NFATC1 --+> CCND1","Expression","Heit et al. showed that transgenic activation of NFATc1 in ß-cells induces proliferation by inducing Cyclin D and Cdk4 levels [23].","20689817:1266",2,1,null,"positive"]
["NFATC1 --+> ID3","Expression","Accordingly, we propose a model whereby early growth response1-NF-ATc1 cooperatively induces inhibitor of DNA binding 3 expression, which in turn promotes traversal of the ß-selection checkpoint by suppressing the activity of E proteins (54, 56, 68).","17878368:1298",2,1,null,"positive"]
["NFATC1 --+> PDPN","Expression","In vitro, endogenous and VEGF-A-induced VEGFR-3 and podoplanin expression by human microvascular endothelial cells was reduced by siRNA to NFATc1, to levels comparable to reductions seen with siRNA to Prox-1.","19233265:8",2,1,null,"positive"]
["NCF1 --+> TLR2","Expression","Small inhibitory RNA to p47Phox in THP-1 cells abrogated high-glucose-induced TLR2 and TLR4 expression.","18650365:10",2,1,null,"positive"]
["TLR2 --+> ITGB2","Expression","Peptidoglycan (TLR2 ligand), flagellin (TLR5 ligand), and Imiquimod R837 (TLR7 ligand) could significantly upregulate cell surface expression of intercellular adhesion molecule (ICAM)-1 and CD18, and induce the release of IL-1beta, IL-6, IL-8, growth-related oncogene -alpha, and superoxides of eosinophils.","17332440:5",2,1,null,"positive"]
["TLR2 --+> CEBPD","Expression","TLR2 signaling by LpqH induced expression of liver inhibitory protein and C/EBPd and enhanced expression of LAP at time points that correlated kinetically with the onset of inhibition of IFN-?-induced CIITA expression., Toll-like receptor2 stimulation also induces C/EBPd expression and binding to the CIITA promoter [31].","17982082:1080, 19629181:349",2,2,null,"positive"]
["TLR2 --+> LCN2","Expression","LCN2 expression is increased in response to activation of TLR2 and TLR4 signaling by bacterial peptides (42).","18317594:1267",2,1,null,"positive"]
["TLR2 --+> CD86","Expression","TLR2 is essential for neisserial porin up-regulation of B7-2 and class II MHC in B cells ., Anti-TLR2 blocked increases in the CD86 median fluorescence intensity, but not the percentage of cells positive for CD86., There may be some differences in the Toll-like receptor2-mediated signaling pathway between cytokine production and CD83/CD86 expression., This indicates that the up-regulation of B7-2 and class II MHC surface expression was dependent on the normal expression of TLR2 on the B cell., They also showed that, in human Immature dendritic cells, cytokine production and CD83/CD86 expression were independently induced by M161Ag through TLR2. <more data available...>","11823477:142, 11160304:195, 11160323:247, 11823477:146, 11160323:191, 19109203:128, 11316801:237, 19109203:149, 11160304:179, 11823477:182",2,10,null,"positive"]
["TLR2 --+> ITGAX","Expression","The TLR2 agonist Pam3Cys significantly stimulated the maturation of DCs by enhancing the surface expression of CD11c, MHC class I, MHC class II, CD40, CD80, and CD86.","19109203:128",2,1,null,"positive"]
["TLR2 --+> HSPB1","Expression","TLR1/2 ligand palmitoyl-3-cysteine-serine-lysine-4 (Pam3CSK4) induces activation of PKDs via a PKC-independent manner, and Pam3CSK4-induced expression of heat shock protein 27 and MCP-1, as well as activation of PKDs, is inhibited by Gö6976, but not by broad-spectrum PKC inhibitors, in mouse bone marrow-derived mast cells (26).","19414785:65",2,1,null,"positive"]
["TLR2 --+> STAT3","Expression","TLR2 activation triggers STAT3 and Smad3 activation., TLR2 activation sequentially stimulates NF-?B, STAT3 and Smad3 activation., In addition, blockade of TLR2 abrogated peptidoglycan-SA-induced STAT3 and Smad3 activation. [thumbnail] ., Secondly, HSP60 activation of TLR2 mediates the expression and phosphorylation of Stat3 in tumor cells., These finding indicated that peptidoglycan-SA-stimulated TLR2 activation increased NF-?B, STAT3 and Smad3 activities depending on a time pattern., Moreover, targeting TLR2 in the host or in the melanoma cells markedly inhibited the B16 cell-induced phosphorylation of Stat3 (Fig. 3F). <more data available...>","20520770:250, 20520770:260, 20520770:255, 19654875:266, 20520770:318, 19654875:200, 20520770:319, 19654875:159, 19654875:164",2,9,null,"positive"]
["CD14 --+> CD86","Expression","In contrast, immature dendritic cells cultured in G4 plus human pancreatic RNase or eosinophil-derived neurotoxin for 48 h, although still CD14-, up-regulated the surface expression of CD83, CD86, and HLA-DR, indicating that human pancreatic RNase and eosinophil-derived neurotoxin treatment induced phenotypic maturation of DCs (Fig. 7A).","15528350:1252",2,1,null,"positive"]
["CD14 --+> CD83","Expression","In contrast, immature dendritic cells cultured in G4 plus human pancreatic RNase or eosinophil-derived neurotoxin for 48 h, although still CD14-, up-regulated the surface expression of CD83, CD86, and HLA-DR, indicating that human pancreatic RNase and eosinophil-derived neurotoxin treatment induced phenotypic maturation of DCs (Fig. 7A).","15528350:1252",2,1,null,"positive"]
["CD14 --+> ITGAX","Expression","Treatment of U937 cells with PMA markedly increased CD14, CD11a, CD11b and CD18 antigen expression, and slightly increased CD11c expression., In particular, those for CD11c and tumor necrosis factor a (TNFa) were markedly increased, and there were lesser, but significant, increases in Spp1, CD14, CD45, CCL9, Toll-like receptor 4 (TLR4), and interleukin-1B (IL-1ß) (Fig. 6G,H).","1689274:1, 18160655:1251",2,2,null,"positive"]
["CD14 --+> CD68","Expression","human microglia cell line clone 3 cells are typical microglia, as suggested by the constitutive expression of Iba-1 and CD14, and IFN-gamma-induced expression of CD11b, CD68 and MHCII.","20375612:3",2,1,null,"positive"]
["SOX9 --+> CLU","Expression","Mutant Kras blocks acinar regeneration in favor of a persistently dedifferentiated state. (A-H) Clusterin and Sox9 (I-P) expression during regeneration and Kras-induced acinar-to-ductal metaplasia. (A and I) Clusterin expression is limited to some normal ducts in PBS-treated Pdx1-CreEarly mice, while Sox9 is restricted to ducts and centroacinar cells (arrowheads). (E and M) Acini in PBS-treated Pdx1-CreEarly;LSL-KrasG12D mice are negative for Clusterin and Sox9, while normal ducts and spontaneous pancreatic intraepithelial neoplasias are positive (asterisks). (B, F, J, and N) Damaged duct-like cells of both genotypes display clusterin- and Sox9-positive cells (insets). (C, D, K, and L) Clusterin and Sox9 are mainly restricted to duct cells (arrowheads) following regeneration in Pdx1-CreEarly pancreata.","20071774:1134",2,1,null,"positive"]
["SOX9 --+> LXN","Expression","BMP-2 treatment upregulated Sox9 expression, and Sox9 stimulated the promoter activity of latexin.","19059214:7",2,1,null,"positive"]
["TGM2 --+> TGFB1","Expression","In addition, TG2 also activates transforming growth factor-beta (TGF-beta)., Particularly relevant is the finding that both TGF-beta and IL-12 regulations were significantly altered in the absence of TG2., Free Gd3+ ions may also activate tissue transglutaminase, which in turn activates transforming growth factor beta (TGF-beta) produced by dendritic cells., Increased TG2 expression in these fibroblasts led to NF-kappaB activation, resulting in the increased expression of transforming growth factor beta(1). <more data available...>","18688035:2, 15905580:8, 19886227:11, 19657147:2, 18558621:6, 12810961:2, 18523305:1259, 15199098:1330, 11686302:1320",2,9,null,"positive"]
["TGM2 --+> CYBB","Expression","Inhibition of cross-linking activity of TG2 by monodansylcadaverin in these cells led to diminished nitroblue tetrazolium positivity, production of less superoxide anion, and decreased expression of GP91PHOX, the membrane-associated subunit of NADPH oxidase.","16763214:3",2,1,null,"positive"]
["CD83 --+> CD86","Expression","However, the increase in surface expression of HLA-DR and CD86 after addition of LPS was significantly attenuated in cord DCs, with CD25 and CD83 expression also markedly reduced., Specifically, IRX-2-treated DC increased expression of CD83 and CCR7, markers for DC maturation and migration, respectively, and increased the expression of HLA-DR, CD54, and the costimulatory molecules CD86 and CD40, which are critical mediators of T cell activation., Correlating with CD83 expression, the basic as well as the lipopolysaccharide induced expression of the activation markers CD86 and MHC-II are significantly increased in CD83transgenic B cells and reciprocally decreased in CD83 mutant B cells. <more data available...>","11982599:2, 17667526:4, 17710154:3, 17056542:1160, 17878352:1075",2,5,null,"positive"]
["GFAP --+> VIM","Expression","As for GFAP, increased lesion-induced up-regulation of vimentin expression is also already apparent at 1 dpl, with knock-out animals showing higher expression than wild-type animals (Fig. 5b).","12843240:1209",2,1,null,"positive"]
["GFAP --+> APOD","Expression","ApoD levels increased by 35% in the peri-infarct area after 10 and 30 days after pMCAO, mainly in neuron-specific nuclear protein (NeuN) positive neurons and glial fibrillary acidic protein (GFAP) positive astrocytes.","20083089:4",2,1,null,"positive"]
["GFAP --+> MET","Expression","Both Nf1(GFAP)CKO and wild-type astrocytes induced MET expression in neurites of wild-type hippocampal neurons in vitro, suggesting that astrocyte-derived signals may induce MET in Nf1 mutant mice.","17348023:5",2,1,null,"positive"]
["B2M --+> TGFB1","Expression","AGE-beta2m also induced TGF-beta1 production by macrophages in a dose-dependent manner (410 +/- 80 pg/mL at 12.5 microg/mL, 621 +/- 62 pg/mL at 25 microg/mL, and 776 +/- 62 pg/mL at 50 microg/mL of AGE-beta2m).","10652049:6",2,1,null,"positive"]
["B2M --+> CCND1","Expression","Cyclin D1 and cyclin D2 transcripts are strongly induced by epidermal growth factor, and beta 2-microglobulin transcripts are strongly induced by TGF-beta in BALB keratinocytes released from quiescence by addition of epidermal growth factor.","8845303:4",2,1,null,"positive"]
["ITGAX --+> CD86","Expression","We found that the expression level of co-stimulatory molecules, CD40, CD54, CD80, CD86 and CD11b, were elevated evidently, except CD11c, I-A(d) and H-2K(d)., As reported previously (24), bone marrow-derived macrophage-derived dendritic cells expressed high levels of CD11c, CD86, and I-Ab, and LPS up-regulated the expression of CD86 and I-Ab.","20499643:4, 19336404:170",2,2,null,"positive"]
["FLI1 --+> TGFBR2","Expression","Introduction of EWSR1-FLI1 into cells lacking the EWSR1-FLI1 fusion suppresses TGF-beta RII expression, whereas antisense to EWSR1-FLI1 in ES cell lines positive for this gene fusion restores TGF-beta RII expression., Regulation of the TGF-ß RII promoter by EWS-FLI1, FLI1, dnFLI1, EWS-ERG, ERG, dnERG, EWS-ETV1, ETV1, and dnETV1., The ERT (also called ESX/ESE-1) regulates the expression through the Z element (10) , whereas another ets family gene FLI1 fused with the EWSR1 gene down-regulates the Transforming growth factorßRII expression in Ewing sarcomas (11) .","10508522:7, 10749119:1136, 11719467:1050",2,3,null,"positive"]
["ITGB2 --+> TLR2","Expression","The anti-CD18 monoclonal antibody markedly reduced TLR2 expression in endothelial cells as induced by polymorphonuclear neutrophils.","14561708:1314",2,1,null,"positive"]
["AIF1 --+> GFAP","Expression","Following paw incision and at spinal L5 segment GFAP expression was increased in laminae I-II and Iba1 in deep laminae on day 1, in the entire dorsal horn on day 4 and dissipated on day 7 after paw incision in parallel with the allodynia.","18538310:6",2,1,null,"positive"]
["AIF1 --+> CCND1","Expression","In contrast, the down-regulation of daintain/AIF-1 expression decreased cyclin D1 expression and inhibited the transcriptional activity of nuclear factor-kappa B.","18341653:7",2,1,null,"positive"]
["AIF1 --+> CD68","Expression","human microglia cell line clone 3 cells are typical microglia, as suggested by the constitutive expression of Iba-1 and CD14, and IFN-gamma-induced expression of CD11b, CD68 and MHCII.","20375612:3",2,1,null,"positive"]
["TREM2 --+> CD86","Expression","Ligation of triggering receptor expressed on myeloid cells-2 induced increased cell surface expression of CD40, CD86, and MHC class II but Ag-capturing mechanisms were not down-regulated (53)., KARAP/DAP12-TREM2 triggering on human Dendritic cells promotes incomplete maturation process, i.e., Dendritic cells up-regulation of CCR7, CD40, CD86, and MHC class II molecules, but not TNF-alpha nor IL-12 production (32).","14978127:315, 15128777:291",2,2,null,"positive"]
["LCN2 --+> GFAP","Expression","Third, the LCN2-induced GFAP expression was blocked by a nitric oxide synthase inhibitor NG-monomethyl-L-arginine (Fig. 8F,G)., Because LCN2 also induced GFAP expression in astrocytes in our study (Fig. 6), we next attempted to determine whether NO is involved in the LCN2 actions in astrocytes., Rho/ROCK pathway appeared to play a pivotal role in regard to LCN2 actions on astrocyte morphology, based on the following results: (1) a ROCK inhibitor, Y27632, partly blocked LCN2-induced morphological changes (Fig. 9A,B); (2) Y27632 also inhibited the LCN2-induced GFAP expression (Fig. 9C,D); and (3) LCN2 induced Rho activation in astrocytes (Fig. 9E). <more data available...>","19129400:366, 19129400:358, 19129400:384, 19129400:439",2,4,null,"positive"]
["PTPN6 --+> ITGB2","Expression","Surface expression of ß2 integrins is increased on motheaten polymorphonuclear leukocytes .","11067945:1301",2,1,null,"positive"]
["PTPN6 --+> CYBB","Expression","Consistent with this, SHP1 inhibition increases gp91PHOX and p67PHOXmRNA in undifferentiated U937 cells., In undifferentiated U937 cells, we found that overexpression of CS453-SHP1 increases gp91PHOX and p67PHOX mRNA abundance relative to control vector transfectants (Fig.2 C).","11483597:208, 11483597:223",2,2,null,"positive"]
["CSF1R --+> PTPN6","Expression","Traumatic injury to the central nervous system activates microglia and strongly increases expression of SHP-1, which physically associates with and is activated by c-Fms in these cells (17).","12361947:312",2,1,null,"positive"]
["CX3CR1 --+> TGFB1","Expression","CX3CR1 promotes TGF-ß1 expression and myofibroblast accumulation in wounded skin ., CX3CR1 promotes TGF-ß1 expression and activated fibroblast accumulation in wounded skin., These results suggest that CX3CR1 activity in vivo promotes TGF-ß1 production, which promotes accumulation of a-smooth muscle actin+-activated fibroblasts, which are the direct source of collagen, a key constituent of granulation tissue in skin wound repair. [Figure 10] View larger version (76K): [in this window] [in a new window] .","18097059:296, 18097059:303, 18097059:301",2,3,null,"positive"]
["P2RX7 --+> CASP1","Expression","We recently reported that P2X7 receptor (P2X7R)-induced activation of caspase-1 inflammasomes is accompanied by release of MHC class II protein into extracellular compartments during brief stimulation of murine macrophages with ATP., Furthermore, the production of IL-18 and IL-1beta and caspase-1 activation were induced independently of a P2X7 purinergic receptor, and the inability of Delta\"region of difference 1\" in caspase-1 activation was compensated for by nigericin, an agent inducing the potassium ion efflux.","19342685:0, 19596775:7",2,2,null,"positive"]

{"sheet":"Centrality analysis","index":3,"n_rows":78,"n_cols":10,"rows_kept":78,"flags":["formulas_cached_only"]}
["#","symbol","module","in degree","out degree","P","z","node role","Betweenness centrality","normalized centrality"]
[27,"TGFB1",2,5,40,0.68,4.43,"R6",1042.87,6.104847203760833]
[35,"CSF1",2,2,14,0.44,2.32,"R3",674.53,3.831529351750908]
[29,"TLR2",2,3,7,0.37,1.12,"R3",436.37,2.3616553776110276]
[9,"CEBPA",2,3,2,0,0.22,"R1",356,1.8656284574664934]
[33,"LGALS3",3,1,2,0.44,-0.33,"R3",353.87,1.8524825405832304]
[8,"STAT3",2,1,12,0.5,0.82,"R3",268.23,1.3239302767885572]
[30,"ITGB2",2,3,1,0,-0.08,"R1",149.52,0.5912768527452869]
[21,"CEBPD",2,1,4,0.64,-0.38,"R3",133.57,0.4928367709199127]
[65,"STAT1",2,1,10,0.51,1.12,"R3",113.33,0.3679197015690931]
[66,"PTPN6",2,1,2,0,-0.08,"R1",72,0.11283953969807665]
[26,"B2M",2,1,2,0.44,-0.38,"R3",63,0.05729341202231696]
[3,"CD14",2,3,4,0,1.12,"R1",52.73,-0.0060908914476888384]
[36,"NFATC1",2,2,3,0.48,-0.08,"R3",48,-0.03528346743728252]
[51,"NCF1",2,1,1,0,-0.38,"R1",44,-0.05997063529317572]
[24,"GFAP",2,3,3,0.61,-0.08,"R3",37,-0.10317317904098881]
[19,"CCND1",4,7,1,0.41,2,"R3",31,-0.1402039308248286]
[50,"SOX9",3,1,2,0.67,3,"R6",24,-0.1834064745726417]
[43,"CSF1R",2,2,1,0,-0.08,"R1",20,-0.2080936424285349]
[31,"LCN2",3,1,1,0,-0.33,"R1",16.33,-0.2307441189363169]
[42,"P2RX7",3,1,1,0.5,-0.33,"R3",11,-0.26363977010429457]
[17,"CXCL10",2,2,1,0.44,-0.38,"R3",9.67,-0.2718482534163791]
[6,"FLI1",3,1,1,0,-0.33,"R1",6,-0.2944987299241611]
[28,"AIF1",2,1,3,0.38,-0.08,"R3",5.5,-0.2975846259061477]
[1,"ITGAX",2,3,1,0,0.22,"R1",5,-0.30067052188813437]
[38,"TREM2",2,1,1,0,-0.38,"R1",1.53,-0.3220866400031217]
[2,"CD86",2,5,0,0,0.52,"R1",0,-0.3315294817080009]
[4,"CD83",2,1,1,0,-0.38,"R1",0,-0.3315294817080009]
[5,"CD68",2,2,0,0,-0.38,"R1",0,-0.3315294817080009]
[7,"TGFBR2",2,2,0,0.5,-0.68,"R3",0,-0.3315294817080009]
[10,"OSMR",2,1,0,0,-0.68,"R1",0,-0.3315294817080009]
[11,"CD9",3,1,0,0,-0.33,"R1",0,-0.3315294817080009]
[12,"HPGD",3,2,0,0,-0.33,"R1",0,-0.3315294817080009]
[13,"SYNPO",3,2,0,0,-0.33,"R1",0,-0.3315294817080009]
[14,"SBNO2",3,1,0,0,-0.33,"R1",0,-0.3315294817080009]
[15,"VIM",2,3,0,0,-0.08,"R1",0,-0.3315294817080009]
[16,"TF",3,3,0,0,-0.33,"R1",0,-0.3315294817080009]
[18,"MET",3,3,0,0,-0.33,"R1",0,-0.3315294817080009]
[20,"HSPB8",4,1,0,0,2,"R1",0,-0.3315294817080009]
[22,"SOCS3",4,2,0,0,-0.5,"R1",0,-0.3315294817080009]
[23,"ISG15",3,2,0,0,-0.33,"R1",0,-0.3315294817080009]
[25,"APOD",1,1,0,0,0,"R1",0,-0.3315294817080009]
[32,"HSPB1",4,3,0,0,-0.5,"R1",0,-0.3315294817080009]
[34,"TGFBR1",2,1,1,0,-0.68,"R1",0,-0.3315294817080009]
[37,"CYBB",2,5,0,0.32,0.22,"R3",0,-0.3315294817080009]
[39,"SERPING1",1,1,0,0,0,"R1",0,-0.3315294817080009]
[40,"C3",2,1,0,0,-0.68,"R1",0,-0.3315294817080009]
[41,"TNFRSF1A",2,1,0,0,-0.68,"R1",0,-0.3315294817080009]
[44,"A2M",1,1,0,0,0,"R1",0,-0.3315294817080009]
[45,"INPP5D",3,1,0,0,-0.33,"R1",0,-0.3315294817080009]
[46,"THBS2",2,1,0,0,-0.68,"R1",0,-0.3315294817080009]
[47,"S100A4",3,1,0,0,-0.33,"R1",0,-0.3315294817080009]
[48,"ITGB5",3,1,0,0,-0.33,"R1",0,-0.3315294817080009]
[49,"RBP1",4,1,0,0,-0.5,"R1",0,-0.3315294817080009]
[52,"TGM2",4,1,2,0,-0.5,"R1",0,-0.3315294817080009]
[53,"FCGR2B",2,1,0,0,-0.68,"R1",0,-0.3315294817080009]
[54,"ABCA1",1,1,0,0,0,"R1",0,-0.3315294817080009]
[55,"CLU",4,2,0,0.5,-0.5,"R3",0,-0.3315294817080009]
[56,"GUSB",3,1,0,0,-0.33,"R1",0,-0.3315294817080009]
[57,"MCL1",4,2,0,0,-0.5,"R1",0,-0.3315294817080009]
[58,"PTGS1",1,1,0,0,0,"R1",0,-0.3315294817080009]
[59,"IL13RA1",3,1,0,0,-0.33,"R1",0,-0.3315294817080009]
[60,"SRGN",3,1,0,0,-0.33,"R1",0,-0.3315294817080009]
[61,"CX3CR1",2,1,1,0,-0.68,"R1",0,-0.3315294817080009]
[62,"ALOX5AP",3,1,0,0,-0.33,"R1",0,-0.3315294817080009]
[63,"Ctla2a",2,1,0,0,-0.68,"R1",0,-0.3315294817080009]
[64,"ADAMTS1",1,1,0,0,0,"R1",0,-0.3315294817080009]
[67,"PROS1",2,1,0,0,-0.68,"R1",0,-0.3315294817080009]
[68,"CASP1",4,2,0,0.5,-0.5,"R3",0,-0.3315294817080009]
[69,"LXN",3,1,0,0,3,"R5",0,-0.3315294817080009]
[70,"HLA-E",2,1,0,0,-0.68,"R1",0,-0.3315294817080009]
[71,"IFIT3",2,1,0,0,-0.68,"R1",0,-0.3315294817080009]
[72,"IFI27",2,1,0,0,-0.68,"R1",0,-0.3315294817080009]
[73,"ID3",4,1,0,0,-0.5,"R1",0,-0.3315294817080009]
[74,"PDPN",2,1,0,0,-0.68,"R1",0,-0.3315294817080009]
[]
[{"$nulls":8},53.7168918918919]
[{"$nulls":8},162.02749636366815]

{"sheet":"Original list of DEG","index":4,"n_rows":333,"n_cols":1,"rows_kept":333,"flags":["formulas_cached_only"]}
["0610011I04RIK"]
["1110032A04RIK"]
["1810009M01RIK"]
["1810059G22RIK"]
["2310014H01RIK"]
["2310033F14RIK"]
["2810459M11RIK"]
["4632428N05RIK"]
["4921524J06RIK"]
["4933411K20RIK"]
["4933428I03RIK"]
["5830458K16RIK"]
["6430529G09RIK"]
["9230105E10RIK"]
["9830147J24RIK"]
["A2M"]
["A330042H22"]
["A530050D06RIK"]
["ABCA1"]
["ABCA9"]
["ABHD4"]
["ADAMTS1"]
["ADCY7"]
["AI452102"]
["AI838057"]
["AIF1"]
["ALDH1L2"]
["ALDOC"]
["ALOX5AP"]
["AMPD3"]
["ANGPT1"]
["ANTXR1"]
["ANXA3"]
["ANXA4"]
["APLN"]
["APOD"]
["AQP4"]
["ARHGAP25"]
["ARHGDIB"]
["ARPC1B"]
["AU020206"]
["AXL"]
["B2M"]
["B4GALT1"]
["BC025600"]
["BC032204"]
["BCL2A1A"]
["BLNK"]
["BMP2K"]
["BZRP"]
["C1QA"]
["C1QB"]
["C1QG"]
["C3"]
["C3AR1"]
["C4"]
["CASP1"]
["CASP12"]
["CASP8"]
["CCL3"]
["CCL6"]
["CCL9"]
["CCND1"]
["CD14"]
["CD151"]
["CD300D"]
["CD44"]
["CD48"]
["CD52"]
["CD53"]
["CD68"]
["CD83"]
["CD84"]
["CD86"]
["CD9"]
["CEBPA"]
["CEBPD"]
["CHI3L1"]
["CKLFSF6"]
["CLEC5A"]
["CLEC7A"]
["CLIC1"]
["CLU"]
["CNN3"]
["COTL1"]
["CP"]
["CRISPLD2"]
["CSF1"]
["CSF1R"]
["CST7"]
["CTLA2A"]
["CTLA2B"]
["CTSC"]
["CTSD"]
["CTSH"]
["CTSL"]
["CTSS"]
["CTSZ"]
["CTTNBP2NL"]
["CX3CR1"]
["CXCL10"]
["CXCL14"]
["CYBA"]
["CYBB"]
["CYP4F14"]
["CYP7B1"]
["D11ERTD759E"]
["D12ERTD647E"]
["DBI"]
["DHRS1"]
["DOCK2"]
["DPYD"]
["DTX3L"]
["E030018N11RIK"]
["E230029C05RIK"]
["EDEM1"]
["EDG3"]
["ELA1"]
["ELK3"]
["EMR1"]
["EYA4"]
["FBXO39"]
["FCER1G"]
["FCGR2B"]
["FCGR3"]
["FGFRL1"]
["FLI1"]
["FTL1"]
["FXYD1"]
["FYB"]
["G1P2"]
["GAL3ST4"]
["GALNT4"]
["GBF1"]
["GBP2"]
["GBP4"]
["GFAP"]
["GGTA1"]
["GMFG"]
["GNG5"]
["GP49A"]
["GPNMB"]
["GPR34"]
["GRN"]
["GUSB"]
["GVIN1"]
["H2-AA"]
["H2-AB1"]
["H2-D1"]
["H2-DMB1"]
["H2-K1"]
["H2-T23"]
["HERC5"]
["HEXB"]
["HFE"]
["HIST1H1C"]
["HIST1H2BC"]
["HPGD"]
["HRSP12"]
["HSD3B7"]
["HSPB1"]
["HSPB6"]
["HSPB8"]
["ID3"]
["IFI27"]
["IFI30"]
["IFI35"]
["IFIH1"]
["IFIT1"]
["IFIT2"]
["IFIT3"]
["IFITM2"]
["IFITM3"]
["IGTP"]
["II"]
["IIGP1"]
["IIGP2"]
["IL13RA1"]
["INPP5D"]
["IRF8"]
["IRGM"]
["ISGF3G"]
["ITGAX"]
["ITGB2"]
["ITGB5"]
["KCNK6"]
["KIF5C"]
["LAIR1"]
["LAMP2"]
["LAPTM5"]
["LCN2"]
["LCP1"]
["LGALS1"]
["LGALS3"]
["LGALS3BP"]
["LGALS9"]
["LGI4"]
["LGMN"]
["LOC386462"]
["LOH11CR2A"]
["LPXN"]
["LRRFIP1"]
["LST1"]
["LXN"]
["LYN"]
["LYZS"]
["LZP-S"]
["MAFB"]
["MCL1"]
["MDFIC"]
["MGI:2182965"]
["MGST1"]
["MPA2L"]
["MPEG1"]
["MS4A11"]
["MS4A6B"]
["MS4A6D"]
["MSN"]
["MSR2"]
["MT1"]
["MT2"]
["NAGLU"]
["NAPRT1"]
["NCF1"]
["NCKAP1L"]
["NEK6"]
["NFATC1"]
["NFE2L2"]
["NKTR"]
["NPC2"]
["NPL"]
["NRK"]
["NUPR1"]
["OAS1A"]
["OASL2"]
["OLFML3"]
["OSMR"]
["P2RX7"]
["P2RY13"]
["P2RY6"]
["PARP12"]
["PARP3"]
["PBXIP1"]
["PDLIM4"]
["PDPN"]
["PHYHD1"]
["PLAT"]
["PLCE1"]
["PLD4"]
["PLEK"]
["PLSCR2"]
["PP11R"]
["PRDX6"]
["PRG1"]
["PROS1"]
["PRSS18"]
["PRSS19"]
["PSCD4"]
["PSMB8"]
["PSMB9"]
["PTGDS2"]
["PTGS1"]
["PTPN6"]
["PTPRC"]
["PYCARD"]
["RAB7L1"]
["RAPGEF3"]
["RBP1"]
["RENBP"]
["RHOC"]
["RHOJ"]
["RNASE4"]
["RNASET2"]
["RRAS"]
["S100A1"]
["S100A11"]
["S100A13"]
["S100A16"]
["S100A4"]
["S100A6"]
["SCAP2"]
["SCARA3"]
["SCN1A"]
["SCRG1"]
["SDC4"]
["SELPL"]
["SERPINA3N"]
["SERPING1"]
["SGPL1"]
["SHOX2"]
["SIGLEC5"]
["SLC13A3"]
["SLC14A1"]
["SLC1A4"]
["SLC25A18"]
["SLC39A14"]
["SLCO2B1"]
["SOAT1"]
["SOCS3"]
["SOX9"]
["SPATA13"]
["STAT1"]
["STAT3"]
["STNO"]
["SYNE1"]
["SYNGR2"]
["SYNPO"]
["TCFCP2L1"]
["TCN2"]
["TGFB1"]
["TGFBR1"]
["TGFBR2"]
["TGM2"]
["THBS2"]
["TLR2"]
["TLR3"]
["TNFAIP8L2"]
["TNFRSF1A"]
["TNNC1"]
["TOR3A"]
["TREM2"]
["TRF"]
["TRIM25"]
["TRIM30"]
["TYROBP"]
["UCP2"]
["UGT1A2"]
["UNC93B1"]
["USP53"]
["VIM"]
["VWA1"]
["X99384"]
["ZFPN1A1"]

{"sheet":"Expanded list of DEG","index":5,"n_rows":100,"n_cols":1,"rows_kept":100,"flags":["formulas_cached_only"]}
["ACAT1"]
["ADRB2"]
["AGER"]
["APP"]
["AR"]
["BCL2"]
["BCL2L1"]
["BDNF"]
["BID"]
["CAST"]
["CAT"]
["CCL12"]
["CCND3"]
["CD4"]
["CD74"]
["CD80"]
["CD8A"]
["CDH1"]
["CEBPB"]
["CTGF"]
["CTNNB1"]
["DUSP1"]
["EDN1"]
["EGFR"]
["EGR1"]
["EP300"]
["ESR1"]
["ETS1"]
["ETS2"]
["FAS"]
["FGF9"]
["FN1"]
["FOXO1"]
["FTL1"]
["GLI1"]
["H2-Q1"]
["HBEGF"]
["HES1"]
["HGF"]
["HMOX1"]
["HRAS1"]
["HSP90AA1"]
["HSPA1A"]
["ID1"]
["IGF1"]
["IGF2"]
["IGFBP3"]
["IL15"]
["IL18"]
["IL1B"]
["ILK"]
["INHBA"]
["IRF1"]
["IRF7"]
["JUN"]
["KITL"]
["MAPK14"]
["MAPK3"]
["MET"]
["MIF"]
["MMP2"]
["MMP9"]
["MYB"]
["MYC"]
["MYD88"]
["MYH11"]
["NGF"]
["NOTCH1"]
["NR3C1"]
["POMC"]
["PPARD"]
["PPARG"]
["PRKCD"]
["PRL"]
["PTGS2"]
["PTHLH"]
["PTK2"]
["RHOA"]
["RHOB"]
["RUNX1"]
["SELPLG"]
["SFPI1"]
["SMAD3"]
["SMAD4"]
["SMAD7"]
["SP1"]
["SPARC"]
["SPP1"]
["TGFB2"]
["TGFB3"]
["THBS1"]
["TLR4"]
["TNF"]
["TNFSF10"]
["TRF"]
["TRP53"]
["VEGFA"]
["VIP"]
["WNT4"]
["ZEB2"]

{"sheet":"Reduced list of DEG","index":6,"n_rows":226,"n_cols":1,"rows_kept":226,"flags":["formulas_cached_only"]}
["1110032A04RIK"]
["2310033F14RIK"]
["2810459M11RIK"]
["4933411K20RIK"]
["A2M"]
["ABCA1"]
["ABCA1"]
["ADCY7"]
["ADCY7"]
["AF251705"]
["AIF1"]
["ANXA3"]
["ANXA4"]
["APOD"]
["APOD"]
["APOD"]
["AQP4"]
["AQP4"]
["ARHGAP25"]
["ARPC1B"]
["AU020206"]
["B2M"]
["B2M"]
["BCL2A1A"]
["BLNK"]
["C1QA"]
["C1QB"]
["C1QB"]
["C1QB"]
["C1QC"]
["C3"]
["C3AR1"]
["C3AR1"]
["C3AR1"]
["C4B"]
["CASP12"]
["CASP12"]
["CCL3"]
["CCL9"]
["CCL9"]
["CD14"]
["CD44"]
["CD44"]
["CD44"]
["CD48"]
["CD52"]
["CD53"]
["CD68"]
["CD74"]
["CD84"]
["CD86"]
["CD9"]
["CEBPA"]
["CEBPD"]
["CELA1"]
["CHI3L1"]
["CLEC7A"]
["CRISPLD2"]
["CSF1"]
["CSF1"]
["CSF1R"]
["CSF1R"]
["CST7"]
["CTLA2B"]
["CTSC"]
["CTSD"]
["CTSH"]
["CTSH"]
["CTSS"]
["CTSZ"]
["CTSZ"]
["CTSZ"]
["CX3CR1"]
["CX3CR1"]
["CXCL10"]
["CYBA"]
["CYBB"]
["CYTH4"]
["DHRS1"]
["DOCK2"]
["E230029C05RIK"]
["E230029C05RIK"]
["EMR1"]
["EYA4"]
["FCER1G"]
["FCGR2B"]
["FCGR2B"]
["FCGR2B"]
["FERMT3"]
["FERMT3"]
["FYB"]
["GBF1"]
["GBP2"]
["GBP2"]
["GBP6"]
["GFAP"]
["GFAP"]
["GFAP"]
["GGTA1"]
["GGTA1"]
["GMFG"]
["GP49A"]
["GPNMB"]
["GPR34"]
["GRN"]
["GRN"]
["GRN"]
["GUSB"]
["H2-AA"]
["H2-AA"]
["H2-AB1"]
["H2-D1"]
["H2-D1"]
["H2-D1"]
["H2-D1"]
["H2-D1"]
["H2-D1"]
["H2-K1"]
["H2-K1"]
["HEXB"]
["HEXB"]
["HPGD"]
["HSPB1"]
["HSPB6"]
["IFI30"]
["IFIT3"]
["IIGP1"]
["IKZF1"]
["IL13RA1"]
["INPP5D"]
["IRF8"]
["IRF8"]
["IRF9"]
["IRGM1"]
["IRGM2"]
["ITGAX"]
["ITGB2"]
["ITGB5"]
["ITGB5"]
["KCNK6"]
["KIF5C"]
["KIF5C"]
["KLK6"]
["LAIR1"]
["LAIR1"]
["LAPTM5"]
["LAPTM5"]
["LAPTM5"]
["LCN2"]
["LCP1"]
["LGALS3"]
["LGALS3BP"]
["LPXN"]
["LRRFIP1"]
["LYZ2"]
["LYZ2"]
["MAFB"]
["MPA2L"]
["MPA2L"]
["MPEG1"]
["MS4A6D"]
["MS4A6D"]
["MS4A6D"]
["MS4A6D"]
["MSN"]
["MSN"]
["NCF1"]
["NCF1"]
["NCKAP1L"]
["OAS1A"]
["OASL2"]
["OLFML3"]
["OSMR"]
["P2RY6"]
["PARP3"]
["PARP3"]
["PBXIP1"]
["PDLIM4"]
["PLD4"]
["PLEK"]
["PLEK"]
["PLEK"]
["PLSCR2"]
["PROS1"]
["PSMB8"]
["PSMB9"]
["PTPLAD2"]
["PTPN6"]
["PTPRC"]
["PYCARD"]
["RAB7L1"]
["RENBP"]
["RHOJ"]
["S100A4"]
["S100A6"]
["S1PR3"]
["S1PR3"]
["S1PR3"]
["SERPINA3N"]
["SHOX2"]
["SIGLECH"]
["SLC14A1"]
["SLCO2B1"]
["SOAT1"]
["SOAT1"]
["SOCS3"]
["SOCS3"]
["STAT3"]
["TCFCP2L1"]
["TCN2"]
["TGFBR1"]
["TLR2"]
["TMEM176A"]
["TMEM176A"]
["TMEM176A"]
["TNFAIP8L2"]
["TREM2"]
["TRF"]
["TRIM30"]
["TRIM30"]
["TYROBP"]
["UNC93B1"]
["VIM"]
["VIM"]
["VIM"]
["X99384"]

{"sheet":"Expanded network","index":7,"n_rows":389,"n_cols":9,"rows_kept":389,"flags":["formulas_cached_only"]}
["A2M -> GFAP","Expression","These data demonstrate that a(2)M* induced GFAP expression in the MIO-M1 cell line, which was selectively blocked by RAP, an antagonist of LRP1 binding ligands.","20881288:5",2,1,null,null,"positive"]
["A2M -> PTGS2","Expression","Macrophage stimulation with alpha(2)M* increased total cellular and nuclear COX-2 two- to threefold.","11583915:1",2,1,null,"Macrophages","positive"]
["AIF1 -> CCND1","Expression","In contrast, the down-regulation of daintain/AIF-1 expression decreased cyclin D1 expression and inhibited the transcriptional activity of nuclear factor-kappa B.","18341653:7",2,1,null,null,"positive"]
["AIF1 -> CD68","Expression","human microglia cell line clone 3 cells are typical microglia, as suggested by the constitutive expression of Iba-1 and CD14, and IFN-gamma-induced expression of CD11b, CD68 and MHCII.","20375612:3",2,1,"Homo sapiens","Microglia","positive"]
["AIF1 -> GFAP","Expression","Following paw incision and at spinal L5 segment GFAP expression was increased in laminae I-II and Iba1 in deep laminae on day 1, in the entire dorsal horn on day 4 and dissipated on day 7 after paw incision in parallel with the allodynia.","18538310:6",2,1,null,null,"positive"]
["ANGPT1 -> BCL2","Expression","Angiopoietin-1 could decrease the expression of Bax, caspase3 and 8, and increase that of Bcl-2., In cardiac allografts, both adeno-associated virus-Angiopoietin-1 and adeno-associated virus-Ang2 decreased inflammation and increased antiapoptotic Bcl-2 mRNA and Bcl-2/Bax ratio at 8 weeks., This meant that phosphatidylinositol-3 kinase activation and Bcl-2 upregulation stimulated by VEGF165 and angiopoietin-1 were two independent signaling pathways in H9C2 cells., However, elevated angiopoietin-1 expression in islets significantly ameliorated the deleterious effect of cytokines on Bcl-2 expression, as relatively higher Bcl-2 protein levels were detected in cytokine-treated islets pretransduced with angiopoietin-1 vector (Fig. 5). [Figure 5] View larger version (53K): [in this window] [in a new window] .","16701012:9, 16690881:4, 15510173:1134, 17596403:1246",2,4,null,"Insulin-Secreting Cells","positive"]
["ANGPT1 -> CCND1","Expression","angiopoietin1 up-regulated the expression of cyclin D1 in both of these cells., In addition, COMP-(COMP)-angiopoietin 1 reversed the nutrient-deprived suppression of cyclin D1 mRNA expression.","16061664:5, 21109762:7",2,2,"Homo sapiens","Endothelial Cells","positive"]
["ANGPT1 -> SMAD7","Expression","Treatment with COMP-angiopoietin-1 also decreased the Cyclosporine A-induced increases in TGF-beta1 and Smad 2/3 levels while increasing Smad 7 levels., COMP-Angiopoietin-1 also reduced renal tissue levels of transforming growth factor-beta1 (TGF-beta1), alpha-smooth muscle actin, fibronectin, as well as Smad 2/3 expression, but increased Smad 7 expression., COMP-angiopoietin-1 treatment decreased monocyte/macrophage infiltration, tissue levels of TGF-beta1, and Smad 2/3 phosphorylation and increased Smad 7 in the obstructed kidney.","18463324:9, 17085463:7, 16885409:9",2,3,null,"Monocytes","positive"]
["ANGPT1 -> VEGFA","Expression","Systemic administration of Ad-Angiopoietin-1 restored bone marrow cell-endothelial progenitor cell differentiation and increased myocardial VEGF expression and angiogenesis in streptozotocin mice., Angiopoietin -1 treatment reduces vascular endothelial growth factor (VEGF) protein expression., Overexpression of angiopoietin-1 resulted in a significant increase in VEGF expression (n = 6)., Role of VEGF-A. (A) Both 5-fluorouracil and angiopoietin-1 induce VEGF-A expression in wild-type mice., Angiopoietin-1 gene transfer improves impaired wound healing in genetically diabetic mice without increasing VEGF expression. <more data available...>","18408125:9, 21179479:1268, 18835934:1198, 15817675:1276, 18078386:100, 16778190:1292, 17626153:1223, 9776732:1163, 18497305:1150, 11557733:1028",2,10,"Bos taurus, Oryctolagus cuniculus","Hematopoietic Stem Cells, Endothelial Cells, Adipocytes","positive"]
["AQP4 -> GFAP","Expression","Likewise, AQP4 deficiency significantly downregulated expression of glial fibrillary acidic protein in perivascular processes of astrocytes., The abundance of GFAP, the usual marker of astrocytes and ependymal cells, was increased by 25% with age (data not shown), a variation much smaller than the doubling in UT-B1 or the fourfold increase in AQP-4.","18281883:2, 12933359:1196",2,2,null,"Astrocytes","positive"]
["AQP4 -> SLC14A1","Expression","In aging brain, UT-B1 abundance was increased twofold together with a fourfold increase in aquaporin-4 abundance., These experiments demonstrated that adriamycin-induced nephrotic syndrome is associated with marked decreases in expression of aquaporin-2, aquaporin-3, aquaporin-4, and the vasopressin-regulated urea transporter in renal inner medulla, indicative of a suppression of the capacity for water and urea absorption by the inner medullary collecting duct.","12933359:8, 9573539:2",2,2,null,null,"positive"]
["AXL -> SOCS3","Expression","In this issue, Rothlin et al. (2007) uncover a complex negative feedback mechanism to limit Toll-like receptor signaling involving the Tyro3/Axl/Mer family of receptor tyrosine kinases, which induce expression of the inhibitory proteins SOCS1 and SOCS3.","18083093:1",2,1,null,null,"positive"]
["B2M -> CCND1","Expression","Cyclin D1 and cyclin D2 transcripts are strongly induced by epidermal growth factor, and beta 2-microglobulin transcripts are strongly induced by TGF-beta in BALB keratinocytes released from quiescence by addition of epidermal growth factor., We previously showed that ß2M promoted the expression of cell cycle markers, cyclin D1 and cyclin A, and cell growth in prostate cancer cells through the activation of a cyclic AMP/PKA/CREB signaling pathway (8)., As indicated, ß2M can activate cyclic AMP/PKA signaling, its downstream phosphorylated cyclic AMP -responsive element binding protein, and expression of target genes, including osteocalcin, BSP, VEGF, cyclin A, and cyclin D1. ß2M also has a direct growth-promoting and antiapoptotic action that culminates in cancer cell growth and survival and through induction of epithelial to mesenchymal transition that facilitates further cancer cell migration, invasion, and metastasis.","8845303:4, 18765525:1200, 16982753:1278",2,3,null,"Keratinocytes","positive"]
["B2M -> PTGS2","Expression","BAPTA-AM, a [Ca2+]i chelator, completely inhibited beta2m-induced expression of VCAM-1 and COX-2., Our results suggest that induction of COX-2 expression by beta 2m may be an important component of the inflammatory process in hemodialysis-associated osteoarthropathy., We have shown that beta(2)M increases the expression of matrix metalloproteinase-1, vascular cell adhesion molecule-1 and cyclooxygenase-2 in human synovial fibroblasts, while the effect of AGE-beta(2)M in this model is markedly reduced., Migita and colleagues [11] demonstrated that ß2M increases cyclo-oxygenase-2 (COX-2) protein and mRNA expression in a dose-dependent manner from human synovial cells; however, utilizing the mouse calvarial resorption model, we were unable to demonstrate an effect of ß2M on prostaglandin E2 production [6]. <more data available...>","11849381:4, 9987081:5, 12480959:2, 11390706:1068, 11849381:5, 9987081:3",2,6,"Homo sapiens","Fibroblasts","positive"]
["B2M -> TGFB1","Expression","AGE-beta2m also induced TGF-beta1 production by macrophages in a dose-dependent manner (410 +/- 80 pg/mL at 12.5 microg/mL, 621 +/- 62 pg/mL at 25 microg/mL, and 776 +/- 62 pg/mL at 50 microg/mL of AGE-beta2m).","10652049:6",2,1,null,"Macrophages","positive"]
["B2M -> VEGFA","Expression","The total VEGF message was generally up-regulated in malignant tissues (20.5-728 copies/103 copies of B2M) compared with healthy tissues (4.2-81 copies/103 copies of B2M)., As indicated, ß2M can activate cyclic AMP/PKA signaling, its downstream phosphorylated cyclic AMP -responsive element binding protein, and expression of target genes, including osteocalcin, BSP, VEGF, cyclin A, and cyclin D1. ß2M also has a direct growth-promoting and antiapoptotic action that culminates in cancer cell growth and survival and through induction of epithelial to mesenchymal transition that facilitates further cancer cell migration, invasion, and metastasis.","11274014:1170, 16982753:1278",2,2,null,null,"positive"]
["BCL2 -> CCND1","Expression","We found that bcl-2 overexpression induces cyclin D1 expression in human breast epithelial cell line MCF10A independent of cell anchorage., These results suggest that p21 and cyclin D1 expression in prostatic cancer might be modulated by Bcl-2 and by androgens and in turn this could be relevant to the progression of prostatic cancer., Lupeol treatment of 451Lu cells caused (a) G(1)-S phase cell cycle arrest and apoptosis; (b) down-regulation of Bcl2 and up-regulation of Bax; (c) activation of caspase-3 and induction of polyribose polymerase cleavage; (d) decreased expression of cyclin D1, cyclin D2, and cdk2; and (e) increased expression of p21 protein. <more data available...>","11313702:5, 10884916:9, 18381953:5, 18375822:1322, 21239698:1229, 10666199:1227, 19318573:1057, 11069629:1271",2,8,"Homo sapiens","Epithelial Cells, Melanocytes, Stem Cells, Endothelial Cells","positive"]
["BCL2 -> SOX9","Expression","In addition, Bcl-2 may also play a role in regulating the expression of aggrecan through Sox9 in vivo as well as in vitro., The present study demonstrates that the activity of Sox9, a master transcription factor that regulates the gene expression of chondrocyte matrix proteins, is suppressed by Bcl-2 small interference RNA in the presence of caspase inhibitors.","15936918:13, 15975921:3",2,2,null,"Chondrocytes","positive"]
["BCL2 -> VEGFA","Expression","Bcl-2 overexpression enhanced the synthesis of the hypoxia-stimulated VEGF protein and mRNA., We demonstrated that bcl-2 overexpression in M14 human melanoma cell line enhances hypoxia-induced VEGF mRNA stability and promoter activation., Bcl-2 induces vascular endothelial growth factor (VEGF) expression in neovascular endothelial cells through a signal transducer and activator of transcription 3 (STAT3)-mediated pathway., Finally, we found that the mechanism by which bcl-2 regulates HIF-1-mediated VEGF expression does not require BH1 and BH2 domains, and it is independent of antiapoptotic and prosurvival function of bcl-2. <more data available...>","10744622:3, 12205045:1, 17942898:3, 21233846:6, 18670359:7, 15987743:1123, 20668552:1255, 10744623:1016, 12205027:1283, 14660675:1316 <more data available...>",2,27,null,"Endothelial Cells, Keratinocytes, B-Lymphocytes","positive"]
["BCL2L1 -> BCL2A1","Expression","Fifthly, knockdown of BCL-XL in combination with agents that inhibit BCL2A1 expression completely reversed the resistance (Figure 7).","19008458:1279",2,1,null,"B-Lymphocytes","positive"]
["BCL2L1 -> CCND1","Expression","Moreover, down-regulation of anti-apoptotic genes (Bcl-2, Bcl-xL and survivin) and a cell cycle regulating gene (cyclin D1) was associated with the cell growth inhibition and apoptosis., Compared with normal mouse plasma cells, all of the Bcl-xl/Myc tumors have significantly reduced expression of cyclin D2 and increased expression of cyclin D1., The third cluster is enriched for apoptosis (BAD, BAK, BCL2, BCLXL, BAD.p136, SMAC), cell cycle or differentiation regulating proteins (Myc, CCND1, SSBP2), and activated STAT proteins. <more data available...>","18939995:7, 17483317:1239, 18840713:1174, 11896290:1210",2,4,"Mus musculus","Myocytes, Smooth Muscle, Plasma Cells, Monocytes","positive"]
["BCL2L1 -> TGFB2","Expression","Long-term expression of BCL-xL promotes transforming growth factor-ß2 and MMP-2 expression.","16254573:1105",2,1,null,null,"positive"]
["BCL2L1 -> VEGFA","Expression","We next attempted to understand how Bcl-xL induces VEGF expression., Several genes that are regulated by nuclear factor-kappaB can contribute to carcinogenesis and atherogenesis including gene products which block apoptosis (e.g. TRAF1, TRAF2, cIAP-1, cIAP-2, XIAP, bcl-2 and bcl-xl), gene products which promote angiogenesis (e.g. cell surface adhesion molecules on endothelial cells, vascular endothelial cell growth factor, COX-2, matrix metalloprotease-9 and urokinase plasminogen activator), and inflammatory cytokines (e.g. TNF, interleukin-1, IL-6 and IL-8) (for refs, see 11).","17572663:1114, 12189195:1269",2,2,null,"Endothelial Cells, squamous cells","positive"]
["CASP1 -> CXCL10","Expression","In C57BL/6 mice, the dextran sulfate sodium-induced increase in IP-10 mRNA, but not TNF-alpha mRNA, was completely prevented by ICE inhibition., During PFAPA attacks, complement (C1QB, C2, SERPING1), IL-1-related (IL-1B, IL-1RN, CASP1, IL18RAP), and IFN-induced (AIM2, IP-10/CXCL10) genes were significantly overexpressed, but T cell-associated transcripts (CD3, CD8B) were down-regulated.","17393315:10, 21478439:4",2,2,null,"T-Lymphocytes","positive"]
["CASP1 -> PTGS2","Expression","Because caspase-1 is involved in the induction of COX-2 expression and PGE2 production, our data support the assertion that caspase-1 is a key target to control inflammatory pain., Caspase-1 inhibitors abolish deleterious enhancement of COX-2 expression induced by HIV-1 gp120 in human neuroblastoma cells., This is based in the fact that gp120 induces IL-1 and two inhibitors of IL-1 converting enzyme abolish COX-2 expression enhanced by gp120 and the consequent cell death in human CHP100 neuroblastoma cells (Corasaniti et al. 2003a).","20920345:11, 12628757:100, 16001969:1255",2,3,null,"B-Lymphocytes","positive"]
["CAT -> BCL2","Expression","Overexpression of mitochondrially located catalase (MitoCatalase) specifically increased basal Bcl-2 and decreased basal Bax expression, suppressed cytokine-mediated reduction of Bcl-2, and thereby prevented the release of cytochrome c, Smac/DIABLO and the activation of caspase-9 and -3., Anti-Human erythrocyte catalase antibody also induced the apoptosis of M-Mphi cultured in the presence of M-CSF and granulocyte-macrophage-Mphi and A-Mphi cultured in the presence or absence of GM-CSF and down-regulated the expression of BCL-2 and BCL-X(L) in these Mphis. <more data available...>","20933054:3, 16204228:7, 17911532:1233, 14657380:1167, 15782127:1220",2,5,"Homo sapiens","Erythrocytes, T-Lymphocytes","positive"]
["CAT -> CD68","Expression","Treatment of THP-1 cells with catalase was able to synergize with all-trans retinoic acid to enhance macrophage differentiation, demonstrated by changes of cell adherence, cell cycle arrest, nitroblue tetrazolium reduction, and expression of differentiation markers including CD68, CD11b, and matrix metalloproteinase 9 (MMP9).","17369494:3",2,1,null,null,"positive"]
["CAT -> CYBB","Expression","Furthermore, arecoline increased reactive oxygen species production and upregulated protein expression and mRNA levels of NADPH oxidase 2, which could be attenuated by catalase and NADPH oxidase inhibitors.","20691257:5",2,1,null,"Neurons","positive"]
["CAT -> PTGS2","Expression","Catalase induces COX-2 or iNOS expression in some type of cells, but the mechanism remains unclear., As well, antioxidant-catalase, N-acetyl-cysteine or reduced glutathione-attenuated COX-2 expression in combined cytokines-treated cells., The antioxidant, N-acetyl-cysteine, also reduced the glutathione or catalase- attenuated COX-2 expressions in IL-1beta and TNF-alpha-treated cells., The addition of catalase into Raw 264.7 macrophages induced COX-2 expression that was correlated with increased COX-2 transcription and mRNA stability. <more data available...>","15683737:0, 15106733:4, 12934647:4, 15020231:3, 19467701:4, 14756815:1231, 10899936:1282, 15667946:100, 18073322:1196, 11597987:1108",2,10,"Rattus norvegicus, Homo sapiens, Bos taurus","Osteoblasts, Myocytes, Cardiac, Macrophages, Chondrocytes, Oocytes, Endothelial Cells","positive"]
["CCL3 -> CD86","Expression","It has been reported that the mucosal adjuvanticity of CT involves the selective up-regulation of CD86 expression [45 ] and that MIP-1a significantly up-regulates the expression of CD80 [5 ], like RANTES [4 ], but also increases the CD86 surface level on resting B cells.","15356099:1199",2,1,null,"B-Lymphocytes","positive"]
["CCL3 -> CXCL10","Expression","Up-regulation of RANTES/CCL5, IP-10/CCL3 and CCR2 was associated with leucocyte migration to the brain and increased expression of MCP-1/CCL2, IP-10/CCL3 and CCR5 with leucocyte migration to the lung., In addition, microglia, macrophages, and neutrophils isolated from the brain abscesses of MyD88 knockout mice produced significantly less TNF-alpha, IL-6, MIP-1alpha/CCL3, and IFN-gamma-induced protein 10/CXCL10 compared with wild-type cells., Inflammatory chemokines (CCL3, CCL4, CCL5) and interferon-dependent chemokines (CXCL9, CXCL10, CXCL11) expression is up-regulated between 2 and 8 hours and then decreases progressively (I-P). <more data available...>","18665903:8, 17372011:5, 16317096:1129, 12138184:1194, 16237112:1220, 17167081:1096, 20136829:1321, 16020804:1204, 19332801:1280",2,9,null,"Macrophages, T-Lymphocytes, Monocytes","positive"]
["CCL3 -> VEGFA","Expression","Moreover, CCL3 enhanced VEGF expression by murine peritoneal macrophages at both the mRNA and the protein level.","18776949:9",2,1,"Mus musculus","Macrophages, Peritoneal","positive"]
["CCND1 -> HSPB8","Expression","The transient transfection with cyclin D1 increased HSPB8 levels ~2-fold when these blots were quantified in image analysis; the HSPB8 knockdown was ~8-fold in each case.","18006821:1234",2,1,null,null,"positive"]
["CCND1 -> PTGS2","Expression","Elevated levels of cyclin D1, VEGF and Bax were detected at 48 h in cells and increased Cox-2 expression was observed at 24 h., nuclear factor-kappa B activation is required for induction of COX-2, cyclin D1 and MMP-9 by cigarette smoke condensate Whether MMP-9, COX-2 and cyclin D1 expression was activated through the activation of nuclear factor-kappa B was further investigated., TNF induced cyclin D1, COX-2, and MMP-9 expression in a time-dependent manner, and indeed SCH 66336 blocked TNF-induced expression of cyclin D1, COX-2, and MMP-9, further strengthening our demonstrations that SCH 66336 blocks TNF-induced NF-?B-regulated gene products. <more data available...>","17487372:23, 12807725:1254, 15090542:1281, 17404112:1264, 17404114:1264, 19318580:1148, 15252041:1280, 14711835:1273",2,8,"Homo sapiens","Fibroblasts","positive"]
["CCND1 -> VEGFA","Expression","In vitro studies indicated that antisense to cyclin D1 decreased VEGF protein expression in DLD1 but not in HCT116., Cyclin D1 regulates vascular endothelial growth factor production and thereby, growth of vascular endothelial cells and tumor [35]., The current elegant studies by Yasui et al. suggest that cyclin D1 abundance within epithelial cells regulates production of VEGF, which in turn mediates blood vessel density., Immunoblot analysis for VEGF, cyclin D1, and cyclin E2 in mouse hindlimb muscle 3 days after tissue ischemia showing increased expression of VEGF and cycline D1 mainly from skeletal muscle.","16899623:4, 20459741:1411, 16899588:1028, 16254206:1142",2,4,"Mus musculus","Endothelial Cells, Epithelial Cells","positive"]
["CD14 -> CD68","Expression","human microglia cell line clone 3 cells are typical microglia, as suggested by the constitutive expression of Iba-1 and CD14, and IFN-gamma-induced expression of CD11b, CD68 and MHCII., In addition, cell surface expression of CD14 decreased (from 98% to 80%) and that of CD68 increased (>90%) with cell differentiation.","20375612:3, 12208965:1142",2,2,"Homo sapiens","Microglia, Phagocytes","positive"]
["CD14 -> CD83","Expression","In contrast, immature dendritic cells cultured in G4 plus human pancreatic RNase or eosinophil-derived neurotoxin for 48 h, although still CD14-, up-regulated the surface expression of CD83, CD86, and HLA-DR, indicating that human pancreatic RNase and eosinophil-derived neurotoxin treatment induced phenotypic maturation of DCs (Fig. 7A)., Maturation of Immature dendritic cells was induced by addition of lipopolysaccharide purified from Salmonella (1 µg/ml). Immature dendritic cells and mature dendritic cells were analyzed for expression of CD83 and CD86, which were upregulated in mature dendritic cells, and CD14, which was downregulated in both cell types (5).","15528350:1252, 12874316:1098",2,2,null,"Dendritic Cells","positive"]
["CD14 -> CD86","Expression","In addition, the nuclear translocation of nuclear factor ?B and expression of the costimulatory molecules CD40 and CD86 are diminished in the absence of either of CD14 or TLR2., In contrast, immature dendritic cells cultured in G4 plus human pancreatic RNase or eosinophil-derived neurotoxin for 48 h, although still CD14-, up-regulated the surface expression of CD83, CD86, and HLA-DR, indicating that human pancreatic RNase and eosinophil-derived neurotoxin treatment induced phenotypic maturation of DCs (Fig. 7A). <more data available...>","18462086:1175, 15528350:1252, 12874316:1098",2,3,null,"Macrophages, Dendritic Cells","positive"]
["CD14 -> ITGAX","Expression","Treatment of U937 cells with PMA markedly increased CD14, CD11a, CD11b and CD18 antigen expression, and slightly increased CD11c expression., In particular, those for CD11c and tumor necrosis factor a (TNFa) were markedly increased, and there were lesser, but significant, increases in Spp1, CD14, CD45, CCL9, Toll-like receptor 4 (TLR4), and interleukin-1B (IL-1ß) (Fig. 6G,H).","1689274:1, 18160655:1251",2,2,null,"Microglia","positive"]
["CD14 -> PTGS2","Expression","These results indicate that, like TNF-a and IL-1ß (26), CD14 is essential for the induction of COX-2, IL-12 p35, and IL-12 p40 genes by low concentrations of LPS and Taxol, but not at high concentrations.","11123339:187",2,1,null,"Macrophages","positive"]
["CD44 -> CCND1","Expression","HMW-HA binding to CD44 selectively inhibits the GTP loading of Rac and Rac-dependent signaling to the cyclin D1 gene, whereas LMW-HA binding to CD44 selectively stimulates ERK activation and ERK-dependent cyclin D1 gene expression., Hyaluronan and CD44 antagonize mitogen-dependent cyclin D1 expression in mesenchymal cells., Nuclear CD44 accelerates cell proliferation and cell cycle progression through control of cyclin D1 expression.","18806267:4, 17296798:100, 19506034:1093",2,3,"Homo sapiens",null,"positive"]
["CD44 -> MET","Expression","CD44 isoforms bearing heparin sulfate chains can bind to HGF/SF and facilitate its presentation to c-Met., A blocking antibody to CD44v6 decreased HGF-induced c-Met phosphorylation as well as enhanced random- and site-directed migration., In this paper, we demonstrate that the activation of c-Met induced by InlB is dependent on CD44v6, a member of the CD44 family of transmembrane glycoproteins., In several types of cells, the activation of the receptor tyrosine kinase c-Met by its ligand hepatocyte growth factor (HGF) requires the coreceptor CD44v6. <more data available...>","12670907:1, 20357818:6, 19432801:3, 17065554:0, 17923692:2, 12183053:4, 10485493:1212",2,7,null,"Melanocytes","positive"]
["CD44 -> TGFB1","Expression","CD44 costimulation increased production of IL-10 in a partially IL-2-dependent manner and also promoted cell surface TGF-beta expression., The effect of BMP-7 on TGF-beta1 synthesis in TNF-alpha-stimulated cells was abrogated by disruption of CD44-hyaluronan interactions, suggesting that it was due to increased monocyte binding to hyaluronan on the cell surface., hyaluronan may also be packaged into cable-like structures that have been shown to bind mononuclear leukocytes via their cell surface CD44 resulting in attenuation of monocyte-dependent TGF-ß1 generation and thereby promoting tissue homeostasis (51). <more data available...>","19635906:4, 15574511:12, 17611197:1400, 16900089:1166, 18397995:3, 15084590:1, 19457680:7, 15387373:2",2,8,null,"T-Lymphocytes, Regulatory, Monocytes, Leukocytes, Mononuclear, Epithelial Cells, Fibroblasts","positive"]
["CD44 -> VIM","Expression","Serial transplantation of elongated epithelial cells results in progressive loss of tumorigenic potential; tumor heterogeneity; CD44, E-cadherin, and epithelial cytokeratin expression and increased alpha-smooth muscle actin I and vimentin expression.","18957543:2",2,1,null,"Epithelial Cells","positive"]
["CD80 -> BCL2","Expression","However, the expression level of bcl-2 in T cells was increased 31% and 76% following stimulation with dendritic cell/rF-B7-1 or dendritic cell/rF-TRICOM, respectively.","10922408:1396",2,1,null,"T-Lymphocytes","positive"]
["CD80 -> BCL2L1","Expression","In vitro data show that cross-linking CD80 on the surface of CD4+ T cells activated in the presence of Th1-promoting cytokines increases the level of T cell activation, effector function, and survival by directly up-regulating the expression levels of transcripts for T-bet, IFN-gamma, and Bcl-xL., Thus, CTLA4-CD80/CD86 interactions play an important role in modulating the expression of BclXL., B7-1 and B7-2 interact with CD28 on T cells, thereby inducing expression of Bcl-XL in the T cells (13-18)., CTLA4-CD80/CD86 interaction during the first 12 h of activation with P + I lowers TGF-ß production and induction of apoptosis but enhances IL-2 production and Bcl-XL levels, leading to increased cell-cycle progression and survival. <more data available...>","16920930:4, 15788440:1179, 9520449:1039, 12429713:1257, 16880206:1059, 15746069:1328, 14745033:1189, 11726649:1333",2,8,"Homo sapiens","T-Lymphocytes, memory T-cells, B-Lymphocytes","positive"]
["CD80 -> CD86","Expression","The expression of CD86 was upregulated earlier than that of CD80 after in vitro stimulation., CD86 expression is enhanced faster than CD80 expression and reaches the peak level after 4-6 hr in stimulated cells., This study suggested that CD80 and CD86 activate T cells in IgA nephropathy, CD80/CD86 expressions correlated with renal function at the time of renal biopsy, and monocyte/macrophages and tubular epithelial cells act as antigen-presenting cells., In the treated group, CD80 expression lowered from 18.06 +/- 4.53 before treatment to 13.18 +/- 3.02 after treatment and CD86 expression lowered from 38.61 +/- 10.54 to 29.65 +/- 8.55; while in the control group, the two expressions were lowered from 18.40 +/- 3.86 to 15.34 +/- 3.90, and from 38.29 +/- 11.67 to 35.88 +/- 13.85 respectively, the lowering in both groups were statistically significant (P<0.01 and P<0.05), but it was more significant in the treated group (P<0.05). <more data available...>","14513778:9, 9014827:5, 14871408:14, 20073218:7, 10202049:1041, 16474127:1255, 18523279:1202, 16244115:1113, 19737784:1126, 14742503:1215 <more data available...>",2,12,null,"PBMCs, Monocytes, T-Lymphocytes, Dendritic Cells, Macrophages, myeloid dendritic cells, B-Lymphocytes, Keratinocytes","positive"]
["CD83 -> CD86","Expression","Here, we investigate how CD83, an immunoglobulin protein expressed on the surface of mature DCs, promotes major histocompatability class II and CD86 expression., However, the increase in surface expression of HLA-DR and CD86 after addition of LPS was significantly attenuated in cord DCs, with CD25 and CD83 expression also markedly reduced., Specifically, IRX-2-treated DC increased expression of CD83 and CCR7, markers for DC maturation and migration, respectively, and increased the expression of HLA-DR, CD54, and the costimulatory molecules CD86 and CD40, which are critical mediators of T cell activation. <more data available...>","21220452:3, 11982599:2, 17667526:4, 17710154:3, 17056542:1160, 18701714:1186, 17878352:1075, 12660223:1115",2,8,"Homo sapiens, Mus musculus","Dendritic Cells, Monocytes, B-Lymphocytes","positive"]
["CD86 -> BCL2L1","Expression","Thus, CTLA4-CD80/CD86 interactions play an important role in modulating the expression of BclXL., In contrast, signaling through CD86 increased the expression of anti-apoptotic molecules Bcl-w and Bcl-x(L)., B7-1 and B7-2 interact with CD28 on T cells, thereby inducing expression of Bcl-XL in the T cells (13-18)., It has also been suggested that cross-linking B7-2 up-regulates B cell proliferation, enhances the expression of antiapoptotic molecule Bcl-xL and stimulates the production of IgG1, IgG2a, and IgE (17, 18). <more data available...>","15788440:1179, 11726649:1393, 9520449:1039, 16221763:1058, 16709832:1310, 12429713:1257, 16880206:1059",2,7,null,"T-Lymphocytes, B-Lymphocytes, Antigen-Presenting Cells, activated B-lymphocytes","positive"]
["CEBPA -> CSF1","Expression","For example, when expressed alone, RUNX1, C/EBPa, and PU.1 are poor activators of the M-CSF promoter., However, C/EBPa both positively and negatively modulated the PU.1-induced changes in CSF-1, CSF-1R, and Mac-1 and endogenous PU.1 expression.","15988004:1056, 18424555:1171",2,2,null,"Myeloid Progenitor Cells, Macrophages","positive"]
["CEBPA -> ID1","Expression","Id1 expression is up-regulated by C/EBPa in CD34+ cells (16)., We note that C/EBP factors appear to also regulate the Id1 gene (55)., Thus, C/EBPa-induced Id1 expression alone does not explain inhibition of erythroid differentiation by C/EBPa.","16606850:1157, 15788530:1234, 16469877:1254",2,3,"Homo sapiens","Granulocytes, Macrophages, Hematopoietic Stem Cells","positive"]
["CEBPA -> MT2A","Expression","MTF-1 and C/EBPalpha act in concert to increase MT-2A expression, which probably explains the high level of Metallothioneins expression in the liver.","17363595:9",2,1,null,null,"positive"]
["CEBPA -> PROS1","Expression","Reporter gene analysis suggests that members of the CCAAT/enhancer binding protein (C/EBP) family of transcription factors are potent activators of protein S gene transcription in HepG2 cells.","17061980:6",2,1,null,null,"positive"]
["CEBPB -> BCL2A1","Expression","Most importantly, C/EBP beta overexpression significantly upregulated promoter activities of IL-8, COX-2, and anti-apoptotic Bfl-1 genes., We first determined that the C/EBPbeta-C overexpression or siRNA-mediated C/EBPbeta depletion decreased TNF-alpha-induced promoter activities of Bfl-1, IL-6, and IL-8 genes., Consistent with their concerted binding to the -933/-773 bfl-1 probe, NF-?B, AP-1, and C/EBPß synergistically activated expression from the bfl-1 promoter (Fig. 5A).","18512730:9, 19489038:5, 12665576:1195",2,3,null,null,"positive"]
["CEBPB -> CCL3","Expression","The -300 bp CCL3 promoter and -222 bp CCL4 promoter were strongly up-regulated by co-transfection with the C/EBPß expression vector., We demonstrated that inducible expression of NF-IL6 is able to increase endogenous gene expression of macrophage inflammatory protein -1 alpha, osteopontin and CD14 in M1 cells., For example, expression of MIP1a (Matsumoto et al. 1998), MCP1(Yamamoto et al. 1999), and IL-8 (Kunsch et al. 1994) are in part regulated by C/EBPß., Therefore, phosphorylation of C/EBPß on Thr235 seems to be essential for inducible IL-8, Mip-1a, and Mip-1ß gene expression in neutrophils. [Figure 8] View larger version (21K): [in this window] [in a new window] . <more data available...>","20702408:5, 9885903:4, 11711437:1163, 19109189:1274, 11937564:1054, 14593587:1245",2,6,"Homo sapiens","Chondrocytes, Macrophages, Neutrophils, Monocytes","positive"]
["CEBPB -> CSF1R","Expression","Indeed, when this region was completely removed from the mutants, as in HSF1-(1-279), the repression of NF-IL6-activated c-fms transcription by HSF1-(1-279) was equally effective as wild-type HSF1 (Fig.1 C)., Previous studies have shown that heat shock represses lipopolyliposaccharide activatedTNF-a gene transcription as well as constitutive and NF-IL6-activated transcription of the c-fms gene, which plays an important role in monocyte/macrophage proliferation and differentiation (7).2 Powerful activation of monocytes/macrophages and lymphocytes often leads to the activation of the APR through production of proinflammatory cytokines such as IL-1ß and TNF-a that are potentially lethal to the host (27).","12468538:1163, 11801594:1292",2,2,null,"Macrophages","positive"]
["CEBPB -> MAFB","Expression","C/EBPß isoforms regulate osteoclastogenesis through MafB expression., Furthermore, we have observed that the macrophage-specific expression of MafB depends, at least in part, on the combinatorial action of C/EBPß and SP1 or SP3 proteins (L.M.Kelly, M.H.Sieweke, T.Graf and C.Nerlov, submitted), suggesting that C/EBPß acts upstream of MafB.","19440205:1207, 10790365:1260",2,2,null,"Osteoclasts, Macrophages","positive"]
["CEBPB -> STAT1","Expression","A similar experiment conducted with U3A cells revealed two important pieces of information. 1) Interferon-? did not stimulate reporter gene expression; and 2) C/EBP-ß stimulated gene expression in the absence of STAT1 to a level comparable to that in the parental cell line, 2fTGH.","10995751:1351",2,1,null,null,"positive"]
["CEBPB -> TGFB1","Expression","These observations indicate that an autoregulatory mechanism, involving the MH2 domain of Smads, modulates activation of the TGF-beta1 promoter by C/EBPbeta., The down-regulation of C/EBPß- or d-activated transcription from the peroxisome proliferator-activated receptor?2 and leptin promoters by Transforming growth factor-ß and Smads did not exclude functional interactions with other DNA binding transcription factors, besides C/EBPß and -d., The increased levels of TCF5 and c-Myc can result in the increased expression of fibrogenic growth factors, HB-EGF, TGF-ß, and VEGF, all of which can initiate and sustain the fibroproliferation cascade, a central event in the immunopathogenesis of bronchiolitis obliterans syndrome following human lung transplantation.","19014341:6, 12524424:1239, 10559198:1239, 18354170:1323",2,4,null,"Microglia, Epithelial Cells","positive"]
["CEBPD -> CCND1","Expression","Silencing of C/EBPdelta, Cdc27, or the anaphase promoting complex/cyclosome coactivator Cdh1 (FZR1) in MCF-10A breast epithelial cells increased cyclin D1 protein expression.","20439707:3",2,1,null,"Epithelial Cells","positive"]
["CEBPD -> CD14","Expression","C/EBPd is also involved in the activation of lipopolysaccharide-binding protein after IL-6 signalling in hepatocytes [18] and of the genes a1-acid glycoprotein [20] and serum amyloid A [21], and activates CD14 transcription in transient transfection assays [22].","14979920:1292",2,1,null,"Hepatocytes","positive"]
["CEBPD -> CEBPA","Expression","Previous investigations indicated that transcription of the C/EBPalpha gene is sequentially activated during differentiation, initially by C/EBPbeta and C/EBPdelta and later by C/EBPalpha (autoactivation)., Nuclear expression of the 36-kilodalton C/EBP delta protein increases immediately after birth, followed first by increases in the 38-kilodalton C/EBP beta protein expression and then by increases in the 42-kilodalton C/EBP alpha protein expression., These data demonstrate that Myc specifically inhibits the terminal stages of the adipogenic program and suggest that Myc may act by blocking C/EBPbeta- and C/EBPdelta-directed activation of C/EBPalpha and PPARgamma2 expression, although the precise molecular mechanism is not understood. <more data available...>","10373535:1, 7910803:4, 10623469:4, 18703634:1194, 18930917:1043, 18653467:1203, 12138207:1046, 16754681:235, 12186946:1140, 16154099:1059 <more data available...>",2,43,"Bos taurus","Adipocytes, Fibroblasts, Mesenchymal Stem Cells, myeloblasts, Hepatocytes","positive"]
["CEBPD -> PRL","Expression","C/EBPd, C/EBPß, and LAP all elicited a significant induction of decidual prolactin promoter activity which was further enhanced by the addition of 8-Br-cAMP.","10455153:1293",2,1,null,null,"positive"]
["CEBPD -> SOCS3","Expression","The doxycycline-dependent expression of C/EBP-d neither increased Spi-2 and Socs3 transcripts nor interfered with their induction by IL6RIL6 (Fig. 5B).","14600146:1226, 14600146:227",2,2,null,null,"positive"]
["CEBPD -> TF","Expression","In the non-transferrin-expressing HeLa cells, the transferrin promoter could be activated by C/EBP-delta., Suire et al. (12) showed, in cotransfection assays, that overexpression of C/EBP alpha (C/EBP) and C/EBP delta (NF-IL6beta, CRP3) in Sertoli cells stimulated transcription from the cAMP-regulated transferrin promoter containing a C/EBP binding site.","8226864:7, 9927313:1054",2,2,null,"Sertoli Cells","positive"]
["CLU -> BCL2","Expression","Notably, key pro-survival/proliferation Nuclear factor ?B target genes, such as p-AKT, cyclin D1 and BCL2, were down-regulated in the presence of exogenous CLU., More specifically, we showed that, via a p53-independent mechanism, Secretory clusterin depletion suppresses expression of Bcl-2 and Bcl-XL prosurvival proteins, rendering cells more vulnerable to active Bax; this effect can be reversed by ectopic Bcl-2 overexpression in OS cells.","19903745:1203, 19118032:1361",2,2,null,"Epithelial Cells","positive"]
["CSF1 -> BCL2","Expression","CSF-1 maintained NF-kappaB activation and increased the expression of bcl-2 and bcl-X(L) mRNA, but had no effect on JNK activation., They also reported that M-CSF maintained nuclear factor-?B activation and increased the expression of bcl-2 but had no effect on c-Jun N-terminal kinase (JNK) kinase activation., In M-MF, the transcript of the BCL-2 gene was stronger than that of the BCL-XL gene, and M-CSF withdrawal decreased the expression of the BCL-2 gene but induced a slight decrease in the expression of the BCL-XL gene (Fig. 2A).","10934148:4, 11279167:1217, 16204228:1126",2,3,null,"Osteoclasts, Macrophages","positive"]
["CSF1 -> BCL2L1","Expression","CSF-1 maintained NF-kappaB activation and increased the expression of bcl-2 and bcl-X(L) mRNA, but had no effect on JNK activation., M-CSF activated Akt and extracellular signal-regulated kinase signaling pathways and up-regulated downstream anti-apoptotic Bcl-xL expression in these cells., Macrophage colony-stimulating factor promotes the survival of osteoclast precursors by up-regulating Bcl-X(L)., Ets-2 also mediates M-CSF-dependent macrophage survival through regulation of Bcl-xL expression (11)., In osteoclast precursors, CSF-1 prevents apoptosis by inhibiting the activity of caspase-3 and -9 and by up-regulating Bcl-XL, an inhibitor of procaspase-9 cleavage (16). <more data available...>","10934148:4, 17717142:5, 12526097:100, 16142752:1157, 17068143:1072, 16204228:1126",2,6,"Rattus norvegicus","Osteoclasts, Myocytes, Cardiac, Macrophages","positive"]
["CSF1 -> C3","Expression","Macrophage colony-stimulating factor (M-CSF) enhances complement component C3 production by human monocytes/macrophages.","8477063:100",2,1,"Homo sapiens","Macrophages","positive"]
["CSF1 -> CCL3","Expression","Combined M-CSF/Abeta treatment increased interleukin-1 and macrophage inflammatory protein 1-alpha expression by microglia, whereas inducible nitric oxide synthase (iNOS) expression was localized primarily to astroglia., Furthermore, addition of M-CSF antagonists to HIV-1-infected macrophages, including anti-M-CSF monoclonal or polyclonal Abs or soluble M-CSF receptors, dramatically inhibited HIV-1 replication and reduced production of MIP-1alpha., Although the mechanism is not known, STAT1 could play an important role because STAT-1- and Akt-mediated macrophage priming by IFN-ß is necessary for optimal lipopolysaccharide-stimulated production of several inflammatory mediators, including IL-653 and for poly (I:C)-induced MIP-1a mRNA expression in keratinocytes.54 In contrast, STAT3 is dispensable for CSF-1-induced macrophage proliferation51 and MIP-1a expression54 and has antiproliferative and antiinflammatory effects in macrophages.32,50,55,56 Thus, our data suggest that up-regulation of STAT1 in cmo macrophages could contribute to their increased production of IL-6 and MIP-1a. <more data available...>","11959396:4, 10779806:5, 19608749:1243, 10779806:144, 10779806:147, 10779806:32, 19608749:244",2,7,null,"Microglia, Macrophages","positive"]
["CSF1 -> CCND1","Expression","Induction of cyclin D1 mRNA by CSF-1 was restored in cells forced to express c-myc, and vice versa, suggesting that expression of the two genes is interdependent., Previously we showed that the macrophage-activating agent lipopolysaccharide blocks CSF-1-induced proliferation and cyclin D1 expression in macrophages., We further demonstrated that Cdc42 modulated M-CSF-stimulated cyclin D expression and phosphorylation of Rb and induced caspase 3 and Bim, thus contributing to osteoclast proliferation and apoptosis rates. <more data available...>","7624328:4, 9722538:2, 20501942:5, 9608681:6, 10602507:1124, 9139801:1201, 8798425:1059, 10952989:1048, 11518769:1133, 10329719:1184 <more data available...>",2,24,"Mus musculus","Fibroblasts, Macrophages, Osteoclasts","positive"]
["CSF1 -> CD14","Expression","It has been demonstrated that the expression of CD16 and CD14 is regulated by macrophage colony stimulating factor (M-CSF) and GM-CSF., M-CSF was also shown by flowcytometric analysis to influence the expression of CD14, a receptor for LPS, which might render monocytes more sensitive to LPS., Daily administration of macrophage colony stimulating factor (M-CSF) to the mice resulted in increased levels of MSR-A expression and reduced levels of CD14 as well as several cytokine expressions, leading to shortening of the inflammatory process. <more data available...>","12153694:6, 8877404:9, 10594845:5, 9566797:4, 15256426:1265",2,5,null,"Monocytes, Macrophages","positive"]
["CSF1 -> CD68","Expression","They also demonstrated that M-CSF upregulates in addition to CD 68 also CD 14 mRNA expression, whereas GM-CSF does not affect the expression of CD 14.","18787236:1261",2,1,null,"Monocytes","positive"]
["CSF1 -> CD86","Expression","TNF-a, GM-CSF, and M-CSF differentially upregulate CD40, B7-1, and B7-2 expression on purified Langerhans cells.","10594746:1111",2,1,null,"Langerhans Cells","positive"]
["CSF1 -> CEBPA","Expression","Ectopic expression of THOC5 mimicked M-CSF mediated cell maturation and enhanced protein expression of the myeloid transcription factors C/EBPbeta, C/EBPalpha, Pu-1 and also GAB2 (a PI-3 Kinase and macrophage development regulator)., M-CSF and G-CSF use separate pathways to activate ERK and modify C/EBPa .","19015024:4, 19587381:1161",2,2,null,"Macrophages","positive"]
["CSF1 -> CEBPB","Expression","Ectopic expression of THOC5 mimicked M-CSF mediated cell maturation and enhanced protein expression of the myeloid transcription factors C/EBPbeta, C/EBPalpha, Pu-1 and also GAB2 (a PI-3 Kinase and macrophage development regulator).","19015024:4",2,1,null,"Macrophages","positive"]
["CSF1 -> CSF1R","Expression","However, after 48 h, M-CSF significantly stimulated c-Fms expression., IL-10 together with M-CSF increased the expression of M-CSF receptors., This treatment completely prevented M-CSF-induced c-Fms expression in a dose-dependent manner but had little effect on TNFa-induced c-Fms up-regulation (Fig. 5D)., Incubation with CSF-1 down-regulated CSF-1R expression and was associated with proliferation of mononuclear cells with decreased CSF-1R binding., We demonstrated that one mechanism by which this occurs is PU.1 down-regulation by the negative control of NFI-A on M-CSFR levels (Fig. 7) because M-CSF induces PU.1 expression through M-CSFR in the hematopoietic myeloid-osteoclast lineage (1-3). <more data available...>","16461346:213, 8978307:46, 16461346:221, 19819976:310, 19059913:261, 19628784:169",2,6,"Homo sapiens","Macrophages, Osteoclasts, Stromal Cells, Monocytes","positive"]
["CSF1 -> CYBB","Expression","We find that M-CSF differentiation increases gp91phox and p67phox mRNA abundance in these cells (Fig. 1B)., Of interest to the current studies, HoxA9 overexpression in murine myeloid cells does not impair granulocyte-colony stimulating factor- or macrophage-colony stimulating factor-induced expression of gp91Phox, a phagocyte respiratory burst oxidase protein (4)., Consistent with this, we find that expression of gp91phox and p67phox protein is also increased by M-CSF differentiation in Western blots of cell lysate proteins (Fig. 1C). <more data available...>","16210632:1195, 15681849:1070, 16210632:1196, 15681849:71",2,4,"Mus musculus","Myeloid Progenitor Cells, Myeloid Cells","positive"]
["CSF1 -> DUSP1","Expression","Therefore, M-CSF activates ERK-1/2 and induces MKP-1 expression through different pathways., Decorin also inhibits M-CSF-dependent expression of MKP-1 and extends the kinetics of ERK activity, which is characteristic when macrophages become activated instead of proliferating., JNK kinase is required for the induction of Mkp1 expression by M-CSF or lipopolysaccharide., Macrophage colony-stimulating factor induces the expression of mitogen-activated protein kinase phosphatase-1 through a protein kinase C-dependent pathway. <more data available...>","10452980:5, 11567999:6, 17337450:1154, 11086074:1558, 16709817:1155, 19585511:3",2,6,null,"Macrophages","positive"]
["CSF1 -> FCGR3A","Expression","It has been demonstrated that the expression of CD16 and CD14 is regulated by macrophage colony stimulating factor (M-CSF) and GM-CSF., CD16 expression on rheumatoid arthritis blood monocytes was augmented in vitro by IL-10, M-CSF, and TGFbeta1., The recombinant human macrophage colony-stimulating factor promoted TNF-alpha, IL-6, and IL-8 inductions of monocytes and increased the percentages of CD11b, CD16, HLA I, and HLA II molecule expression on monocytes., CSF-1 also induces the expression of CD16 (Fc?RIII) on the CD14+CD16+ subset of human monocytes [11 ], which exhibit a more activated, macrophage-like character. <more data available...>","12153694:6, 12384915:8, 11501160:3, 16973889:1032, 12186843:1061, 15534180:1269",2,6,"Homo sapiens","Monocytes, Astrocytes","positive"]
["CSF1 -> ITGB2","Expression","The levels of CD11a and CD18 expression on granulocytes were significantly enhanced by administration of M-CSF.","11789672:6",2,1,null,"Granulocytes","positive"]
["CSF1 -> LGALS3","Expression","Macrophage colony-stimulating factor (M-CSF), which is present at increased levels in MRL/lpr mice, but not in MRL/Mp- +/+ mice, induced the expression of Mac-2 antigen and Fas antigen on spleen adherent cells of MRL/Mp- +/+ mice.","8870694:4",2,1,null,null,"positive"]
["CSF1 -> NFATC1","Expression","Furthermore, anti-CD11b antibodies inhibited NFATc1 expression induced by M-CSF and RANKL in BMMs., S3 shows the normal osteoclast differentiation and expression of NFATc1 in NFATc2-/- monocyte/macrophage precursor cells that were stimulated with RANKL/M-CSF., Expression of NFATc1 is induced by CSF-1/RANKL during osteoclast differentiation, and this factor has been implicated as a \"master regulator\" of osteoclast differentiation (13, 31)., Inhibition of c-Fos and NFATc1 expression induced by RANKL and M-CSF in RAGE-deficient prefusion osteoclasts To further understand how RAGE regulates osteoclast maturation and function, we examined expression of transcriptional factors essential for osteoclastogenesis, including c-Fos and NFATc1 (39, 40).","18775427:4, 16275763:1202, 17403683:264, 16606672:1165",2,4,"Mus musculus","Macrophages, Monocyte-Macrophage Precursor Cells, Osteoclasts","positive"]
["CSF1 -> P2RX7","Expression","Furthermore, lipopolysaccharide and M-CSF could up-regulate P2X7 receptor expression in monocytes, while IFN-gamma, TNF-alpha and GM-CSF had weak effects, but pretreatment with these inducers could not further enhance lipopolysaccharide-stimulated P2X7 receptor expression in monocytes.","15830104:6",2,1,null,"Monocytes","positive"]
["CSF1 -> P2RY6","Expression","Using transwell, antibody-mediated depletion, suramin inhibition of purinergic receptors, and competitive experiments with uridine diphosphate /uridine triphosphate , we demonstrate that HNP1-3 secreted by CD14(-)/CD24(+) cells inhibit M-CSF-induced differentiation of CD14(+)/CD24(-) cells at least in part through P2Y6, a receptor involved in macrophage differentiation.","19864642:6",2,1,null,"Macrophages","positive"]
["CSF1 -> SERPING1","Expression","Interferon-gamma and alpha , colony stimulating factor-1, interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) all induce C1-INH synthesis in a variety of cell types., In vitro studies indicate that C1INH mRNA and protein levels are increased by up to 20 fold after stimulation with interferon-gamma (gamma-IFN) and to a lesser extent in response to alpha-interferon , tumor necrosis factor-alpha (TNF-alpha), Interleukin 6 (IL-6) and monocyte colony stimulating factor (M-CSF).","9777421:6, 8172557:8",2,2,null,"Hepatocytes","positive"]
["CSF1 -> TGFB1","Expression","Five days after myocardial infarction, M-CSF increased the number of ED-1-positive cells, messenger ribonucleic acid levels of transforming growth factor-beta-1, collagen I and III, and collagen fibers within the infarct., Transcripts for TGF-ß and Tweak were both decreased by M-CSF treatment., Macrophage colony-stimulating factor accelerates wound healing and upregulates TGF-beta1 mRNA levels through tissue macrophages., Macrophage colony-stimulating factor accelerates wound healing and upregulates TGF-beta 1 mRNA levels through tissue macrophages. <more data available...>","16458148:4, 12193691:1163, 9356238:100, 11030870:1308, 11477167:1227",2,5,null,"Microglia, Macrophages, myofibroblasts","positive"]
["CSF1 -> TLR2","Expression","CSF-1 also down-regulated expression of TLR1, TLR2, and TLR6, but not the LPS receptor, TLR4, or TLR5., TLR-2 expression on monocytes was enhanced by macrophage colony-stimulating factor (M-CSF) and interleukin-10 (IL-10), but was reduced by transforming growth factor beta1, while CD16 expression was inducible by these cytokines., Toll-like receptor 2 and 4 surface expressions on human monocytes are modulated by interferon-gamma and macrophage colony-stimulating factor.","11751985:7, 15146415:10, 11672593:100",2,3,"Homo sapiens","Macrophages, Monocytes","positive"]
["CSF1 -> TNFRSF1A","Expression","Cell surface expression of TNFR1/2 expression on monocytes was induced by IL-10, and more efficiently in combination with M-CSF., The expression of TNFR1 and TNFR2 in monocytes has been shown to be modulated by various cytokines including TNF-a, interleukin-10, and macrophage-colony stimulating factor (Takasugi et al. 2006).","16859503:4, 18310456:1267",2,2,null,"Monocytes","positive"]
["CSF1 -> TREM2","Expression","Addition of macrophage colony stimulating factor (M-CSF) to LN cell culture allowed the proliferation and expression of TREM2 in LN cells, and the addition of neutralizing anti-M-CSF antibodies suppressed the proliferation of LN cells despite the expression of TREM2., Whereas Humphery et al. recently reported that TREM-2 expression is induced during in vitro osteoclastogenesis induced by culture bone marrow-derived macrophages with macrophage CSF (MCSF) and the receptor activator of NF-?B ligand (4), we find that differentiation of macrophages in MCSF alone leads to expression of TREM-2. [Figure 3] View larger version (33K): [in this window] [in a new window] .","20345919:4, 16951310:1159",2,2,null,"Microglia, Macrophages","positive"]
["CSF1 -> VEGFA","Expression","In vivo, M-CSF increased VEGF mRNA expression in skeletal muscles., In this study, we demonstrate the molecular mechanism of M-CSF-induced VEGF production., In mice, M-CSF increased VEGF production in hearts and in freshly isolated cardiomyocytes, which showed M-CSF receptor expression., M-CSF augments the production of vascular endothelial growth factor (VEGF) from the bone marrow cells, especially from myeloid lineage cells., In summary, we demonstrate that MCP-1 and M-CSF, critical for monocyte recruitment, activation, and differentiation, differentially regulate VEGF-A expression and may play an important role in monocyte/macrophage- mediated tumor angiogenesis. <more data available...>","15944252:6, 18852899:3, 17717142:3, 16456135:3, 16318581:9, 12928417:1218, 15749929:1316, 18436538:1449, 18832730:1273, 17283136:1185 <more data available...>",2,15,"Homo sapiens, Mus musculus","Monocytes, Myocytes, Cardiac, Macrophages, Endothelial Cells","positive"]
["CSF1R -> PTPN6","Expression","Traumatic injury to the central nervous system activates microglia and strongly increases expression of SHP-1, which physically associates with and is activated by c-Fms in these cells (17).","12361947:312",2,1,null,"Microglia","positive"]
["CSF1R -> VEGFA","Expression","Anti-M-CSFR mAb treatment significantly impaired the effect of M-CSF on VEGF production, and the VEGF level decreased to a level similar to the control value, whereas control IgG did not (*, p < 0.05).","15944252:1412",2,1,null,"Muscle Fibers, Skeletal","positive"]
["Ctla2a -> TGFB1","Expression","Similarly, CTLA-2alpha via retinal pigment epithelium was able to promote TGF-beta production by the CD4(+) T cells., The CTLA-2alpha effect on T regulatory cell induction occurred through TGFbeta signaling, because CTLA-2alpha promoted activation of TGFbeta in the eye.","19801522:4, 19017942:7",2,2,null,"T-Lymphocytes, T-Lymphocytes, Regulatory","positive"]
["CTSL1 -> BCL2","Expression","Moreover, down-regulation of cathepsin L lowered the expression of antiapoptotic protein Bcl-2, whereas up-regulation increased the expression of Bcl-2, indicating that cathepsin L acts upstream of caspase-3.","12536203:6",2,1,null,null,"positive"]
["CTSL1 -> HLA-DQB1","Expression","Surface I-Ab expression is slightly enhanced by cathepsin L or cathepsin S expression (Fig. 1[Go]A)., However, the surface staining of 15G4, which recognizes both CLIP:I-Ab and small leupeptin-induced peptide:I-Ab, is enhanced by the expression of cathepsin L or cathepsin S, presumably due to the increased surface expression of CLIP:I-Ab resulting from efficient degradation of small leupeptin-induced peptide (Fig. 4[Go]A; also see Fig. 6[Go], upper panel; molecular mass (m) = 1987.9).","11884425:1140, 11884425:141, 11884425:196",2,3,null,"Fibroblasts, Dendritic Cells","positive"]
["CTSS -> HLA-DQB1","Expression","Surface I-Ab expression is slightly enhanced by cathepsin L or cathepsin S expression (Fig. 1[Go]A)., Therefore, Cat S deficiency decreases the expression of Ea peptide-I-Ab complexes in splenic B cells as well as in intestinal epithelial cells., Thus, the absence of cathepsin S drastically inhibits generation of mature peptide-loaded I-Ab dimers.","11884425:1140, 15661874:1228, 10072073:1164, 11884425:141, 15661874:229",2,5,null,"Fibroblasts, B-Lymphocytes","positive"]
["CX3CR1 -> TGFB1","Expression","CX3CR1 promotes TGF-ß1 expression and myofibroblast accumulation in wounded skin ., CX3CR1 promotes TGF-ß1 expression and activated fibroblast accumulation in wounded skin., These results suggest that CX3CR1 activity in vivo promotes TGF-ß1 production, which promotes accumulation of a-smooth muscle actin+-activated fibroblasts, which are the direct source of collagen, a key constituent of granulation tissue in skin wound repair. [Figure 10] View larger version (76K): [in this window] [in a new window] .","18097059:1295, 18097059:296, 18097059:303, 18097059:301",2,4,null,"Fibroblasts","positive"]
["CX3CR1 -> VEGFA","Expression","CX3CR1 promotes VEGF production and angiogenesis in wounded skin ., Activation of fractalkine/CX3CR1 by vascular endothelial cells induces angiogenesis through VEGF-A/KDR and reverses hindlimb ischaemia., In one of the original contributions within this issue, Ryu et al.15 demonstrate that activation of fractalkine and its cognate receptor CX3CR1 upregulates HIF-1a and subsequently VEGF-A, leading to post-ischaemic neovascularization., On the contrary, under our present experimental conditions, genetic depletion of CX3CR1 reduced alkali injury-induced macrophage accumulation but promoted Corneal neovascularization with little effects on intraocular VEGF expression.","18097059:1311, 18006432:100, 18339645:1056, 18322241:1311",2,4,null,"Endothelial Cells, Monocytes, Macrophages","positive"]
["CXCL10 -> CCL3","Expression","We found that treatment with the chemokine IP-10 resulted in significant increases in the amount of MIP-1alpha and MCP-1/JE released from murine mammary cells., Up-regulation of RANTES/CCL5, IP-10/CCL3 and CCR2 was associated with leucocyte migration to the brain and increased expression of MCP-1/CCL2, IP-10/CCL3 and CCR5 with leucocyte migration to the lung., MCP-1/CCL2 (a ligand for CCR2) and MIP-1a/CCL3 (a ligand for CCR5) were also induced in addition to two CXCR3 ligands, IP-10 and I-TAC (Table 3) ., Neutralization of CXCL10 dramatically reduces cellular infiltration into the cornea and suppresses the expression of CCL3, as well as RANTES (CCL5) (Carr et al., 2003[Down]; Wickham et al., 2004[Down]). <more data available...>","15026621:3, 18665903:8, 12773510:1199, 16476970:1076, 16920957:1148, 16982826:1270, 12941914:1285, 20478761:1206",2,8,"Mus musculus",null,"positive"]
["CXCL10 -> ISG15","Expression","Consistent with this finding, Respiratory syncytial virus-induced beta interferon (IFN-beta), interferon-inducible protein 10 (IP-10), chemokine ligand 5 (CCL-5), and IFN-stimulated gene 15 (ISG15) expression levels were decreased in RIG-I-silenced cells during the early phase of infection but not at later times (18 h postinfection)., The genes induced most strongly by human cytomegalovirus infection included three chemokines (CCL5, CCL8, CXCL10) and the interferon-stimulated genes MX1 and G1P2 (Table 2[Up]). <more data available...>","17108032:5, 19439557:1245, 11927648:1067",2,3,"Homo sapiens","Myeloid Progenitor Cells, Killer Cells, Natural","positive"]
["CXCL10 -> PDPN","Expression","Anti-IP-10 mAb treatment clearly decreased the glomerular mRNA expression of podocin, nephrin, and podoplanin, but anti-podocalyxin antibody treatment did not..","14638910:1189",2,1,null,null,"positive"]
["CYBB -> IFIT1","Expression","Here, we found that NOX2 and reactive oxygen species are required for the host cell to trigger an efficient RIG-I-mediated IRF-3 activation and downstream antiviral IFNbeta and IFIT1 gene expression.","20532218:5",2,1,null,null,"positive"]
["CYBB -> PTGS2","Expression","Deficiency of gp91(phox) or suppression of p22(phox) expression decreased NADH oxidase activity and down-regulated COX-2 expression and PGE2 production stimulated by lipopolysaccharide.","15546960:6",2,1,"Mus musculus","Myocytes, Cardiac","positive"]
["DUSP1 -> BCL2","Expression","Importantly, we showed that knockdown of ERK2 or MKP-1 decreases the basal level of Bcl-2 expression, which may suggest the underlying mechanism of cisplatin resistance.","18089824:1084",2,1,null,null,"positive"]
["DUSP1 -> CD14","Expression","The expression level of c-fos, fosB and MKP-1 transcripts increased drastically, peaked within 1h, and that of the CD14 and CCL9 transcripts peaked from 12 to 24h.","18974019:2",2,1,null,null,"positive"]
["DUSP1 -> CD14","Expression","The expression level of c-fos, fosB and MKP-1 transcripts increased drastically, peaked within 1h, and that of the CD14 and CCL9 transcripts peaked from 12 to 24h.","18974019:2",2,1,null,null,"positive"]
["DUSP1 -> CEBPA","Expression","Whereas the induction of PPAR? and C/EBPa expression during adipocyte differentiation was markedly attenuated by depletion of MKP-1, that of C/EBPß expression was unaffected.","15269202:1203",2,1,null,"Adipocytes","positive"]
["DUSP1 -> TLR2","Expression","By using several inhibitors and activators, we found that TLR2 gene induction by glucocorticoids was mediated by the suppression of p38 mitogen-activated protein kinase activity following induction of MAPK phosphatase-1., Inhibition of MKP-1 attenuates dexamethasone-mediated inhibition of nontypeable Haemophilus influenzae-induced p38 phosphorylation and enhancement of TLR2 expression., G, MKP-1 knockdown using MKP-1-siRNA attenuated nontypeable Hemophilus influenzae-induced TLR2 expression at mRNA level and enhanced p38 activation in HeLa cells. <more data available...>","18704103:7, 12356755:1215, 16754688:1281, 12356755:216, 16754688:269",2,5,"Homo sapiens","Keratinocytes","positive"]
["FCGR3A -> CXCL10","Expression","As shown in Figure 5, lipopolysaccharide-activated CD16-mDCs were able to induce in Human umbilical vein endothelial cells the production of significant amounts of GM-CSF, G-CSF, and CXCL10 (IP-10), whereas CD1c-mDCs did not have the same effect.","17332250:1214, 17332250:215",2,2,"Homo sapiens","Endothelial Cells","positive"]
["FCGR3A -> NFATC1","Expression","These results provide the first direct evidence that both cyclosporin A-sensitive transcription factors, NFATp and NFATc, are expressed in human natural killer cells, and that their activation and/or expression can be regulated in primary cells by a single stimulus, that, in the case of CD16 in natural killer cells, results in early activation of NFATp and subsequently induced expression of NFATc mRNA.","7650486:10",2,1,"Homo sapiens","Killer Cells, Natural","positive"]
["FCGR3A -> TGFB1","Expression","Treatment of primary human NK cells with TGF-beta inhibited IFN-gamma production induced by CD16 activation with or without IL-12 or IL-2, and it did so without affecting the phosphorylation/activation of MAP kinases ERK and p38, as well as STAT4.","18768831:2",2,1,"Homo sapiens","Killer Cells, Natural","positive"]
["FGF9 -> SOX9","Expression","In addition, FGF-9 was shown to stimulate enhancer activity and Sox9 expression., Sox9 then up-regulates the expression of Fgf9, which is required for the maintenance of Sox9 expression., SOX9 up-regulates Fgf9, which initiates a Sox9/Fgf9 feed-forward loop that accelerates commitment to the male pathway.","12681949:7, 18216218:1368, 16700629:1322",2,3,null,null,"positive"]
["FGF9 -> TGFB1","Expression","Furthermore, FGF-2 and FGF-9 increased expression of other osteogenic factors BMP-2 and TGFbeta-1., These findings suggest that Fgf9 normally functions to repress Tgfbeta signaling in these cells.","15780951:6, 18653563:4",2,2,null,"Osteoblasts, myofibroblasts","positive"]
["FGF9 -> VEGFA","Expression","Furthermore, the expression levels of angiogenin, brain-derived neurotrophic factor (BDNF), FGF-4, FGF-9, IGFBP-2, IL-8, MIP-1beta, OPG, pulmonary and activation-regulated protein (PARC), TGF-beta2, TIMP-2 and VEGF were significantly associated with the presence of joint effusion; among these, nine cytokines (angiogenin, BDNF, FGF-4, FGF-9, IGFBP-2, MIP-1beta, PARC, TGF-beta2 and TIMP-2) were hitherto not described in Temporomandibular joint disorders., As expected, FGF9 treatment led to induction of Vegf-A, Vegf-B, and Vegf-C expression compared with the BSA control (Fig. 7A,B; Supplementary Fig. 4A,B,G,H). <more data available...>","17082335:6, 16778080:1243, 19097117:1929, 21089029:2324, 21337459:2324, 18079413:1204",2,6,null,null,"positive"]
["FLI1 -> CCL3","Expression","Activation of oncogenic transcription factors (MAFB, FLI1, and CRIP1) promotes overexpression of chemokines (CCL3, CCL5, and CXCL9) and chemokine receptor (CCR1).","16373702:1272",2,1,null,null,"positive"]
["FLI1 -> TGFBR2","Expression","Introduction of EWSR1-FLI1 into cells lacking the EWSR1-FLI1 fusion suppresses TGF-beta RII expression, whereas antisense to EWSR1-FLI1 in ES cell lines positive for this gene fusion restores TGF-beta RII expression., Regulation of the TGF-ß RII promoter by EWS-FLI1, FLI1, dnFLI1, EWS-ERG, ERG, dnERG, EWS-ETV1, ETV1, and dnETV1., The ERT (also called ESX/ESE-1) regulates the expression through the Z element (10) , whereas another ets family gene FLI1 fused with the EWSR1 gene down-regulates the Transforming growth factorßRII expression in Ewing sarcomas (11) .","10508522:7, 10749119:1136, 11719467:1050",2,3,null,null,"positive"]
["GFAP -> APOD","Expression","ApoD levels increased by 35% in the peri-infarct area after 10 and 30 days after pMCAO, mainly in neuron-specific nuclear protein (NeuN) positive neurons and glial fibrillary acidic protein (GFAP) positive astrocytes.","20083089:4",2,1,null,"Neurons","positive"]
["GFAP -> LGALS3","Expression","Measuring the mean Mac-2 fluorescence in pixels selected by their GFAP expression demonstrated that most of the Mac-2 increase after crush occurs within astrocytes: mean Mac-2 expression was approximately twofold higher in the crushed optic nerves and increased at higher segmentation values of GFAP (Fig. S1B).","21199938:1073",2,1,null,"Astrocytes","positive"]
["GFAP -> MET","Expression","Both Nf1(GFAP)CKO and wild-type astrocytes induced MET expression in neurites of wild-type hippocampal neurons in vitro, suggesting that astrocyte-derived signals may induce MET in Nf1 mutant mice.","17348023:5",2,1,null,"Astrocytes","positive"]
["GFAP -> VIM","Expression","As for GFAP, increased lesion-induced up-regulation of vimentin expression is also already apparent at 1 dpl, with knock-out animals showing higher expression than wild-type animals (Fig. 5b).","12843240:1209",2,1,null,"Astrocytes","positive"]
["GUSB -> PTGS2","Expression","K. pneumoniae produced ß-glucuronidase and lipopolysaccharide, which potently induced NO and COX-2 production in murine peritoneal macrophages.","21410316:9",2,1,"Mus musculus","Macrophages, Peritoneal","positive"]
["HBEGF -> BCL2L1","Expression","Recombinant HB-EGF induced the Bcl-2, Bcl-xL mRNA/protein expression in HET-1A and TTn cells.","20593979:6",2,1,"Homo sapiens","Keratinocytes","positive"]
["HBEGF -> CCND1","Expression","These results indicate that HB-EGF mediates the regulatory effects of both estradiol and progesterone on rat uterine epithelial cell proliferation through an effect on the production of G1 phase molecules such as cyclin D1., B, activation of cyclin D1 promoter by HB-EGF., C, Western blot analysis was done and showed that HB-EGF treatment increased expression of cyclin D1., HB-EGF expression is also reported to increase activation of cyclin D1 promoter as well as induction of vascular endothelial growth factor resulting in increased angiogenesis and enhanced tumorigenicity in mice (42). <more data available...>","9492026:5, 15289334:1179, 17909029:1204, 16424019:1329, 16000554:1073",2,5,null,"Epithelial Cells","positive"]
["HBEGF -> CSF1R","Expression","In the present study, we demonstrated that heparin binding epidermal growth factor-like growth factor (HB-EGF) induced the expression of c-fms and the scavenger receptor in normal human medial smooth muscle cells to the level observed in the intima.","8798698:2",2,1,null,"Myocytes, Smooth Muscle","positive"]
["HBEGF -> PLAT","Expression","HB-EGF enhanced the mRNA expression of tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) mRNA.","8609052:8",2,1,null,"Endothelial Cells","positive"]
["HBEGF -> PTGS2","Expression","It has been known that ERK5 activates the myocyte enhancer factor 2 family of transcription factor, we next tested whether activation of MEF2A contributes to HB-EGF-induced COX-2 expression., Furthermore, heparin-binding epidermal growth factor-like growth factor (HB- EGF), a p53 downstream target gene, induced Cox-2 expression, implying that Cox-2 is an ultimate effector in the p53-->HB-EGF-->Ras/Raf/MAPK-->Cox-2 pathway. p53-induced apoptosis was enhanced greatly in Cox-2 knock-out cells as compared with wild-type cells, suggesting that Cox-2 has an abrogating effect on p53-induced apoptosis. <more data available...>","21244855:10, 12411481:3, 12388195:1194, 12796363:1210",2,4,null,"Muscle Cells","positive"]
["HBEGF -> SOCS3","Expression","Knockdown of ErbB4 expression using small interfering RNA transfection impaired the HB-EGF-mediated decrease in SOCS1 and SOCS3 transcript levels, demonstrating that ErbB4 is required for HB-EGF-induced repression of SOCS1 and SOCS3 gene expression.","18653779:1285",2,1,null,null,"positive"]
["HBEGF -> VEGFA","Expression","HB-EGF increased VEGF production., In addition, RT-PCR analysis demonstrated that VEGF165 mRNA levels were increased in vascular smooth muscle cells 4-10-fold by 0.35-2 nM of HB-EGF, respectively., The reduction of HB-EGF expression attenuated the chemotactic invasive ability and the expression of matrix metalloprotease -2 and vascular endothelial growth factor (VEGF), leading to the inhibition of cell invasion and angiogenesis., We also found that soluble form HB-EGF induced vascular endothelial growth factor (VEGF) expression, implicating an autocrine loop that may play a role in regulating these growth factors. <more data available...>","19559571:10, 9563510:5, 18852147:4, 15289334:1078, 17460286:1184, 20110534:1163",2,6,null,"Epithelial Cells, Endothelial Cells","positive"]
["HSPB1 -> DUSP1","Expression","Moreover, phosphorylated heat shock protein 27 up-regulated the levels of p38 mitogen-activated protein kinase and mitogen-activated protein kinase phosphatase-1, an inhibitory protein of extracellular signal-regulated kinase., Interaction between heat shock protein25 or HSP70i and MKP1 Dephosphorylated ERK1/2-Because heat shock increased expressions of the phosphorylated form of MKP1, which was found to be associated with ERK1/2 and JNK1/2 inactivation (22), we determined MKP1 phosphorylation in heat shock protein25- or heat shock protein70i-overexpressed cells.","18477563:4, 16624816:1187",2,2,null,null,"positive"]
["ID1 -> ANGPT1","Expression","In the present study, Id1 gene transfer upregulated the expression of angiopoietin-1 but not Ang2 in human umbilical vein ECs.","16267257:1298",2,1,"Homo sapiens",null,"positive"]
["ID1 -> CCND1","Expression","In summary, Id1 may contribute to early breast cancer by promoting excessive proliferation through cyclin D1., The glycogen synthase kinase-3beta phosphorylation at Ser9, stabilization and nuclear localization of beta-catenin, T-cell factor (TCF)/lymphoid enhancer factor transactivation activity and cyclin D1 expression were enhanced by Inhibitor of differentiation-1., Blockage of the nuclear factor-kappaB activity with pyrrolidine dithiocarbamate or enhancement of the nuclear factor-kappaB activity with p65 (a subunit of nuclear factor-kappaB) in OC1 significantly inhibited or increased, respectively, the cell proliferation and transcription of cyclin D1 induced by Id1. <more data available...>","18413773:6, 19079342:5, 17149750:5, 15489884:1043",2,4,"Mus musculus","Epithelial Cells","positive"]
["ID1 -> CSF1","Expression","We found that SCF, M-CSF, osteopontin, fibroblast growth fadctor-1, transforming growth factor-a, and SDF-1 mRNA expression were decreased in Id1-/- stromal cells relative to Id1+/+ stromal cells.","19478045:1223",2,1,null,"Fibroblasts","positive"]
["ID1 -> VEGFA","Expression","Inhibitor of DNA binding 1 has been implicated in tumor angiogenesis by regulating the expression of vascular endothelial growth factor (VEGF), but its molecular mechanism has not been fully understood., Our recent unpublished data indicate that Id1 contributes to angiogenesis by regulating the expression of angiogenic factors such as vascular endothelial growth factor, interleukin-8, and cyclooxygenase-2., Id1 promotes invasion by production of a 120-kDa gelatinase, mediates tumor angiogenesis by production of vascular endothelial growth factor, facilitates hormone-independent growth, and is involved in the resistance of cancer cells against cytotoxic drugs (19, 26, 27).","17426247:0, 20028744:1326, 18381431:1079",2,3,null,"Keratinocytes","positive"]
["IFIT1 -> IFI27","Expression","Thirteen genes were selectively induced by mitogen-activated protein kinase kinase7-JNK1ß relative to mitogen-activated protein kinase kinase7-JNK1a and included GARG16, GARG49, IGTP, GTPI, interferon-induced 15-kDa protein (ISG15) and a-interferon-inducible protein (ISG12), genes known to be interferon-responsive as well as two genes that are components of the ubiquitin pathway (Table II).","12354774:1169",2,1,null,"Fibroblasts","positive"]
["IFIT2 -> IFIT1","Expression","ISG56 mRNA was induced much more strongly than ISG54 mRNA when the inducer was double-stranded RNA (Fig. 2A).","16973618:1149",2,1,null,null,"positive"]
["IFIT3 -> IFI27","Expression","Thirteen genes were selectively induced by mitogen-activated protein kinase kinase7-JNK1ß relative to mitogen-activated protein kinase kinase7-JNK1a and included GARG16, GARG49, IGTP, GTPI, interferon-induced 15-kDa protein (ISG15) and a-interferon-inducible protein (ISG12), genes known to be interferon-responsive as well as two genes that are components of the ubiquitin pathway (Table II).","12354774:1169",2,1,null,"Fibroblasts","positive"]
["INHBA -> BCL2","Expression","Activin A induced the expression of Bcl-2, and ablation of Bcl-2 by small interfering RNA abrogated its protective action in myocytes., Activin A resulted in a significant time-dependent decrease in Bcl-2 mRNA levels and increase in caspase-3 mRNA levels in SNU-16 cells.","19805648:7, 19148527:4",2,2,null,"Muscle Cells","positive"]
["INHBA -> BCL2L1","Expression","Correlation between Bcl-X expression and B-cell hybridoma apoptosis induced by activin A.","9754721:100, 12456957:1636, 15977175:1669",2,3,null,"B-Lymphocytes","positive"]
["INHBA -> CD80","Expression","Activin A also enhanced CD80 expression, which is a marker of activated macrophages, but did not influence RAW264.7 cell proliferation.","19403063:5",2,1,null,"Macrophages","positive"]
["INHBA -> CSF1","Expression","The contribution of activin A to M1 (GM-CSF) macrophage polarization was evidenced by the capacity of a blocking anti-activin A antibody to reduce M1 (GM-CSF) polarization markers expression while enhancing FRß and other M2 (M-CSF) markers mRNA levels.","21389328:2",2,1,null,"Macrophages","positive"]
["INHBA -> MCL1","Expression","Interestingly, erythropoietin prevented activin A-induced apoptosis with continuous expression of Mcl-1 and caused KU812 cells to undergo erythroid differentiation., Likewise, it has been shown that activin A induces expression of MCL-1 in K562 cells and KU812 cells,19 and both IL-3 and GM-CSF reportedly up-regulate expression of Mcl-1 in Ba/F3 cells and TF-1 cells.50-53 Whether such additional factors can also regulate expression of MCL-1 in primary chronic myeloid leukemia cells in vivo remains at present unknown.","11314004:6, 15626746:1270",2,2,null,null,"positive"]
["INHBA -> SMAD7","Expression","Recombinant TGF-beta1 and activin A increased the expression of inhibitory SMAD7, whereas they reduced c-MYC., Activin A rapidly and transiently increased Smad7 messenger RNA levels of rat anterior pituitary , clonal gonadotrope (alpha T 3-1 and L beta T2), and corticotrope (AtT20) cells with an EC(50) of 0.1-0.2 nM., Activin A and human bone morphogenetic protein-2 induce Smad6 and Smad7 mRNA in HS-72 cells., On the other hand, similar to rat anterior pituitary cells cells (54), activin A rapidly induced Smad7 mRNA levels in this cell line (Fig. 8B). <more data available...>","16837618:5, 11181520:4, 10224135:1098, 12538636:1212, 17405825:1242, 12417591:1242",2,6,"Rattus norvegicus, Homo sapiens","Gonadotrophs, Myocytes, Smooth Muscle","positive"]
["INHBA -> SOCS3","Expression","Our main findings were: (i) activin A treatment reduced the LIF-mediated increase in cardiomyocyte length, perimeter and sarcomeric organization and was accompanied by a substantially decreased alpha-skeletal actin gene expression. (ii) The activin A-mediated phosphorylation of Smad2 was markedly enhanced by LIF. (iii) Activin A markedly induced SOCS3 gene expression, while LIF potently increased the expression of Smad7 mRNA, representing inhibitors of LIF and activin A signaling pathways, respectively. (iv) Inhibiting activation of the Smad2/3 pathway abolished the effects of activin A on LIF-induced changes in cell length, perimeter and sarcomeric organization.","16926021:4",2,1,null,"Myocytes, Cardiac","positive"]
["INHBA -> TF","Expression","Activin-A stimulated both basal and FSH-stimulated inhibin and transferrin production by Sertoli cells after 72 h of culture.","8033824:6",2,1,null,"Sertoli Cells","positive"]
["INHBA -> TGFB1","Expression","Incubation with activin A significantly stimulated TGF-beta1, PAI-1 and connective tissue growth factor RNA expression and increased production of extracellular matrix proteins in mesangial cells., In hepatocytes, activin A enhanced the expression of collagen and TGF-beta(1), promoted matrix metalloproteinase activity, induced mitochondrial beta-oxidation, downregulated fatty acid synthase activity, promoted decreased weight percentage of saturated FAs, and altered the composition of polyunsaturated FAs., Furthermore, activin A increased the mRNA levels of transforming growth factor-ß1 and MCP-1 after both 6 and 24 hours of stimulation (Figure 4C and 4D). <more data available...>","15673690:5, 19532130:8, 14993131:1155, 18234825:1414, 15001548:1217, 17406031:1106",2,6,"Homo sapiens","Mesangial Cells, Hepatocytes, Myocytes, Cardiac, Embryonic Stem Cells, Hepatic Stellate Cells","positive"]
["INHBA -> VEGFA","Expression","These results indicate that an autocrine factor activin A amplifies the effect of VEGF by up-regulating VEGF and its receptors., Activin A stimulated vascular endothelial growth factor gene transcription through Sp1-dependent induction of vascular endothelial growth factor promoter activity., Administration of recombinant activin A in mice increased the area of neovascularization, VEGF expression, and the kinase activities of p38 and p42/44 MAPKs after mechanical debridement., In addition, Activin A, a member of the TGF-ß family, and its receptors are expressed in hepatocellular carcinoma and have been shown to stimulate vascular endothelial growth factor transcription, DNA binding, and the transactivation potential of specificity protein 1 [142 ].","15117880:10, 15188178:6, 15039217:3, 16946019:1364",2,4,"Bos taurus","Endothelial Cells, Epithelial Cells, Hepatocytes","positive"]
["ISG15 -> IFI27","Expression","Thirteen genes were selectively induced by mitogen-activated protein kinase kinase7-JNK1ß relative to mitogen-activated protein kinase kinase7-JNK1a and included GARG16, GARG49, IGTP, GTPI, interferon-induced 15-kDa protein (ISG15) and a-interferon-inducible protein (ISG12), genes known to be interferon-responsive as well as two genes that are components of the ubiquitin pathway (Table II).","12354774:1169",2,1,null,"Fibroblasts","positive"]
["ITGAX -> CD80","Expression","We found that the expression level of co-stimulatory molecules, CD40, CD54, CD80, CD86 and CD11b, were elevated evidently, except CD11c, I-A(d) and H-2K(d).","20499643:4",2,1,null,null,"positive"]
["ITGAX -> CD86","Expression","We found that the expression level of co-stimulatory molecules, CD40, CD54, CD80, CD86 and CD11b, were elevated evidently, except CD11c, I-A(d) and H-2K(d)., As reported previously (24), bone marrow-derived macrophage-derived dendritic cells expressed high levels of CD11c, CD86, and I-Ab, and LPS up-regulated the expression of CD86 and I-Ab.","20499643:4, 19336404:1169, 19336404:170",2,3,null,"Macrophages","positive"]
["ITGB2 -> CCL3","Expression","Blockade of depletion of IkappaB-alpha by proteasome inhibitors (proteasome inhibitor I or acetyl-leucinyl-leucinyl-norleucinal) led to concomitant inhibition of nuclear factor-kappaB DNA-binding activity and expression of MIP-1alpha and MIP-1beta messenger RNA induced by beta(2) integrin ligation., It has previously been shown that recognition of ß2-integrin/ICAM-1 on fibroblast-like synoviocytes induced MIP-1a expression in synovial fluid polymorphonuclear neutrophils [38] ., As mentioned above, cell-to-cell contact enhances these chemoattractive processes; for example, the interaction of rheumatoid arthritis synovial fibroblasts and leucocytes via ß2 integrin/vascular cell adhesion molecule -1 resulted in an upregulation of macrophage inflammatory protein-1a synthesis in polymorphonuclear neutrophils and monocytes from rheumatoid arthritis synovial fluid [12] .","11342414:6, 17875202:1287, 18177509:1122",2,3,"Homo sapiens","Monocytes, Fibroblasts, Leukocytes","positive"]
["ITGB2 -> CD80","Expression","CD80 expression increased in infected cells but expression of l-selectin and beta2 integrin was unaltered.","19703127:4",2,1,"Homo sapiens","Monocytes","positive"]
["ITGB2 -> TLR2","Expression","The anti-CD18 monoclonal antibody markedly reduced TLR2 expression in endothelial cells as induced by polymorphonuclear neutrophils.","14561708:1314",2,1,null,"Endothelial Cells","positive"]
["LCN2 -> GFAP","Expression","LCN2 protein induced upregulation of glial fibrillary acidic protein (GFAP), cell migration, and morphological changes similar to characteristic phenotypic changes termed reactive astrocytosis., Third, the LCN2-induced GFAP expression was blocked by a nitric oxide synthase inhibitor NG-monomethyl-L-arginine (Fig. 8F,G)., Because LCN2 also induced GFAP expression in astrocytes in our study (Fig. 6), we next attempted to determine whether NO is involved in the LCN2 actions in astrocytes., Rho/ROCK pathway appeared to play a pivotal role in regard to LCN2 actions on astrocyte morphology, based on the following results: (1) a ROCK inhibitor, Y27632, partly blocked LCN2-induced morphological changes (Fig. 9A,B); (2) Y27632 also inhibited the LCN2-induced GFAP expression (Fig. 9C,D); and (3) LCN2 induced Rho activation in astrocytes (Fig. 9E). <more data available...>","19129400:7, 19129400:366, 19129400:358, 19129400:384, 19129400:439",2,5,null,"Astrocytes","positive"]
["LGALS1 -> CD80","Expression","Compared with eGFP-Dendritic cells, galectin-1-Dendritic cells had enhanced levels of IAd, H2Kd, CD40, CD54, CD80, and CD86 expression (Fig. 4A).","16751364:1259",2,1,null,"Dendritic Cells","positive"]
["LGALS1 -> CD83","Expression","Furthermore, galectin-1 induced both CD83 and CD86 expression in a dose-dependent manner (Fig. 1D).","16785517:1209",2,1,null,"Monocytes","positive"]
["LGALS1 -> CD86","Expression","Furthermore, galectin-1 induced both CD83 and CD86 expression in a dose-dependent manner (Fig. 1D)., Compared with eGFP-Dendritic cells, galectin-1-Dendritic cells had enhanced levels of IAd, H2Kd, CD40, CD54, CD80, and CD86 expression (Fig. 4A)., Incubation of nontransduced Dendritic cells for 18 h with medium supplemented with 10 µM soluble human Galectin-1 induced an increase of IAd and CD86 expression similar to that triggered by recombinant adenovirus-Galectin-1 infection at a MOI of 50 (Fig. 4B).","16785517:1209, 16751364:1259, 16751364:260, 16751364:264",2,4,null,"Monocytes, Dendritic Cells","positive"]
["LGALS1 -> GFAP","Expression","Expression of GFAP was increased 50-fold following the addition of galectin-1 (Figure 2F).","14693917:1096",2,1,null,"Astrocytes","positive"]
["LGALS1 -> TGFB1","Expression","We demonstrate here that Recombinant galectin-1 treatment induces the production of substantial amounts of TGF-ß1 and IL-10, which in turn may be responsible for counterregulating the uveitogenic Th1 response.","16670344:282",2,1,null,"T-Lymphocytes","positive"]
["LGALS3 -> CCND1","Expression","Recombinant galectin-3 induced cardiac fibroblast proliferation, collagen production, and cyclin D1 expression., Interestingly, galectin-3 induces cyclin D1 expression (an early G1 cyclin) and its associated kinase activity in the absence of cell anchorage., We found that galectin-3 induces cyclin D(1) promoter activity in human breast epithelial cells independent of cell adhesion through multiple cis-elements, including the SP1 and CRE sites., Finally, we demonstrated that silencing of galectin-3 enhanced apoptosis induction with chemotherapeutic agents by further reducing the expression of anti-apoptotic and/or cell survival molecules such as survivin, cyclin D1, and XIAP, and increasing the expression of pro-apoptotic XAF-1. <more data available...>","15520318:6, 10463621:6, 12439750:3, 19843071:10, 11062152:1131, 11724777:1182, 17047062:1062, 19190323:1248, 17403142:1279, 11062152:1156 <more data available...>",2,13,"Rattus norvegicus, Homo sapiens","Fibroblasts, Epithelial Cells","positive"]
["LGALS3 -> TGFB1","Expression","Thus disruption of the Galectin-3gene blocks fibrosis despite similar expression levels of TGF-ß., Gal-3 increased transforming growth factor-ß1, -ß2, and -ß3 expression in left ventricle compared with vehicle group; Ac-SDKP inhibited this effect.","16549783:1133, 19098114:1203, 16549783:134",2,3,null,"Macrophages","positive"]
["LST1 -> CD80","Expression","Besides activating receptors expressed on their endogenous state, such as NKp46, NKp30, NKG2-D, MHC-I-specific CD94/NKG2-C, and triggering counterparts of killer inhibitory receptors (1, 2, 3), activation of human NK cells induces the de novo expression of other triggering receptors, such as CD69, NKp44, CD40 ligand, and CD80/CD86 counterstructures, which endow activated NK cells with new recognition capability (3, 4, 5, 6, 7).","12077230:1039",2,1,"Homo sapiens","Killer Cells, Natural","positive"]
["LST1 -> CD86","Expression","Besides activating receptors expressed on their endogenous state, such as NKp46, NKp30, NKG2-D, MHC-I-specific CD94/NKG2-C, and triggering counterparts of killer inhibitory receptors (1, 2, 3), activation of human NK cells induces the de novo expression of other triggering receptors, such as CD69, NKp44, CD40 ligand, and CD80/CD86 counterstructures, which endow activated NK cells with new recognition capability (3, 4, 5, 6, 7).","12077230:1039",2,1,"Homo sapiens","Killer Cells, Natural","positive"]
["MAFB -> CCL3","Expression","Activation of oncogenic transcription factors (MAFB, FLI1, and CRIP1) promotes overexpression of chemokines (CCL3, CCL5, and CXCL9) and chemokine receptor (CCR1).","16373702:1272",2,1,null,null,"positive"]
["MAFB -> HBEGF","Expression","Likewise, MafB efficiently induced HB-EGF transcription.","16247450:1238",2,1,null,null,"positive"]
["MET -> CCND1","Expression","CCND1 is induced in human c-Met/ß-catenin tumors., Thus, HGF/c-Met may mediate the upregulation of HNF4a, Cyclin D1, and Survivin in CD133+CD45- OCs., For instance, whereas activation of ErbB2 induces formation of abnormal noninvasive structures consisting of individual units, overexpression of CSF-1R induces large filled structures, overexpression of the HGF-MET induces development of abnormal, invasive structures, and overexpression of cyclin D1 and Akt results in formation of large acini (23).","19118011:1121, 17585168:1463, 16707444:1248",2,3,null,"oval cells","positive"]
["MET -> HBEGF","Expression","Additional data show that HGF-driven MET activation can lead to increased EGFR phosphorylation as a result of enhanced transforming growth factor-a and heparin-binding EGF-like growth factor expression, suggesting that the cross talk between the two receptors can occur in both directions (54).","18829470:1128",2,1,null,null,"positive"]
["MET -> NR3C1","Expression","RU486 + MET before restraint stress and acoustic trauma caused an immediate increase in glucocorticoid receptor mRNA followed by increased glucocorticoid receptor protein expression (24 h after trauma).","16777974:4",2,1,null,null,"positive"]
["MET -> PTGS2","Expression","Our data suggest that the increased expression of Met protein in Thyroid papillary carcinoma cells has a role in up-regulating the expression of COX-2, which in turn contributes to the invasive capacity of Thyroid papillary carcinoma cells., These data suggest that c-Met signaling can both stabilize already transcribed COX-2 mRNA and activate COX-2 gene transcription., The expression of COX2 was down-regulated by miR-15b, miR-16, and miR-20b, and c-MET was down-regulated by all three of these MicroRNAs plus miR-20a. <more data available...>","19391129:10, 17550984:1243, 17205120:1238, 19359592:1073, 12393863:1277, 10593866:1228, 16230363:1123, 16204019:1140",2,8,"Rattus norvegicus","Macrophages","positive"]
["MET -> VEGFA","Expression","The angiogenic properties of the c-Met/HGF axis are well known (3) and can result in a critical angiogenic switch by Shc for VEGF production (15)., The presence of NRP1 and Phosphorylated c-MET in the protein complex exhibited a similar time course following VEGF165 stimulation, with the peak at 30 min (Figure 5b, low)., HGF/c-Met signaling increases vascular endothelial growth factor levels in tumor and VEGFR2 on endothelial cells (36, 37)., Blocking HGF or inhibiting c-Met would abrogate the effect of IL-6 on HGF expression and in turn prevent the induction of VEGF, IL-8, and GRO-1. <more data available...>","17440059:1169, 20085644:1217, 19318488:1077, 17545511:1052, 19318576:1343, 15221009:1095, 14613995:1068, 17942923:1247, 18779539:1202",2,9,null,"Endothelial Cells","positive"]
["NCF1 -> ALOX5AP","Expression","Similarly, transfection of transformed human brain endothelial cell with siRNA for p47phox, a subunit of NADPH-oxidase, completely antagonized hypoxia-induced FLAP mRNA expression (Fig. 2B, lane 4).","20194722:1164",2,1,"Homo sapiens","Endothelial Cells","positive"]
["NCF1 -> TLR2","Expression","Small inhibitory RNA to p47Phox in THP-1 cells abrogated high-glucose-induced TLR2 and TLR4 expression., Our data show that NADPH oxidase and Toll-like receptor signaling are significantly upregulated in the vascular tissue of diet-induced obesity mice, and deletion of the NADPH oxidase p47phox abolishes both TLR2 and TLR4 expression in vascular tissue.","18650365:10, 18779779:1174",2,2,null,null,"positive"]
["NFATC1 -> CCND1","Expression","Heit et al. showed that transgenic activation of NFATc1 in ß-cells induces proliferation by inducing Cyclin D and Cdk4 levels [23].","20689817:1266",2,1,null,"Insulin-Secreting Cells","positive"]
["NFATC1 -> ID3","Expression","Accordingly, we propose a model whereby early growth response1-NF-ATc1 cooperatively induces inhibitor of DNA binding 3 expression, which in turn promotes traversal of the ß-selection checkpoint by suppressing the activity of E proteins (54, 56, 68).","17878368:1298",2,1,null,"thymocytes","positive"]
["NFATC1 -> PDPN","Expression","In vitro, endogenous and VEGF-A-induced VEGFR-3 and podoplanin expression by human microvascular endothelial cells was reduced by siRNA to NFATc1, to levels comparable to reductions seen with siRNA to Prox-1.","19233265:8",2,1,"Homo sapiens","Endothelial Cells","positive"]
["NFATC1 -> PTGS2","Expression","Interestingly, COX-2 promoter activity was similarly enhanced by NFATc cotransfection (Fig. 4A).","10816557:168",2,1,null,"T-Lymphocytes","positive"]
["NFATC1 -> TGFB1","Expression","In Jurkat T cells, the TGF-beta1 promoter was activated by calcineurin and NFATc and inhibited by Cyclosporin A and FK506.","15716327:3",2,1,null,"T-Lymphocytes","positive"]
["NR3C1 -> CEBPA","Expression","These data support a role for glucocorticoid receptor-inducible C/EBPalpha and C/EBPbeta expression in the transactivation of hepatic SULT2A-40/41 expression., The glucocorticoid signaling pathway that leads to a G1 cell cycle arrest is complex because the ligand-bound glucocorticoid receptor must induce the expression of C/EBPa and then physically associate with this transcription factor.","15502011:6, 9872941:1232",2,2,null,null,"positive"]
["NR3C1 -> CP","Expression","We found ceruloplasmin that was strongly induced by Lipopolysaccharide (neuroprotection) and completely inhibited by the Glucocorticoid receptor blockade (a neurotoxic condition).","17375196:1182",2,1,null,"Neurons","positive"]
["NR3C1 -> PDPN","Expression","The levels of T1alpha mRNA were reduced from 0.4 ± 0.05 arbitrary units in wild-type fetal mice to 0.23 ± 0.07 arbitrary units in glucocorticoid receptor-null fetal mice, a reduction of ~ 50%.","14578211:1174",2,1,"Mus musculus",null,"positive"]
["NR3C1 -> PTGS2","Expression","The induction of the COX-2 promoter activity and the phosphorylation of CREB-1 were also blocked by the glucocorticoid receptor antagonist RU486., dexamethasone-mediated suppression of COX-2 expression is modulated by glucocorticoid receptor, which will explain the distinct effect of dexamethasone on COX-2 expression between macrophages and endothelial cells (16)., Moreover, lipopolysaccharide down-regulates PPAR? mRNA but up-regulates glucocorticoid receptor mRNA, although PPAR? and glucocorticoid receptor suppressed COX-2 promoter activity by interfering with the NF-?B signaling pathway (13) (Fig. 5). <more data available...>","19797430:64, 10827178:109, 10827178:183, 19797430:103, 19797430:201",2,5,"Bos taurus, Homo sapiens","Fibroblasts, Macrophages, Endothelial Cells","positive"]
["NR3C1 -> TGFBR2","Expression","We found that expressions of TbetaRII and RhoB were up-regulated by ligand-bound glucocorticoid receptor at mRNA and protein levels., The up-regulation of TbetaRII expression by dexamethasone was mediated by glucocorticoid receptor and occurred at the transcriptional level.","19278840:5, 16887915:3",2,2,null,null,"positive"]
["OSMR -> CEBPB","Expression","As observed with RANKL, mouse OSM effects on Cebpd, Cebpb, and Pparg mRNA levels were ablated in the absence of OSMR (Figure 5, E-G).","20051625:1183",2,1,null,"Osteoblasts","positive"]
["OSMR -> CEBPD","Expression","As observed with RANKL, mouse OSM effects on Cebpd, Cebpb, and Pparg mRNA levels were ablated in the absence of OSMR (Figure 5, E-G).","20051625:1183",2,1,null,"Osteoblasts","positive"]
["P2RX7 -> CASP1","Expression","We recently reported that P2X7 receptor (P2X7R)-induced activation of caspase-1 inflammasomes is accompanied by release of MHC class II protein into extracellular compartments during brief stimulation of murine macrophages with ATP., Furthermore, the production of IL-18 and IL-1beta and caspase-1 activation were induced independently of a P2X7 purinergic receptor, and the inability of Delta\"region of difference 1\" in caspase-1 activation was compensated for by nigericin, an agent inducing the potassium ion efflux.","19342685:0, 19596775:7",2,2,"Mus musculus","Macrophages","positive"]
["P2RX7 -> CCL3","Expression","In vitro study indicated that treatment with ATP and BzATP (an agonist for ATP ionotropic receptor P2X(7) R) caused an increase in the intracellular levels of microglial MIP-1a and MCP-1.","21162127:5",2,1,null,"Macrophages","positive"]
["P2RX7 -> PTGS2","Expression","These observations are noteworthy, given that the promoter region of many P2RX7-modulated proinflammatory genes, such as IL-1ß, TNF-a, iNOS, IL-6, and COX-2 contain consensus sites for CREB binding., Our data clearly suggest that P2X7 purinergic receptor antagonists can block the lipopolysaccharide-induced expression of Group V secretory phospholipase A2s and COX-2, which leads to inhibited arachidonic acid metabolism., It is noteworthy that our studies in human monocytes are the first to indicate that stimulation of the P2X7 receptor by concentrations of BzATP in the low micromolar range (100 µM) can promote an increase in the expression of the enzyme COX-2. <more data available...>","18625910:1255, 10593984:1161, 12101284:1287, 17475804:1328",2,4,"Homo sapiens","Monocytes, Macrophages, Microglia","positive"]
["P2RX7 -> TGFB1","Expression","In conclusion, activation of P2X(7) receptors enhanced TGF-beta 1 mRNA expression and the effect involved protein kinase C/MAPK signalling pathway in RBA-2 type-2 astrocytes., The P2X(7) inhibitor oxidized adenosine triphosphate attenuated the extracellular matrix and TGF-beta up-regulation induced by adenosine triphosphate and, to a lesser extent, that caused by high glucose., Activation of P2X7 purinoceptor-stimulated TGF-beta 1 mRNA expression involves PKC/MAPK signalling pathway in a rat brain-derived type-2 astrocyte cell line, RBA-2. <more data available...>","14575868:9, 15698427:7, 16969386:1316, 19052563:1324",2,4,"Rattus norvegicus","Astrocytes","positive"]
["P2RY6 -> TGFB1","Expression","Furthermore, a P2Y6 receptor antagonist MRS2578 suppressed the stress-induced expression of periostin and transforming growth factor-ß messenger ribonucleic acids in vitro and in vivo.","19008857:1266",2,1,null,"Fibroblasts","positive"]
["P2RY6 -> TGFB2","Expression","We also demonstrated that p115-RGS and the P2Y6 receptor antagonist inhibit the expression of transforming growth factor-ß2 messenger ribonucleic acid by pressure overload (Figure 2 and Figure 6).","19008857:1249",2,1,null,null,"positive"]
["PLAT -> CCND1","Expression","Ectopic overexpression of an uninhibitable GSK3ß mutant eliminated tPA-induced cyclin D1 expression., Gel shift experiments revealed the activation of beta-catenin/T-cell-specific transcription factor /lymphoid enhancer factor-1 (Lef) transcriptional complex, evidenced by an increased binding of nuclear extracts to oligonucleotides containing the cyclin D1 Lef/transcription factor site. beta-Catenin silencing through small interfering RNA and antisense oligonucleotides inhibited both the tPA-mediated cyclin D1 expression and cell proliferation. <more data available...>","20724593:6, 15695395:3, 20724593:4",2,3,null,"Fibroblasts, T-Lymphocytes","positive"]
["PPARD -> ABCA1","Expression","Unexpectedly, PPARdelta activation led to enhanced fecal neutral sterol loss in both groups without any changes in intestinal Abca1, Abcg5, Abcg8, and 3-hydroxy-3-methylglutaryl-coenzyme A reductase expression., In FHS74 human intestinal cells (26), the PPARdelta agonist produced a 2.1-fold increase in ABCA1 expression., Nevertheless, PPARd activators appear to induce ABCA1 expression and cholesterol efflux moderately, and they can increase HDL levels in an obese-monkey model (17)., The peroxisome proliferator-activated receptord ligand GW501516 was reported to increase expression of ABCA1 and induce apoAI-specific cholesterol efflux from human THP-1 cells. <more data available...>","15604518:5, 11309497:1148, 12370265:1076, 18337495:1198, 16825673:1158, 12704191:1140, 18182682:1256, 12547832:1278, 12006382:1136, 11557774:1275 <more data available...>",2,14,"Homo sapiens","Macrophages, Keratinocytes, Monocytes","positive"]
["PPARD -> BCL2L1","Expression","Importantly, the activation of PPARbeta/delta induces Akt phosphorylation correlated with up-regulation of PDK1, down-regulation of PTEN, and increased expression of Bcl-xL and COX-2.","18566335:6",2,1,null,null,"positive"]
["PPARD -> CAT","Expression","Activation of PPAR-delta upregulated the expression of antioxidant genes superoxide dismutase 1, catalase, and thioredoxin and decreased reactive oxygen species production in ECs., Indeed, Peroxisome proliferator-activated receptord activation led to inhibition of H2O2-induced apoptosis and upregulated the expression of the antioxidative enzyme catalase., Also, the PPARß/d isoform has been shown to protect cardiac myocytes from oxidative stress-induced apoptosis by activating expression of catalase, which scavenges hydrogen peroxide [53].","18048767:4, 16337160:1069, 17010956:1129",2,3,"Homo sapiens","Endothelial Cells, Myocytes, Cardiac","positive"]
["PPARD -> HBEGF","Expression","On the protein level, HB-EGF expression was increased on activation of PPARd (Figure 5c, left) and decreased after lentivirus-mediated knockdown of PPARd in primary keratinocytes (Figure 5c, right)., We also showed that activation of PPARd enhances proliferation of epidermal keratinocytes and that it induces transcription of heparin-binding epidermal growth factor-like growth factor, which in turn induces epidermal hyperplasia in vivo (Zheng et al., 2003; Kimura et al., 2005; Shirakata et al., 2005), suggesting that activation of PPARd contributes to the hyperproliferative phenotype in psoriasis, at least in part, by inducing heparin-binding epidermal growth factor-like growth factor expression.","17637826:1168, 18305567:1038",2,2,null,"Keratinocytes","positive"]
["PPARD -> PTGS2","Expression","Activation of PPARdelta resulted in increased COX-2 mRNA and protein expression., Thus, PPARdelta induces COX-2 expression and the cyclooxygenase-2-derived PGE(2) further activates PPARdelta via cPLA(2)alpha., Importantly, the activation of PPARbeta/delta induces Akt phosphorylation correlated with up-regulation of PDK1, down-regulation of PTEN, and increased expression of Bcl-xL and COX-2., Taken together, these observations reveal that PPARdelta induces COX-2 expression in human cholangiocarcinoma cells and that the COX-2-derived prostaglandin E2 further activates PPARdelta through phosphorylation of cPLA2alpha. <more data available...>","12901877:4, 17178883:7, 18566335:6, 16966336:9, 17693664:1, 19483106:1426, 17965409:1209, 12740443:1048, 12901877:11, 16966336:157 <more data available...>",2,19,null,"Macrophages, Peritoneal, Hepatocytes","positive"]
["PPARD -> SERPINA3","Expression","Depletion of the PPARdelta receptor, but not of PPARalpha or gamma, attenuated the suppressive effect of GW501516 on interleukin-6-induced alpha1-antichymotrypsin mRNA expression, indicating that PPARdelta specifically mediated this effect.","17461989:5",2,1,null,"Hepatocytes","positive"]
["PPARD -> UCP2","Expression","PPAR(delta) also activates the heat-producing uncoupling enzymes in brown adipose tissue (UCP1 and 3) and muscle (UCP2)., A specific agonist of peroxisome proliferator-activated receptor beta (L165041) increased UCP-2 mRNA levels in myotubes, whereas activation of PPARalpha or PPARgamma was ineffective., The addition of a PPAR-ß agonist (L165,041) for the final 24 hours of 1% treatment resulted in increased levels of UCP-2 mRNA and protein whereas Rosiglitazone induced SIRT1, PGC-1a, RXR-a, PPAR-a, CPT-1b, and UCP-2 mRNA and SIRT1 protein. <more data available...>","14677574:4, 11278377:8, 21113404:5, 20040361:3, 16467150:1179, 12600885:1131, 12118038:1274, 19465504:1197",2,8,null,"Muscle Fibers, Skeletal, Myoblasts, Insulin-Secreting Cells, Macrophages, Myocytes, Cardiac","positive"]
["PPARD -> VEGFA","Expression","Increased expression of vascular endothelial growth factor in colon tumors vs normal colon was suppressed by loss of PPAR-delta expression., Activation of both Peroxisome-proliferator-activated receptor? and Peroxisome-proliferator-activated receptorß/d induced expression of VEGF mRNA and protein in a Peroxisome-proliferator-activated receptor-dependent way., Contradictory findings are also reported suggesting that PPARbeta/delta ligands potentiate tumorigenesis by increasing cell proliferation, by inhibiting apoptosis through phosphorylation of Akt and by increasing cyclooxygenase-2 (COX2) and vascular endothelial growth factor (VEGF) expression. <more data available...>","19436036:6, 20221637:3, 17693664:1, 15930337:1264, 17148604:1141, 18492772:1234, 19741045:1201, 18599600:1168, 17965409:1209",2,9,"Homo sapiens","Endothelial Cells, Epithelial Cells, Keratinocytes","positive"]
["PRL -> A2M","Expression","Hysterectomy of day 10 pregnant rats combined with hormone replacement determined that alpha 2M mRNA levels are regulated primarily by PRL through day 12 and by placental lactogens during midgestation (days 12-15)., In addition, the orphan receptor response element and PRL response element act independently of, rather than synergistically with, each other to regulate basal and PRL-induced expression of alpha2M in ovarian luteal cells., In summary, results of this study reveal that constitutive expression of SOCS-1 can prevent PRL signaling and that the lack of PRL-induced expression of alpha2-macroglobulin in a defined decidual cell population is largely due to SOCS-1 expression in these cells. <more data available...>","2479532:7, 9731707:14, 10770492:12, 16959875:1221, 16123161:1296, 11181541:1290, 10598581:1064, 9661641:1264",2,8,null,"Luteal Cells, decidual cells","positive"]
["PRL -> BCL2","Expression","In the previous studies, prolactin induced Bcl-2 expression to prevent apoptosis and also provoked the activity of ornithine decarboxylase ., Prolactin increases Bcl-2 expression, suppresses stress-induced lymphocyte apoptosis, and improves survival from experimental sepsis., Results from stability studies indicated that increased bcl-2 messenger RNA evoked by PRL in Nb2 cell lines was most likely not attributable to increased stability of its transcripts., Expression of the anti-apoptotic gene bcl-2, which was stimulated within 1 h by PRL, was upregulated by L-arginine or DEA/Nitric oxide alone at 2 h and 8 h, respectively. <more data available...>","16520895:1, 15749917:1, 8940371:7, 10771518:11, 10456673:4, 14647416:1089, 12531884:1256, 9867250:100, 11380682:1207, 12140755:1107 <more data available...>",2,21,"Mus musculus","Lymphocytes, B-Lymphocytes, Precursor Cells, B-Lymphoid","positive"]
["PRL -> BCL2L1","Expression","The results indicated that a 0.9 kb bcl-x(L) transcript was rapidly induced by PRL., In another study, it was shown that Bcl-xl expression is dependent on prolactin stimulation (44)., As shown in Fig. 8A, PRL-induced Bcl-XL expression was not affected by 50 nM of control, scrambled siRNA., DIP hormone treatment induced STAT-5a phosphorylation by 5 min and bcl-xL expression in mammary epithelial cells by day 4, which indicates that the prolactin/STAT-5a and/or glucocorticoid-signaling pathways may be involved in regulating bcl-x transcription. <more data available...>","12904174:3, 19240166:1274, 17728251:1244, 11085510:1094, 17728251:245, 17728251:246, 17728251:265, 17728251:253, 17728251:81, 9163473565e7552cff17c5039d90b0c5",2,10,null,"T-Lymphocytes, Insulin-Secreting Cells, Epithelial Cells","positive"]
["PRL -> CCND1","Expression","This suggests a role for Oct-1 in PRL-dependent control of cyclin D1 transcription., Unmodified PRL employed multiple pathways to increase cellular proliferation and cyclin D1 levels in PRL-deficient MCF-7 cells., Finally, PRL induces expression of c-Myc and Cyclin D1 and leads to increased cell proliferation, which is specifically antagonized by ICI 182,780 or ERalpha depletion., Moreover, we show that both c-Src/phosphatidylinositol 3-kinase and c-Src/Fak/Erk1/2 pathways are involved in the up-regulation of c-myc and cyclin d1 expression mediated by PRL. <more data available...>","15885880:6, 12970160:2, 19169277:6, 12907754:8, 11773438:5, 20075866:3, 11356126:4, 18403642:1, 17519353:1228, 15746189:1165 <more data available...>",2,21,"Mus musculus, Mesocricetus auratus, Homo sapiens","Epithelial Cells, hepatic stem cells, hematopoietic cells","positive"]
["PRL -> CEBPB","Expression","In this report we demonstrate that PRL, a lactogenic hormone, enhances C/EBPbeta and PPARbeta mRNA expression and augments adipogenic conversion of NIH-3T3 cells., Although PRL alone can induce ß-casein expression through Stat5, glucocorticoid receptor and C/EBPß are not capable of inducing transcription in the absence of a Stat5., Whether or not lactogen action is also required for white adipose tissue differentiation is unclear, but PRL induces PPAR? and C/EBPß mRNA levels in NIH 3T3 cells [36] and adult female PRLR knockout mice have reductions in abdominal fat mass and decrease in adipocyte numbers [37]-[39]. ?his illustrates that beyond the role of PRLR signaling in adaptive thermogenesis at birth, this pathway may also affect later, white adipose tissue development and metabolism.","10674402:3, 16973758:1087, 18253483:1307",2,3,null,"Mesenchymal Stem Cells, Adipocytes","positive"]
["PRL -> CXCL10","Expression","PRL but not growth hormone selectively induced significantly enhanced production of MCP-1 and IP-10., In parallel with protein secretion, PRL enhanced interferon-?-induced CXCL9, CXCL10, and CXCL11 mRNA expression (Fig. 2D[Go])., Kanda N, Watanabe S (2007) Prolactin enhances interferon-gamma-induced production of CXC ligand 9 (CXCL9), CXCL10, and CXCL11 in human keratinocytes., Moreover, with the activation of STAT1, NF-?B, and IRF-1, PRL enhances IFN-?-induced transcription and secretion of key chemokines (for example, CXCL9, CXCL10, CXCL11), thus promoting the infiltration of type 1-T helper cells into psoriatic lesions (Kanda and Watanabe, 2007).","18248819:6, 17255201:1153, 19924133:1190, 19110541:1266",2,4,"Homo sapiens","Macrophages, Keratinocytes, T-Lymphocytes, Helper-Inducer","positive"]
["PRL -> GFAP","Expression","Prolactin induced expression of glial fibrillary acidic protein and tumor necrosis factor-alpha at a wound site in the rat brain.","7758825:100",2,1,"Rattus norvegicus",null,"positive"]
["PRL -> LST1","Expression","Prolactin selectively up-regulates the surface expression of the NKp46 and NKp30.","15654827:1334",2,1,null,null,"positive"]
["PRL -> PPARD","Expression","In this report we demonstrate that PRL, a lactogenic hormone, enhances C/EBPbeta and PPARbeta mRNA expression and augments adipogenic conversion of NIH-3T3 cells.","10674402:3",2,1,null,"Mesenchymal Stem Cells","positive"]
["PRL -> PTGS2","Expression","Prolactin up-regulates prostaglandin E2 production through increased expression of pancreatic-type phospholipase A2 and prostaglandin G/H synthase 2 in uterine cells.","8898352:100",2,1,null,null,"positive"]
["PRL -> SERPINA3","Expression","We find that PRL stimulated tyrosine phosphorylation of Stat5, induced nuclear protein binding to the Growth hormone-responsive element of the serine protease inhibitor 2.1 promoter, and activated Spi 2.1 gene expression., Prolactin was not able to stimulate expression of Spi 2.1 and/or insulin-like growth factor I mRNA under conditions that produced a growth hormone response(29, 30).","8892312:4, 7559615:1327",2,2,"Mus musculus","Myeloid Cells","positive"]
["PRL -> SOCS3","Expression","SOCS-3 expression was enhanced by PRL or by IFN-gamma., Finally, we show that PRL-induced SOCS3 expression can be potentiated by co-treatment with PGE(2)., PRL administration, however, significantly increased adrenal SOCS-3 mRNA expression (P<0.05)., Expression of SOCS-2 mRNA was increased with frequent milking or PRL treatment, whereas expression of SOCS-3 mRNA was reduced by frequent milking or exogenous PRL., The cytotoxic T-lymphocyte clone expressed conventional PRL receptor (PRLR), and PRL induced the expression of suppressor of cytokine signaling-3 (SOCS-3) and increased the expression of SOCS-2 and cytokine-inducible src homology-2 containing protein (CIS, another member of the SOCS family). <more data available...>","10969179:2, 19115200:7, 16809484:7, 17106096:7, 12668883:1, 11606470:1162, 19502454:1161, 17205581:1167, 16284084:1231, 18325991:1225 <more data available...>",2,16,"Homo sapiens","Leukocytes, Mononuclear, T-Lymphocytes, Cytotoxic, Epithelial Cells, endometrial stromal cells, Adipocytes","positive"]
["PRL -> TF","Expression","Experiments carried out in vitro using isolated rabbit epithelial mammary cells cultured on collagen I gel indicated that transferrin mRNA was abundant and only weakly inducible by the lactogenic hormones insulin, cortisol and prolactin, as opposed to caseins and WAP mRNAs., Bovine prolactin promotes the expression of human transferrin in the milk of transgenic mice.","8180682:8, 20213525:100",2,2,"Oryctolagus cuniculus",null,"positive"]
["PRL -> VEGFA","Expression","The mRNA of the angiogenic and survival factors VEGF and HIF-1alpha, was also induced by PRL treatment., The induction of VEGF by PRL was PRL receptor-, Jak2- and MAP kinase kinase-dependent., First, the pregnancy hormone PRL induces insulin and VEGF-A expression in ß-cells., Prolactin increases HO-1 expression and induces VEGF production in human macrophages., VEGF is up-regulated by prolactin, the principal hormone driving mammary development in advance of lactation (6) ., Second, others have found that mixed PRL preparations elevate mRNA for VEGF in other cell types (Hovey et al. 2001, Goldhar et al. 2005), whereas we observed either no effect of unmodified PRL or a decrease with S179D PRL.","19170064:7, 15737464:7, 16439446:1336, 15352176:100, 18032632:1035, 16601282:1298",2,6,"Rattus norvegicus, Homo sapiens","Insulin-Secreting Cells, Macrophages","positive"]
["PTGS1 -> PPARD","Expression","Cells were pretreated with a cyclooxygenase-2-selective inhibitor (NS398; 10 µM) or a cyclooxygenase-1-selective inhibitor (valeryl salicylate; 500 µM) for 30 min, followed by the addition of 2-arachidonyl glycerol or DMSO (vehicle) for 16 h (*, P < 0.05, compared with vehicle). (B) Transactivation of the PPRE reporter plasmid in Human umbilical vein ECs (blue), but not in HCT116 (gray), which is a cyclooxygenase-2-null cell line. (B, insets) mRNA levels of cyclooxygenase-1 and -2 in these cells by qRT-PCR (*, P < 0.05; **, P < 0.01, compared with vehicle). (C) Overexpression of COX-2 enhances 2-arachidonyl glycerol-induced peroxisomal proliferator-activated receptord transactivation.","17724132:1093",2,1,"Homo sapiens",null,"positive"]
["PTGS1 -> PTGS2","Expression","A, expression of COX-2 and PGES was induced coincident with cyclooxygenase-1 overexpression in HeLa cells., Overexpression of cyclooxygenase-1 in HeLa cells up-regulates expression of COX-2 and PGES concomitant with increased prostaglandin E2 production., C, partial inhibition of the cyclooxygenase-1-mediated up-regulation of COX-2 and PGES expression was observed after cotreatment with the selective COX-2 inhibitor NS-398., Overexpression of cyclooxygenase-1 in HeLa cells resulted in induced expression of cyclooxygenase-2 (COX-2) and prostaglandin E synthase (PGES) concomitant with increased prostaglandin E2 synthesis. <more data available...>","11809691:290, 11809691:346, 11809691:292, 11809691:41, 17202378:255, 17635918:373, 9430720:216, 9242654:190, 11809691:387, 12960371:171",2,10,"Mus musculus","Macrophages, Peritoneal, Endothelial Cells, Leukocytes","positive"]
["PTGS1 -> VEGFA","Expression","We have recently demonstrated that treatment of ovarian carcinoma cells with endothelin-1 (ET-1) induces expression of both Cyclooxygenase-1 and COX-2, which contributes to vascular endothelial growth factor (VEGF) production., Alphavbeta3 engagement also led to vascular endothelial cell growth factor (VEGF) generation and endothelial cells proliferation that was attenuated by inhibition of both cyclooxygenase-1 and COX-2., Induced overexpression of cyclooxygenase-1 resulted in an increase in bFGF, VEGF, Ang-1, and Ang-2 expression. <more data available...>","15347673:1, 12670347:5, 11809691:1373, 15269139:1250, 18339887:1279, 17308114:1196, 15458923:1218, 16741061:1109",2,8,null,"Endothelial Cells, mesothelial cells","positive"]
["PTGS2 -> BCL2","Expression","However, we did not observe any changes in Bcl-2, Bcl-XL, or Bax expression induced by COX-2 or prostaglandin E2., Chronic inflammation in benign prostatic hyperplasia causes an overexpression of COX-2, which induces the increased expression of Bcl-2 and VEGF., In vitro studies suggest that cox-2 regulates expression of the anti-apoptotic protein bcl-2, thus possibly accounting for reduced apoptosis in carcinogenesis., In summary, modulation of DR-5 and Bcl-2 levels by COX-2 attenuates TRAIL-induced apoptosis and represents a novel mechanism of intrinsic drug resistance in human colon cancer cells. <more data available...>","16127422:11, 21556211:13, 16550596:1, 12208739:6, 17541981:7, 18717758:6, 15754411:11, 17504996:1176, 16912190:1159, 12414664:1168 <more data available...>",2,32,"Rattus norvegicus","Epithelial Cells, Stromal Cells, Kupffer Cells, B-Lymphocytes, Endothelial Cells","positive"]
["PTGS2 -> BCL2L1","Expression","Suppression of COX-2 increased Bax protein and decreased Bcl-x(L) protein in vitro., However, we did not observe any changes in Bcl-2, Bcl-XL, or Bax expression induced by COX-2 or prostaglandin E2., Moreover, phosphatidic acid notably increased cyclooxygenase -2 protein expression, and phosphatidic acid-induced expression of both Bcl-2 and Bcl-xL was inhibited by NS-398, a specific inhibitor of COX-2., COX-2 deficiency impaired Bcl-2 and Bcl-xL down-regulation in liver ischemia/reperfusion injury .","15585639:7, 16127422:11, 17541981:7, 18209082:1199",2,4,null,null,"positive"]
["PTGS2 -> CCL3","Expression","The deficiency of COX-2 significantly attenuated mRNA expression in the abdominal aorta of the macrophage marker CD68, and the inflammatory cell recruitment chemokines, monocyte chemotactic protein-1 and macrophage inflammatory protein-1alpha.","17137566:9",2,1,null,"Macrophages","positive"]
["PTGS2 -> CCND1","Expression","COX-2 inhibitor can inhibit the expression of BCL-3 and cyclin D1 in a dose-dependent manner., The continued increase of COX-2 (up to 18 h) resulted in increased intracellular prostaglandin E(2) and cyclin D1 expression significantly after 8 and 12 h of EGF treatment., COX-2 activity is known to induce expression of cyclin D1 in neoplastic cells, and cyclin D1 expression can induce cell death in postmitotic neurons., As shown in Figure 4d, the expression of cyclin D1 was significantly inhibited and there was a further increase in the levels of COX-2 when RIE-Tr cells were treated with TGF-ß1 for 8 and 24 h. <more data available...>","20737317:10, 17077316:5, 15548426:1, 10023661:1187, 15090542:1281, 17404112:1264, 17404114:1264, 15731178:1230, 16731743:5, 9101092:9 <more data available...>",2,12,"Rattus norvegicus","Epithelial Cells, Neurons","positive"]
["PTGS2 -> CD44","Expression","Cyclooxygenase 2 is overexpressed in most non-small cell lung cancer and upregulates the cell adhesion receptor CD44., In contrast, expression of CD44 was markedly increased in KB/COX-2 as compared to KB/Neo., Furthermore, expression of CD44 on the surface of these cells was reduced by treatment with either NS-398 or COX-2 antisense oligonucleotide., CD44 expression is up-regulated in COX-2 cDNA in the sense-modified non-small cell lung cancer cells., In other cell models, cox-2 modulates cell adhesion to ECM by regulating expression of ß120 and a526 integrins or CD44.27 To address this, we tested expression of these molecules in our isogenic ANBL-6 cell lines. <more data available...>","16872953:1, 20664981:7, 16035618:5, 11320076:1151, 16497971:1253, 15358636:1086, 11320076:6",2,7,null,null,"positive"]
["PTGS2 -> CD68","Expression","The deficiency of COX-2 significantly attenuated mRNA expression in the abdominal aorta of the macrophage marker CD68, and the inflammatory cell recruitment chemokines, monocyte chemotactic protein-1 and macrophage inflammatory protein-1alpha.","17137566:9",2,1,null,"Macrophages","positive"]
["PTGS2 -> IFIT2","Expression","Cyclooxygenase 2 (Cox-2), chemokine (C-X-C motif) ligand 2 (Cxcl2), and IFN-induced protein with tetratricopeptide repeats 2 (Ifit2) mRNAs were all strongly up-regulated at 10 h post-LPS treatment and were superinduced by trichostatin A + LPS (Fig. 3 a).","16816106:1146",2,1,null,"Macrophages","positive"]
["PTGS2 -> MCL1","Expression","These data suggest that the expression level of Mcl-1 is tightly regulated by COX-2., Furthermore, COX-2 enhanced Mcl-1 expression in the anoikis process, implying that Mcl-1 also may be involved in mediating the survival function of COX-2., Our data clearly show that COX-2 inhibitors can directly interfere with this protumorigenic effect of COX-2 via down-regulating the expression of Mcl-1 protein., Recently, Mcl-1 expression has been shown to be upregulated by COX-2/prostaglandin E2 in lung adenocarcinoma cell line (Lin et al., 2001). <more data available...>","11585835:6, 16000874:3, 16849551:1261, 16528365:1189, 19933775:1259, 12438243:1154, 11585835:29, 11585835:27, 11585835:32, 11585835:35 <more data available...>",2,13,"Homo sapiens","Plasma Cells","positive"]
["PTGS2 -> PTGS1","Expression","cadmium at 1 microM and above markedly stimulated COX-2 mRNA expression and slightly increased the level of cyclooxygenase-1 mRNA., To elucidate the role of COX-2 in blood pressure homeostasis using Cyclooxygenase-1>COX-2 mice, in which the Cyclooxygenase-1 expression is controlled by COX-2 regulatory elements., However, in the choroid plexus, cyclooxygenase-1 mRNA was enhanced (p<0.05) at 30 and 120 min after lipopolysaccharide endotoxin injection and Cox-2 showed a similar (NS) change., At 2 to 4 hours after surgery, PTGS1 expression was slightly decreased (36%, P < .001) and PTGS2 expression was markedly increased (300%, P < .001) with wide interindividual variation; at 48 hours after surgery, little detectable change in PTGS1 and PTGS2 expression was found in the control group. <more data available...>","11351503:8, 19940265:2, 9845005:5, 16678543:3, 12713596:1127, 10945606:1220, 12533422:1268, 15934081:1128, 9388257:1228, 14678996:1344 <more data available...>",2,11,"Ovis aries, Mus musculus","Osteoblasts, Macrophages, Endothelial Cells, Keratinocytes","positive"]
["PTGS2 -> S100A4","Expression","In addition, a COX-2 inhibitor suppressed stromal formation and reduced expression of CXCL12/CXCR4 and a fibroblast marker (S100A4) in a micropore chamber model.","20110411:5",2,1,null,"Fibroblasts","positive"]
["PTGS2 -> VEGFA","Expression","In this model, VEGF expression was down-regulated by selective COX-2 inhibition with NS-398., As Cox-2 modulates expression of VEGF, also the VEGF promoter might be controllable., COX-2 may contribute to VEGF expression in non-small cell lung cancer., Only in those cell lines without expression of COX-1 was VEGF production blocked meaningfully by small interfering RNA of COX-2., Moreover, COX-2 may participate in polyp enlargement through angiogenesis by promoting VEGF production., Inhibition of COX-2 or iNOS attenuated retinal neovascularization and decreased VEGF and MMP-2 expression. <more data available...>","14563940:3, 18698374:4, 21219643:8, 21301321:3, 12743436:10, 17923259:4, 15010822:14, 21294088:1, 10841517:7, 20881304:8 <more data available...>",2,121,"Mus musculus, Homo sapiens","Fibroblasts, Epithelial Cells, Endothelial Cells, Embryonic Stem Cells, T-Lymphocytes, Stromal Cells, Macrophages, D-cells, Neutrophils","positive"]
["PTK2 -> BCL2","Expression","Finally, Bit-1-mediated regulation of bcl-2 was dependent on focal adhesion kinase, PI3K, and AKT., Furthermore, expression of FRNK blocked the activation of bcl-2transcription by wild type Shc (compare Figs. 2 A and3 A) in the a5?cß1 cells., FAK- and Shc-dependent increases in Bcl-2 protein expression in response to integrin engagement that protect Chinese hamster ovary cells from apoptosis have also been described (17)., Apoptosis-associated proteins Bax, Bcl-2, BAD and survivin have all been demonstrated to be involved in the chemoresistance of pancreatic cancer cells and be regulated by FAK or Akt [29-33] . <more data available...>","21383007:10, 11333270:1157, 12637511:1343, 20021699:1252, 16527907:1258, 16648868:1180",2,6,null,"Epithelial Cells","positive"]
["PTK2 -> CCND1","Expression","Using Northern blotting and cyclin D1 promoter/luciferase assays, we showed that FAK signaling regulated cyclin D1 expression at the transcriptional level., Cell adhesion to the extracellular matrix activates focal adhesion kinase (FAK), which is essential for cyclin D1 expression., By flow cytometry analysis, it was found that FAK promoted G1/S transition and enhanced the expression of cyclin D1 while FAKY397F inhibited these steps compared with the control NIH3T3 cells., Finally, we also found that DeltaC14 blocked cyclin D1 upregulation and induced p21 expression, while wild-type FAK increased cyclin D1 expression and decreased p21 expression. <more data available...>","11739801:8, 11313702:1, 14577571:6, 9864370:5, 18520069:6, 12907754:8, 19625610:8, 20658539:7, 20038548:1419, 15557280:1321 <more data available...>",2,23,"Homo sapiens, Mus musculus","Fibroblasts, Embryonic Stem Cells, Endothelial Cells","positive"]
["PTK2 -> PTGS2","Expression","The study of the mechanism implicated in COX-2 upregulation by collagen I showed focal adhesion kinase (FAK) activation., These results suggest that FAK regulates the production of prostaglandin E(2) via the transcriptional regulation of COX-2 mRNA in compressive stimulated PDL cells., In contrast to phosphatidylinositol 3-kinase and protein kinase C, inhibition of FAK and Src effectively reduced Kaposi's sarcoma-associated herpesvirus infection-induced COX-2 transcription and protein levels., Inhibition of focal adhesion kinase (FAK) or downstream phosphoinositide 3-kinase and p70S6 kinase by specific chemical inhibitors prevented COX-2 induction by Col-I, and C/EBP and CREB from binding to their consensus DNA oligonucleotides. <more data available...>","21209362:5, 20924071:5, 20943963:8, 15163555:9, 12237848:3, 16540596:1229",2,6,"Homo sapiens","Mesangial Cells, Endothelial Cells, Microglia, Osteoblasts","positive"]
["PTPN6 -> CYBB","Expression","Consistent with this, overexpression of SHP1 decreases gp91PHOX and p67PHOX mRNA abundance in IFN?-treated U937 transfectants., Expression of a dominant-negative form of SHP1 increased ICSBP tyrosine phosphorylation and CYBB and NCF2 transcription in undifferentiated myeloid cell lines [3 ]., Consistent with this, SHP1 inhibition increases gp91PHOX and p67PHOXmRNA in undifferentiated U937 cells., In undifferentiated U937 cells, we found that overexpression of CS453-SHP1 increases gp91PHOX and p67PHOX mRNA abundance relative to control vector transfectants (Fig.2 C).","11483597:1223, 18089853:1048, 11483597:208, 11483597:223",2,4,null,"Myeloid Cells","positive"]
["PTPN6 -> ITGB2","Expression","Surface expression of ß2 integrins is increased on motheaten polymorphonuclear leukocytes .","11067945:1301",2,1,null,"Granulocytes","positive"]
["PTPRC -> BCL2","Expression","Bcl-2 expression was upregulated between CD3(-)CD4(+)CD8(+)CD45R0(+) and CD3(+)CD4(+)CD8(+)CD45R0(+) stages.","11975983:7",2,1,"Homo sapiens","thymocytes","positive"]
["S100A4 -> CD44","Expression","Furthermore, S100A4 siRNA down-regulated the expression of CD44 and MMP2, suggesting that S100A4 may promote the proliferation, invasion and metastasis of osteosarcoma cells by regulating the expression of other proteins that are crucial in modulating cell-ECM adhesion and facilitating ECM degradation.","20855150:4",2,1,null,null,"positive"]
["S100A6 -> S100A4","Expression","Six hours after shaving, both S100A4 and S100A6 mRNAs were upregulated in the outer layer of the epithelial sac, and the S100A6 signal extended to the hair germ (Figure 4e,f).","11407987:1168",2,1,null,null,"positive"]
["S1PR3 -> PTGS2","Expression","Transfection with the antisense oligonucleotides to S1P1 or S1P3 significantly suppressed sphingosine 1-phosphate-mediated COX-2 expression and PGE2 production (Fig. 7, A and B)., Transfection of S1P1 or S1P3 but not of S1P2 antisense oligonucleotide inhibited sphingosine 1-phosphate-induced COX-2 expression and PGE2 production in WISH cells, indicating the involvements of S1P1 and S1P3 in the processes., As shown in Fig. 7, sphingosine 1-phosphate-induced COX-2 expression and PGE2 synthesis were inhibited by the down-regulation of S1P1 and S1P3 but not S1P2, which suggests that S1P1 and S1P3, but not S1P2, are involved in sphingosine 1-phosphate-induced COX-2 expression in WISH cells.","12796504:239, 12796504:51, 12796504:279",2,3,null,null,"positive"]
["SLC14A1 -> GFAP","Expression","The abundance of GFAP, the usual marker of astrocytes and ependymal cells, was increased by 25% with age (data not shown), a variation much smaller than the doubling in UT-B1 or the fourfold increase in AQP-4.","12933359:1196",2,1,null,"Astrocytes","positive"]
["SMAD7 -> CEBPD","Expression","While C/EBPß levels were not strongly affected, Smad6 or Smad7 overexpression increased the levels of C/EBPd, which is normally downregulated during differentiation.","10791980:1246",2,1,null,"Adipocytes","positive"]
["SOCS3 -> PTGS2","Expression","Keratinocyte-specific overexpression of SOCS-3 led to atrophied wound-margin epithelia and augmented the inflammatory response of wound keratinocytes by an increase in chemokine (MIP-2) and inflammatory enzyme (COX-2 and iNOS) expression.","19924141:3",2,1,null,"Keratinocytes","positive"]
["SOX9 -> CLU","Expression","Mutant Kras blocks acinar regeneration in favor of a persistently dedifferentiated state. (A-H) Clusterin and Sox9 (I-P) expression during regeneration and Kras-induced acinar-to-ductal metaplasia. (A and I) Clusterin expression is limited to some normal ducts in PBS-treated Pdx1-CreEarly mice, while Sox9 is restricted to ducts and centroacinar cells (arrowheads). (E and M) Acini in PBS-treated Pdx1-CreEarly;LSL-KrasG12D mice are negative for Clusterin and Sox9, while normal ducts and spontaneous pancreatic intraepithelial neoplasias are positive (asterisks). (B, F, J, and N) Damaged duct-like cells of both genotypes display clusterin- and Sox9-positive cells (insets). (C, D, K, and L) Clusterin and Sox9 are mainly restricted to duct cells (arrowheads) following regeneration in Pdx1-CreEarly pancreata.","20071774:1134",2,1,null,"centroacinar cells","positive"]
["SOX9 -> FGF9","Expression","In the mouse XY gonad, Sry normally initiates a feed-forward loop between Sox9 and Fgf9, which up-regulates Fgf9 and represses Wnt4 to establish the testis pathway., Sox9 upregulates fibroblast growth factor 9, which is required to maintain Sox9., Sox9 then up-regulates the expression of Fgf9, which is required for the maintenance of Sox9 expression.","16700629:5, 16881057:1303, 18216218:1368",2,3,null,null,"positive"]
["SOX9 -> LXN","Expression","BMP-2 treatment upregulated Sox9 expression, and Sox9 stimulated the promoter activity of latexin.","19059214:7",2,1,null,"Chondrocytes","positive"]
["STAT1 -> B2M","Expression","The same authors also show that transcription of the ß2-microglobulin gene is down-regulated in mouse Stat1-null T lymphocytes., A direct target of EOMES, IL2RB (CD122) (29), is also 7.4-fold up-regulated. ß-2 microglobulin , which is up-regulated by STAT1 and is part of MHC I, is fivefold up-regulated in L&H cells.","10921891:1271, 18794340:1113",2,2,null,"T-Lymphocytes, B-Lymphocytes","positive"]
["STAT1 -> CASP1","Expression","Activation of caspase-1 gene expression requires IRF-1 and Stat-1 (24, 32)., In addition, overexpression of STAT-1 together with interferon-? treatment further enhanced the activity of the caspase-1 promoter., In addition, activation of the STAT-1 signaling pathway can cause expression of caspase 1 and subsequent apoptosis (43)., The activation of the Stat1-signaling pathway by interferon-? and EGF can lead to expression of caspase 1 and apoptosis (Chin et al., 1997; Kumar et al., 1997)., Furthermore, activation of STAT1 through the IFN-? receptor led to increased expression of caspase-1, -3, and -8 and sensitized cells to apoptosis (51, 52, 53, 54). <more data available...>","16135520:1077, 10744676:1203, 18566411:1327, 11971185:1169, 15494489:1282, 17339457:1350, 10051540:1210, 16135520:78, 10744676:204, 10744676:201 <more data available...>",2,17,"Homo sapiens","Fibroblasts, memory T-cells, Macrophages, T-Lymphocytes, Myocytes, Cardiac, Chondrocytes, Lymphocytes, Null","positive"]
["STAT1 -> CD80","Expression","MHC class I and CD80 expression is reduced by STAT-1 mutation or deficiency., Thus, comparable to the results with DCs, STAT1 appears to be required for the CpG-induced up-regulation of CD40 and CD80 by macrophages (Fig. 4C).","19620292:1217, 17513775:1238",2,2,null,"Dendritic Cells, Macrophages","positive"]
["STAT1 -> CEBPB","Expression","C, STAT1 restores Interferon-?-stimulated gene expression via C/EBP-ß in U3A cells., Several transcription factors such as EGR-1, C/EBPß, and c-jun are induced in STAT-1 null cells (Ramana et al, 2001).","10995751:1364, 16117790:1144",2,2,null,"Fibroblasts, Lymphocytes, Null","positive"]
["STAT1 -> CXCL10","Expression","STAT1 was critical for IFN-gamma induction of both the Cxcl9 and Cxcl10 genes in microglia and in microglia and astrocytes, respectively.","20585034:7",2,1,null,"Microglia","positive"]
["STAT1 -> CYBB","Expression","At the same time, STAT1 and IRF-1 together promote the interferon-?-induced transcription of the CYBB gene (26).","16162660:1069",2,1,null,"Myeloid Cells","positive"]
["STAT1 -> GFAP","Expression","The expression of glial fibrillary acid protein (GFAP) is activated by the cooperation of Smad1 and Stat1/3 proteins that in turn require p300/CBP as a coactivator., Mice were sacrificed, and paraffin-embedded brain sections were immunostained for GFAP, Iba-1, STAT-1 (which is involved in gene transcription), and iNOS, which is regulated by STAT-1 (51).","19020048:1366, 12594292:1179",2,2,null,"Neurons","positive"]
["STAT1 -> HSPB1","Expression","STAT-1 was required for transcriptional activation of the HSP27 gene, but not for the HSP70 gene, and cDNA transfection of STAT-1 in mumps virus-infected cells restored thermotolerance.","12917439:6",2,1,null,null,"positive"]
["STAT1 -> IFI27","Expression","From results presented here, it is reasonable to propose that up-regulated STAT1 may enhance IFI27 and OAS1 expression in breast tumors.","19478064:183",2,1,"Homo sapiens","Epithelial Cells","positive"]
["STAT1 -> IFIT3","Expression","Ectopic expression of STAT1, but not mutant STAT1-S727A, almost completely restored interferon-alpha2a-induced IFIT4 expression., Induction of IFIT4 transcription by IFN-a depends upon the sequential activation of protein kinase Cd, c-Jun amino-terminal kinase, and STAT1 (signal transducer and activator of transcription 1) [36] ., We found that enforced expression of STAT1 in U3A cells could rescue the response of RIG-G gene to IFNa, but mutant signal transducer and activator of transcription1-Y701F had no such an effect ( Fig. 1C), suggesting that phosphorylation of STAT1 was required for RIG-G expression in IFNa-treated U3A cells. <more data available...>","17933493:3, 18706081:1111, 19351818:1136, 19351820:1136, 17933493:6",2,5,null,"PBMCs, Myeloid Progenitor Cells","positive"]
["STAT1 -> ISG15","Expression","A single mutation (K161A) in the p48 contact region of Stat1 inhibited the Stat1-p48 interaction as well as the IFN-a-triggered ISG15 gene induction, whereas this mutation had no effect on either the Stat1-Stat2 interaction or the IFN-? response which is independent of p48 (Horvath et al., 1996).","10851063:1089",2,1,null,null,"positive"]
["STAT1 -> MCL1","Expression","Further, mutation of STAT1/STAT2 prevented the effect of both Abeta and SGK1 on Mcl-1 expression.","19609277:10",2,1,null,null,"positive"]
["STAT1 -> PSMB8","Expression","In the secondary responses, IRF1 activates transcription of IRF2, cyclin-dependent kinase inhibitor 1A, caspases, and the major histocompatibility complex class Ia genes by binding IFN response elements , whereas STAT1 and IRF1 cooperate to transactivate expression of other genes, such as guanylate binding protein , proteasome subunit beta type 8, PSMB9, and CIITA.","19164174:1091",2,1,null,null,"positive"]
["STAT1 -> SMAD7","Expression","STAT-1 is activated, homodimerizes, and translocates to the nucleus to regulate transcription of the inhibitory SMAD7., Stat1 also enhances the expression of SOCS1 and Smad7, which inhibit the IL4 and transforming growth factor-ß signaling pathways, respectively . [Space]., Conversely, IFN-? antagonizes TGF-ß activity in many cellular responses, for which Smad7 induction by Jak1/STAT1 seems to be a major mechanism 199., Smad7, a key negative regulator of TGF-ß-mediated signaling (28), is also induced by excessive STAT1 activation, which is associated with chronic infection with the gastric class I carcinogen H. pylori (29). <more data available...>","12668667:1291, 10851061:1603, 19002158:1304, 18431520:1078, 16308570:1175, 11518734:1278, 10652273:1204, 19516008:1261",2,8,"Homo sapiens","Epithelial Cells, T-Lymphocytes, Cytotoxic, Macrophages, Monocytes, Endothelial Cells, Keratinocytes","positive"]
["STAT3 -> CD14","Expression","STAT3 inhibitor pretreatment could also down-regulate high CD14 and CD16 expression by BxPC-3 conditioned medium treatment.","17545630:1248",2,1,null,"Monocytes","positive"]
["STAT3 -> CD9","Expression","Furthermore, activation of STAT3 induced the expression of CD9, indicating the LIF/STAT3 pathway is critical for maintaining CD9 expression., In a previous study, the addition of leukemia inhibitory factor or STAT3 activation induced CD9 expression in embryonic stem cells [13], which indicates that the leukemia inhibitory factor/STAT3 pathway is critical for maintaining CD9 expression., In addition, we examined the expression of CD9, a tetraspan transmembrane protein expressed by undifferentiated mouse Embryonic stem cells, which appears to be regulated by activation of the LIF/STAT3 pathway and is decreased upon differentiation of the cells (Oka et al., 2002).","11950938:5, 12954725:1222, 14745950:1225",2,3,"Mus musculus","Embryonic Stem Cells","positive"]
["STAT3 -> CEBPA","Expression","Gene expression profile and quantitative PCR analysis of G-CSF-stimulated cell lines revealed that the expression of C/EBPalpha was up-regulated by the activation of Stat3., Treatment of freshly isolated adult rat hepatocytes with 10-100 mM ethanol rapidly (< 3 min) inhibits interleukin-6 (IL-6)-induced STAT3 activation, tyrosine and serine phosphorylation and IL-6-induced CCAAT enhancer binding protein (C/EBP) alpha and beta mRNA expression., One is that activated Stat3 binds to the promoter region of C/EBPa and induces the transcription of C/EBPa. <more data available...>","15664994:3, 10486586:2, 15664994:261, 15664994:66, 15664994:47, 15664994:255, 15664994:266",2,7,"Rattus norvegicus","Neutrophils, Hepatocytes, Granulocytes","positive"]
["STAT3 -> CXCL10","Expression","Inhibitors of p38 mitogen-activated protein kinase, c-Jun N-terminal kinase (JNK), phosphatidylinositol-3-OH kinase and signal transducer and activator of transcription 3 decreased OSM-induced CXCL10 production.","19616927:6",2,1,"Homo sapiens","Fibroblasts","positive"]
["STAT3 -> FCGR3A","Expression","STAT3 inhibitor pretreatment could also down-regulate high CD14 and CD16 expression by BxPC-3 conditioned medium treatment.","17545630:1248",2,1,null,"Monocytes","positive"]
["STAT3 -> FLI1","Expression","A recent study showed that an enhanceosome responsible for activating SCL transcription was required for GATA-2, Fli-1, and Elf-1.37 As the expression of Fli-1 was induced via the STAT3 transcription factor,38 phosphorylation of STAT3 by the binding of HGF to c-met39 might activate Fli-1 or Elf-1.","14701703:1187",2,1,null,null,"positive"]
["STAT3 -> HPGD","Expression","Activation of signal transducer and activator of transcription3 may augment potently the androgen bound receptor signaling and contribute to synergistic induction of 15-PGDH expression by combined treatments with IL-6 and dihydrotestosterone.","14749354:1215",2,1,null,null,"positive"]
["STAT3 -> MET","Expression","The resulting increase in the concentration of unphosphorylated STAT3 drives a second wave of expression of genes such as RANTES, IL6, IL8, MET, and MRAS that do not respond directly to tyrosine-phosphorylated signal transducer and activator of transcription 3., U-STAT3 induces the expression of well-known oncogenes, such as MRAS and MET, which are late-phase genes induced by IL-6., Unphosphorylated STAT3 could drive overexpressions of certain oncogenes (such as M-RAS and MET), which contributed to cellular transformation ( 34). <more data available...>","17510282:1, 19478064:1202, 19351818:1254, 19351820:1254, 18364677:1189, 15007380:1295, 19478064:203",2,7,"Homo sapiens","Monocytes, Keratinocytes","positive"]
["STAT3 -> OSMR","Expression","STAT3 activation further enhances OSMR expression, thereby establishing a positive-feedback loop., We found that Stat3flx/flx/NIC tumors expressed lower levels of both cebpd and osmr, two genes that are induced by Stat3 (28, 29)., We show that OSMR expression is dependent on LIF-induced STAT3 and that the subsequent OSMR-mediated signal inhibits the phosphorylation of STAT5 and coordinately activates signal transducer and activator of transcription3-dependent apoptosis in the involuting mammary gland.","20348953:1139, 19690134:1181, 18927239:1084",2,3,null,null,"positive"]
["STAT3 -> SBNO2","Expression","IL-10-mediated induction of ETV3 and SBNO2 expression was dependent upon both STAT3 and a stimulus through the TLR pathway., IL-10-mediated induction of ETV3 and SBNO2 expression was dependent on STAT3 and a stimulus through the TLR pathway [32] .","18025162:2, 19741156:1099",2,2,"Homo sapiens","Macrophages","positive"]
["STAT3 -> SYNPO","Expression","Stat3-DN inhibited nef-containing vector-induced cyclin E expression and significantly increased synaptopodin expression (Figure 5C).","15343382:1157",2,1,null,"Podocytes","positive"]
["STAT3 -> TF","Expression","proteolysis-inducing factor activates both the transcription factors NF-kB and STAT3, which result in the increased production of IL-8, IL-6, and C-reactive protein and the decreased production of transferrin.","11259367:4",2,1,"Homo sapiens","Hepatocytes","positive"]
["STAT3 -> VIM","Expression","Specific inhibition of STAT3 activation by Janus kinase2-specific inhibitor AG490 blocked STAT3 phosphorylation, cell motility, induction of N-cadherin and vimentin expression and IL6 production., Stat3 can enhance transcription of the vimentin gene.","19088723:9, 14712222:1097",2,2,null,null,"positive"]
["TF -> BCL2L1","Expression","The expression of Bcl-xL was increased by Apo-transferrin (Figures 4 and 5a).","14704719:1284",2,1,"Rattus norvegicus","Hepatocytes","positive"]
["TGFB1 -> A2M","Expression","It was blocked when bovine adrenocortical cells were exposed to 5,6-dichlorobenzimidazole riboside, a potent inhibitor of RNA polymerase II, suggesting that TGF-beta 1 acts as an activator of alpha 2-M gene expression at the transcriptional level., This is supported by the following observations: (i) Treatment of adrenocortical cells by FGF-2 resulted in a time-dependent and dose-dependent increase of alpha 2M synthesis, (ii) FGF-2 did not modify alpha 2M secretion rate; (iii) The induction of alpha 2M synthesis by FGF-2 was not observed in the presence of the transcription inhibitor DRB; (iv) The amount of alpha 2M mRNA was increased by 2 to 3 fold under either FGF-2 or TGF beta 1 treatment; (v) Optimal doses of TGF beta and FGF-2 synergistically increased alpha 2M synthesis. <more data available...>","1689294:5, 7524573:1, 9570034:1745, 15618353:1348",2,4,null,"Germ Cells","positive"]
["TGFB1 -> ABCA1","Expression","TGF-beta1 significantly increased expressions of ABCA1, ABCG1 and SR-BI at both transcriptional and translational levels in a dose-dependent and time-dependent manner., Proatherogenic cytokines such as interferon -? and interleukin -1ß have been shown to inhibit the expression of ABCA1, while antiatherogenic cytokines, including IL-10 and transforming growth factor -ß1, have been shown to promote the expression of ABCA1., transforming growth factor-ß increases ABC-1 expression and inhibits its down-regulation by interferon-?. <more data available...>","20057170:4, 20485864:4, 11352993:1189, 11742878:1055, 15995168:2634",2,5,null,"Macrophages","positive"]
["TGFB1 -> ADAMTS1","Expression","Expression of ADAMTS1 is induced by transforming growth factor-ß in keratinocytes.","15843381:262",2,1,null,"Keratinocytes","positive"]
["TGFB1 -> AIF1","Expression","Furthermore, functional studies showed specific allograft inflammatory factor-1 isoform expression stimulation by transforming growth factor-beta., These data suggest that AIF-1 plays an important role in the pathogenesis of systemic sclerosis owing to its increased expression in affected tissues and to the specific stimulation of AIF-1 isoform 2 by TGFbeta., A substantial induction was seen, however, in cells treated with IFN-? (7.5-fold), whereas TGF-ß1 produced a more modest increase in aif-1message (2.5-fold). [Figure 1] View larger version: In this window. <more data available...>","17053503:3, 16868985:10, 11861656:1123, 10894811:1159, 17522098:1077, 16868985:9",2,6,"Homo sapiens","Macrophages, PBMCs","positive"]
["TGFB1 -> ALOX5AP","Expression","The addition of anti-TGF-beta1 antibody reduced hydroxynonenal-induced 5-LOX and FLAP expression by 40%, indicating the partial involvement of a TGF-beta1-dependent mechanism., The expression of FLAP in Osteoarthritis osteoblasts is also modulated differently by 1,25(OH)2D3 and TGF-beta depending on their endogenous low and high prostaglandin E2 levels., TGFbeta1 and/or 1,25(OH)(2)D(3) induced a rapid and marked enhancement ( approximately 4-13-fold) in FLAP messenger RNA levels, which was associated with a subsequent and late increase in leukotriene B(4) production and prostaglandin E(2) synthesis. <more data available...>","20144213:12, 17156456:12, 15593193:4, 11090070:5",2,4,null,"Chondrocytes, Osteoblasts, Dendritic Cells","positive"]
["TGFB1 -> CCND1","Expression","TGF-ß1 also up-regulated cyclin D1 and E protein levels while down-regulating p27, thus stimulating cell cycle progression., The expression of cyclin D1 in MCF10A cells is regulated by TGF-ß treatment., These results strongly suggest that TGF-ß regulates cyclin D1 expression in a ß-catenin-dependent manner., In addition, Sox17 counteracted repression of the cyclin D1 promoter by TGF-ß1 and Smad3., TGF-ß stimulates cyclin A expression without affecting cyclin D-cdk4/6 activity in suspended NRK cells., TGF-ß stimulated cyclin D1 expression in Ad-GFP-infected but not Ad-Cre-infected chondrocytes (Fig. 7a). <more data available...>","20876581:7, 18715870:116, 16690606:242, 19479035:326, 10702223:90, 16690606:239, 16690606:67, 19479035:260, 16517699:263, 15811853:143 <more data available...>",2,19,"Mus musculus","Mesangial Cells, Chondrocytes, Epithelial Cells, T-Lymphocytes","positive"]
["TGFB1 -> CD14","Expression","At 2 hr, 50 ng/ml TGF-beta 1 significantly lowered CD14 expression (51%, P = 0.043)., TGF-beta and VD3 synergistically increased the expression of differentiation-associated markers such as the CD11b and CD14 antigens, whereas TGF-beta and dexamethasone did not., Furthermore, TGF-beta/D3 treatment (but not D3 alone) elicits the expression of membrane CD14, FcRI, FcRII, CD11a, CD11b, CD11c, ICAM-1, and PECAM-1 Ag at a level comparable to that observed on normal human monocytes., The same CCAAT/enhancer-binding protein site was also involved in the TGF-ß/Vit D3-dependent activation of CD14 expression (42). <more data available...>","7526045:5, 10547074:1, 8383719:5, 11698458:1270, 12821938:1143, 18497880:1254",2,6,"Homo sapiens","Monocytes, Stromal Cells","positive"]
["TGFB1 -> CD9","Expression","However, CD9 levels induced by TGFß1 were substantially greater than those caused by culture in the presence of IL-2 (data not shown).","17360654:1191",2,1,null,"Killer Cells, Natural","positive"]
["TGFB1 -> CLU","Expression","At the same time, TGFbeta1 enhanced clusterin protein and mRNA expression., TGF-beta 1 induced a bilateral increase in clusterin mRNA per astrocyte., A single T to G base mutation in the AP-1 site (5'-TGAGGCA) abolishes TGFbeta-induced clusterin promoter transactivation., We hypothesize that activation of the TGF-beta signaling pathway, which often occurs after ionizing radiation exposure, can in turn activate the CLU promoter., The expression of clusterin mRNA and protein in nonpigmented ciliary epithelial cells was significantly downregulated by TGF-beta1 in vitro. <more data available...>","10066375:3, 7730444:2, 9334243:5, 15530543:10, 16639006:8, 8892344:4, 9407436:5, 8170537:2, 10406964:1149, 15671065:1426 <more data available...>",2,43,"Sus scrofa, Homo sapiens, Bos taurus, Mustela lutreola","Epithelial Cells, Astrocytes, Fibroblasts, myofibroblasts, Endothelial Cells, sperm cell, Myocytes, Smooth Muscle","positive"]
["TGFB1 -> CSF1","Expression","Transforming growth factor beta (TGF-beta) increased both the synthesis of CSF-1 and its accumulation in the matrix., In a time-dependent manner, TGF-beta1 produced a 10- and a 6-fold increase in M-CSF mRNA and protein levels after 12 h, respectively., In turn, treatment with transforming growth factor beta1 reduced the expression of granulocyte-macrophage and macrophage colony stimulating factor mRNA., Our present studies suggest that Platelet-derived growth factor autocrine loop-dependent and loop-independent pathways could modulate the M-CSF production stimulated by TGF-beta or interleukin-1 and account for the complexity of the cytokine network involving M-CSF in vivo under various physiological and pathological conditions. <more data available...>","8591991:10, 9278333:2, 10381274:7, 8048485:6, 16707491:1362, 16443656:1082, 9492032:1246, 7804125:8, 8048485:1, 9278333:1 <more data available...>",2,12,"Mus musculus","Macrophages, Osteoblasts, Myeloid Progenitor Cells","positive"]
["TGFB1 -> CSF1R","Expression","In contrast, TGF-beta 1 down-modulated IL-3 and CSF-1 receptor expression by 54 and 55%, respectively, by 24 h., TGF-beta1 significantly induced the expression of c-fms mRNA and c-fms cell-surface expression., Cell surface expression of the monocyte/macrophage-specific marker c-fms was increased 3.1-fold following TGF-beta 1 treatment., TGF-ß1 induces the expression of c-fms., transforming growth factor-ß1 induces CSF-1R expression and in vivo invasion of MDA-MB-231 cells., Antagonists of TGF-beta1 signaling significantly inhibited both the induction of c-fms expression and cellular invasiveness, suggesting that additional studies are warranted to assess the therapeutic potential of TGF-beta antagonists in endometriosis. <more data available...>","8409417:3, 19505996:6, 8930403:10, 17332318:1233, 19934330:1236, 19505996:8, 17332318:234, 17332318:219, 17332318:248, 17332318:223 <more data available...>",2,16,"Mus musculus","Macrophages, mesothelial cells, Epithelial Cells, Myeloid Progenitor Cells","positive"]
["TGFB1 -> CX3CR1","Expression","These results showed that TGFß enhanced CX(3)CR1 expression and attenuated the LPS-induced increase in IL-1ß expression., TGF-beta1 upregulates CX3CR1 expression and inhibits fractalkine-stimulated signaling in rat microglia., In this regard, several recombinant cytokines, including TGF-ß1 (27), IL-2, and IL-15 (28), have been reported to modulate CX3CR1 expression.","20570721:11, 12446007:100, 15347678:1068",2,3,"Rattus norvegicus","Microglia, Leukocytes","positive"]
["TGFB1 -> CX3CR1","Expression","These results showed that TGFß enhanced CX(3)CR1 expression and attenuated the LPS-induced increase in IL-1ß expression., TGF-beta1 upregulates CX3CR1 expression and inhibits fractalkine-stimulated signaling in rat microglia., In this regard, several recombinant cytokines, including TGF-ß1 (27), IL-2, and IL-15 (28), have been reported to modulate CX3CR1 expression.","20570721:11, 12446007:100, 15347678:1068",2,3,"Rattus norvegicus","Microglia, Leukocytes","positive"]
["TGFB1 -> CYBB","Expression","Cyclosporine A, TGF-beta1 and angiotensin II increased Nox-2 mRNA levels 2- to 7-fold in vitro (NRK52E cells)., Transfection of wild-type mouse cardiac fibroblasts with AAV/TGFbeta (ACT)(1) markedly enhanced the expression of NADPH oxidases (p22(phox), p47(phox), and gp91(phox) subunits) and LOX-1, formation of reactive oxygen species, and collagen synthesis, concomitant with an increase in the activation of p38 and p44/42 mitogen-activated protein kinases ., TGF-ß1 upregulates the expression of p22phox, p47phox, p67phox, and gp91phox in rat mesangial cells (Figure 2B) and p22phox mRNA in tubular epithelial cells (Figure 2C), suggesting that TGF-ß1-induced reactive oxygen species may be NADPH oxidase dependent. <more data available...>","18976289:8, 18182394:3, 12874439:1080, 12482831:1145",2,4,"Rattus norvegicus, Mus musculus, Homo sapiens","Fibroblasts, Mesangial Cells, Myocytes, Smooth Muscle","positive"]
["TGFB1 -> DUSP1","Expression","Both TYP 1 and CL100 mRNAs are induced upon TGF-beta treatment of squamous cell lines sensitive to the growth factors antiproliferative effects., In cells treated with Ro-31-8220, the TGF-ß1-induced expression of MKP-1 was abrogated (n = 5 independent experiments)., As shown in Fig. 4, LPS induced a small increase in MKP-1 expression that was substantially enhanced with the addition of TGF-ß., As shown in Fig. 6B, TGF-ß1 or nontypeable Hemophilus influenzae indeed induced MKP-1 expression at the protein level (Fig. 6B). <more data available...>","8545112:5, 17848599:1164, 16394011:1176, 16754688:1248, 12734193:1303",2,5,null,"squamous cells, Myocytes, Smooth Muscle, Epithelial Cells","positive"]
["TGFB1 -> FCGR2B","Expression","Furthermore, TGF-beta/D3 treatment (but not D3 alone) elicits the expression of membrane CD14, FcRI, FcRII, CD11a, CD11b, CD11c, ICAM-1, and PECAM-1 Ag at a level comparable to that observed on normal human monocytes., IFN-a, IFN-?, TGF-ß, IL-10, and soluble IgG modulated CD32a and/or CD32b on circulating conventional DCs, which was similar to their effects on cytokine-induced monocyte-derived DCs.","8383719:5, 16167082:1141",2,2,"Homo sapiens","Monocytes","positive"]
["TGFB1 -> FCGR3A","Expression","CD16 expression was increased by 10 ng/ml of TGF-beta 1., In this study we show that the T cell-derived cytokine, IL-4, antagonizes the ability of TGF-beta to induce the expression of CD16., CD16 expression on rheumatoid arthritis blood monocytes was augmented in vitro by IL-10, M-CSF, and TGFbeta1., SCC VII/SF tumors in the oral cavity of the mice secrete high quantities of TGF-beta1, which reduce the expression of NK cell receptor NKG2D as well as CD16 and inhibits biological functions of NK cells., Functional CD16 expression on peripheral blood monocytes was induced with TGFß (32). <more data available...>","7526045:8, 1653804:1, 12384915:8, 16210663:13, 15188374:1182, 12687542:1698, 1309559:100, 8666430:100, 16282534:1054, 16301325:1198 <more data available...>",2,14,"Mus musculus, Homo sapiens","Monocytes, T-Lymphocytes, Killer Cells, Natural, Phagocytes, Macrophages","positive"]
["TGFB1 -> GFAP","Expression","FGF-2 also inhibited the TGF-beta1-mediated increase in GFAP mRNA and protein., Whereas untreated control cells expressed progressively the glial fibrillary acidic protein (GFAP) after arrest of multiplication, the addition of TGF beta 1 to proliferative cells prevented GFAP expression and accumulation of its mRNA., TGF-beta induced CysC and GFAP expression in AP-16 cells, an astrocyte progenitor-like cell line expressing GLAST (a glutamate transporter subtype specifically expressed in immature astrocytes). <more data available...>","9537840:4, 1397085:4, 15509901:2, 8170537:2, 8361632:2, 19057972:3, 12118088:4, 9688751:1192, 11867550:1092, 15078546:100 <more data available...>",2,18,null,"Astrocytes, Neurons","positive"]
["TGFB1 -> GUSB","Expression","Beta-glucuronidase expression was increased by TGF-beta and decreased by IFN-gamma., Cells were counterstained with methylene blue. (c) ß-Glucuronidase production (red staining) was stimulated by TGF-ß in cultured bone-marrow-derived macrophages at day 5.","9712070:10, 12091424:1110",2,2,null,"Granulocytes, Macrophages","positive"]
["TGFB1 -> HBEGF","Expression","We also show that production of sol- and tm-HB-EGF is differentially modulated by TNF alpha and TGF beta., TGF-beta, which is expressed by TbetaT-FH, mediates up-regulation of TGF-alpha and HB-EGF expression in those cells., TGFß induces proHB-EGF shedding and EGFR transactivation through ADAM activation in gastric cancer cells., Figure 5, B and C, illustrates that the expression of both amphiregulin and HB-EGF could be up-regulated in response to treatment with FGF-2 and/or TGF-beta1., The present study extends these previous reports suggesting the involvement of MMPs in the pathophysiology of glomerulosclerosis and adds new evidence that the glomerular MMPs also are involved in TGF-ß-mediated fibronectin synthesis via processing and release of HB-EGF.","15562026:5, 16828470:9, 20934403:100, 10579352:1196, 12164862:1206",2,5,null,"endometrial stromal cells","positive"]
["TGFB1 -> HPGD","Expression","Induction of 15-PGDH expression by TGF-beta1 was synergistically stimulated by the addition of Wnt3A which was inactive by itself., A number of anti-cancer agents, such as transforming growth factor-beta1 (TGF-beta1), glucocorticoids and some histone deacetylase inhibitors were found to induce 15-PGDH expression., Fig. 5. 15-PGDH induction by TGF-ß but not by cell growth arrest., A number of anti-cancer molecules, such as transforming growth factor-ß1, glucocorticoids and some histone deacetylase inhibitors, were found to induce 15-PGDH expression (Tai et al., 2007; Wakimoto et al., 2008), suggesting that their beneficial action may, in part, be related to their ability to induce 15-PGDH expression.","16844092:6, 17481556:12, 15574495:1194, 20023295:1213",2,4,null,null,"positive"]
["TGFB1 -> HSPB1","Expression","Retinoic acid enhanced the TGF-beta-induced increase of mRNA for HSP27., The TGF-beta-stimulated increase in the level of mRNA for HSP27 was also attenuated by T(3)., The TGF-beta1-induced down-regulation of LEDGF, Hsp27, and alphaB-crystallin promoters activity was reversed by cotransfection with a plasmid expressing LEDGF., SP600125, a specific inhibitor of stress-activated protein kinase /c-Jun N-terminal kinase (JNK), markedly reduced the HSP27 expression induced by TGF-beta., TGF-ß1 incubation resulted in increased expression of HSP-27 and decreased expression of HSP-72. <more data available...>","11909638:7, 12706291:3, 12649267:8, 18407296:5, 18577533:1198, 18596079:1181, 16055503:1191, 18552392:1225",2,8,"Homo sapiens, Mus musculus","Osteoblasts, Epithelial Cells, Fibroblasts, renal tubular epithelial cells, Astrocytes","positive"]
["TGFB1 -> ID3","Expression","Expression of ID1 and ID3 mRNA is induced in HUVECs by VEGF or TGFß. a and b, Id1 and Id3 mRNA levels were measured in HUVECs with or without stimulation with VEGF (20 ng/ml), TGFß (0.5 ng/ml) (a), TNF-a (20 ng/ml), or IL-1ß (1 ng/ml) (b) for 24 h.","15494533:1134",2,1,null,"Endothelial Cells","positive"]
["TGFB1 -> IL13RA1","Expression","transforming growth factor-ß can enhance the effects of IL-13 on activation and survival of eosinophils, and on the surface expression of IL-13Ra1 on eosinophils (Myrtek et al., 2004[Go])., As depicted in Figure 1a, transforming growth factor-ß1 (1 ng/ml) upregulated the expression of IL-13Ra1 significantly (mean fluorescence intensity[plusminus]SEM in unstimulated; 10.93[plusminus]1.7 and transforming growth factor-ß1; 14.72[plusminus]2.4, P=0.002, paired t-test, n=7).","16888081:1218, 17235327:1030",2,2,null,"Eosinophils","positive"]
["TGFB1 -> INHBA","Expression","The expression of activin A was induced by TGF-beta 1 or activin A itself., Activin A messenger RNA expression in cultured hepatocytes was increased significantly by TGF-beta1 and by activin A itself., TGF-beta1 highly enhanced expression levels of FLRG mRNA in astroglial cells, compared with those of follistatin and activin A mRNAs., Activin A is a homodimeric protein structurally and functionally related to transforming growth factor beta (TGF-beta), and the expression of activin A is modulated by TGF-beta. <more data available...>","14694161:6, 9496947:8, 12645077:3, 7541220:0, 20573232:7, 11451587:3, 9566800:4, 15001548:1219, 13130463:1146, 19668241:1336 <more data available...>",2,14,"Homo sapiens","Hepatocytes, Astrocytes, Lymphocytes, Null, synoviocytes, Chondrocytes, Hepatic Stellate Cells, myofibroblasts, Macrophages","positive"]
["TGFB1 -> INPP5D","Expression","Activin/TGF-beta-induced expression of SHIP results in intracellular changes in the pool of phospholipids, as well as in inhibition of both Akt/PKB (protein kinase B) phosphorylation and cell survival., TGF-beta1 treatment does not increase IRAK-M or SHIP1 protein expression in shSMAD4 THP-1 cells, whereas it does so in shLUC THP1 cells, indicating that TGF-beta1 regulates IRAK-M and SHIP1 expression through a SMAD4-dependent pathway., Interestingly, the antiinflammatory monokine transforming growth factor-ß/activin induces transcriptional up-regulation of SHIP1. <more data available...>","12447389:5, 20404275:8, 15604218:1211, 15778380:1182, 17947710:1361, 16428799:1147, 16636301:1257, 19542365:1298, 19139077:1132, 19139077:265 <more data available...>",2,20,"Mus musculus","Killer Cells, Natural, Mast Cells, hematopoietic cells, T-Lymphocytes, Regulatory, Macrophages, T-Lymphocytes","positive"]
["TGFB1 -> ITGAX","Expression","Furthermore, TGF-beta/D3 treatment (but not D3 alone) elicits the expression of membrane CD14, FcRI, FcRII, CD11a, CD11b, CD11c, ICAM-1, and PECAM-1 Ag at a level comparable to that observed on normal human monocytes.","8383719:5",2,1,"Homo sapiens","Monocytes","positive"]
["TGFB1 -> ITGB5","Expression","Both PPARalpha ligands also suppressed TGF-beta-induced beta5 integrin mRNA levels., Thus, TGF-beta increases expression of the integrin beta(5) gene by mechanisms involving Sp1/Sp3 and Smad transcription factors., In contrast, Smad3 siRNA significantly attenuated ß5 integrin expression induced by TGFß1 (Fig. 2B). [FIGURE 2.] View larger version: In this window., E. (2002) PPARa inhibits TGF-ß-induced ß5 integrin transcription in vascular smooth muscle cells by interacting with Smad4., Moreover, Transforming growth factor-ß stimulated the ßV-integrin subunit expression and p57kip2proteolysis via Smad signaling in osteoblastic cells (14). <more data available...>","12456495:6, 10964912:9, 18353785:1136, 19244313:1245, 12130649:1043, 17098824:1241, 16249187:1329, 19228122:1069, 14684628:1206, 12456495:3 <more data available...>",2,11,null,"Fibroblasts, Osteoblasts","positive"]
["TGFB1 -> LGALS1","Expression","high glucose conditions and TGF-ß1 treatment augment expression and nuclear translocation of galectin-1., Thus, TGF-beta(1) may trigger a Smad-dependent pathway to control galectin-1 expression, suggesting that distinct mechanisms might cooperate in tilting the balance toward an immunosuppressive environment at the tumor site., PDGF, TGFß and Ang II slightly induced galectin-1 mRNA levels in quiescent venous smooth muscle cells and the PAC1 cells., Interestingly, transforming growth factor beta regulates galectin-1 expression in a dose-dependent manner within breast cancer cells.19 Transforming growth factor beta is present in two thirds of primary classic Hodgkin lymphoma tumors20 and within Hodgkin Reed-Sternberg cell lines.21 .","20828557:4, 16900348:5, 10728371:1252, 17438085:1104",2,4,"Homo sapiens","Epithelial Cells, Myocytes, Smooth Muscle, T-Lymphocytes","positive"]
["TGFB1 -> MCL1","Expression","We have shown that TGF-ß promotes osteoclast survival in part by rapid stimulation of Bcl-XL and Mcl-1 expression (12)., The increased levels of the cytokines, IL-4, IL-10, prostaglandin E2, and TGF-ß enhance the expressions of c-FLIP, Bcl-xL, and Mcl-1, which are involved in the resistance to apoptosis (32-34).","20181800:1072, 16740684:1107, 9163473565e7552cff17c5039d90b0c5",2,3,null,"Osteoclasts, Macrophages","positive"]
["TGFB1 -> MET","Expression","In contrast, a combination of IL-6 and TGFbeta1 down-regulated c-met expression as well as Sp1 DNA binding activity., Real-time RT-PCR and Northern and Western blot analyses revealed that TGF-beta1 significantly induced c-met expression in HKC cells, which primarily took place at the gene transcriptional level., Transforming growth factor-beta, a negative regulator of fetal liver growth, increased c-met mRNA levels 48 hours after the addition of the factor, whereas glucocorticoids had a negative effect., We report that c-met message and protein levels are up-regulated by the cytokines IL-5, IL-10, TGF-beta, PDGF and basic FCF while down-regulation occurred after treatment with IFN-gamma. <more data available...>","11469916:13, 15339794:3, 7526865:4, 21594411:3, 18652820:6, 15770602:6, 15675950:1113",2,7,"Rattus norvegicus, Homo sapiens","mesothelial cells, Fibroblasts","positive"]
["TGFB1 -> NCF1","Expression","In addition, LPS-induced ERK phosphorylation and subsequent Ser345 phosphorylation on p47phox were significantly inhibited by TGF-beta1 pretreatment., TGF-beta1 at 10 ng/mL significantly increased the intercellular reactive oxidative species production and p47phox expression (P < 0.05)., Transfection of wild-type mouse cardiac fibroblasts with AAV/TGFbeta (ACT)(1) markedly enhanced the expression of NADPH oxidases (p22(phox), p47(phox), and gp91(phox) subunits) and LOX-1, formation of reactive oxygen species, and collagen synthesis, concomitant with an increase in the activation of p38 and p44/42 mitogen-activated protein kinases . <more data available...>","18566433:6, 19292057:5, 18182394:3, 12874439:1080",2,4,"Rattus norvegicus, Mus musculus","dopaminergic neurons, Fibroblasts, Mesangial Cells","positive"]
["TGFB1 -> NFATC1","Expression","Similarly, TNF-alpha activates osteoclastogenesis by stimulating translocation of TGF-beta-induced NFATc1., Addition of Transforming growth factor-ß during differentiation to either lineage inhibited NFATc activation., Using quantitative real-time PCR, we found that transforming growth factor-ß1 treatment results in a 4.5-fold increase in NFATc1 transcript levels in neural crest stem cells (Fig. 6).","18060870:6, 12810687:1296, 15148306:1175",2,3,null,"Monocytes, Th1 Cells, Stem Cells","positive"]
["TGFB1 -> NR3C1","Expression","Therefore, we conclude that glucocorticoid receptor function is mediated by the activation of latent-TGF beta 1 in MG-63 osteosarcoma cells., Therefore, it is conceivable that uPA, TGF beta 1 and IGF-I mediate at least in part cell-cell interactions and glucocorticoid receptor function in osteoblastic metastases., These data suggested that TGFbeta1, uPA, and IGF-I mediate at least in part cell-cell interactions and glucocorticoid receptor function in PA-III prostate cancer and UMR 106 osteosarcoma cells., TGF-ß1 increases glucocorticoid receptor expression by up-regulating glucocorticoid receptor gene transcription.","7768643:4, 9179184:7, 9174122:7, 12753290:1130",2,4,null,"Osteoblasts","positive"]
["TGFB1 -> PTGS1","Expression","Release of histamine, cysteinyl-leukotrienes, and tumour necrosis factor alpha was strongly reduced whereas prostaglandin D2 generation and cyclooxygenase 1 and 2 expression were upregulated by TGF-beta1., Prostaglandin E2, transforming growth factor-beta, and interleukin-1 beta variably regulate the expression of cyclooxygenase 1, cyclooxygenase 2, and lysyl oxidase in IMR90, human embryo lung fibroblasts., In a few experiments in MC3T3-E1 cells, TGFbeta stimulated PGHS-1 messenger RNA levels up to 5-fold at 4 h, with little change in glyceraldehyde 3-phosphate dehydrogenase (Fig. 1). <more data available...>","15951536:7, 8872612:0, 9348193:1158, 7536192:1058",2,4,"Bos taurus","Mast Cells, Fibroblasts, Endothelial Cells","positive"]
["TGFB1 -> PTGS2","Expression","TGFbeta-stimulated luciferase activity paralleled PGHS-2 messenger RNA induction., The addition of TGF-beta1 further stabilized the COX-2 mRNA (t1/2 > 50 min)., Transforming growth factor-beta1 (TGF-beta 1) is one of the most potent stimulators of cyclooxygenase-2 expression., TGFbeta1 increased COX2 expression in astrocytes and neurons., TGF-beta 1 induced COX-2 mRNA, COX-2 protein and PGE(2) biosynthesis., Both TGF beta and TNF could independently increase COX-2 mRNA levels and Prostaglandin biosynthesis. <more data available...>","9348193:9, 10692471:6, 10455907:1, 9681442:12, 15288474:6, 9093911:6, 18316610:4, 17302909:7, 10069452:8, 9815044:7 <more data available...>",2,95,"Homo sapiens, Rattus norvegicus, Mus musculus, Bos taurus","Epithelial Cells, Neurons, Hepatic Stellate Cells, Osteoblasts, Fibroblasts, Macrophages, Hepatocytes, Mesangial Cells, endometrial stromal cells, Astrocytes <more data available...>","positive"]
["TGFB1 -> PTK2","Expression","TGFbeta1 also stimulated surface expression of integrin alphavbeta3 and FAK activation., The expression of focal adhesion kinase and integrin-linked kinase proteins was also upregulated by treatment with TGF-beta., Our results showed that TGF-beta 1 could rapidly attenuated cell adhesion onto Fn without changing the expression of alpha 5 beta 1 integrin, and at the meantime dephosphorylated FAK., In addition to that, Hcy-mediated TGF-beta1 induction was inhibited by TGF-beta R1 kinase inhibitor II (ALK5 inhibitor II) and attenuated FAK phosphorylation and alpha-smooth muscle actin expression. <more data available...>","12234017:3, 20410683:7, 12549072:3, 16972260:8, 19340459:2, 18669633:3, 12733346:4, 18787183:4, 11477097:1141, 18583311:100 <more data available...>",2,12,"Homo sapiens, Mus musculus","myofibroblasts, Endothelial Cells, Epithelial Cells, Fibroblasts","positive"]
["TGFB1 -> PTPRC","Expression","intravenous immunoglobulin suppressed cord blood mononuclear cells and CD3(+) T-cells proliferation, secretions of IL-10, INF-? and TGF-ß(1), but not IL-4, and PHA-induced expressions of surface molecules (CD25, CD45RA and CD45RO), with more pronounced effects for cord blood mononuclear cells., Purified B cells (B220+) were stimulated with 10 µg/mL lipopolysaccharide for 48 hours with or without 3 ng/mL TGF-ß1., Tran et al. demonstrated that TGF-ß is required for induction of FOXP3 expression, particularly in naive CD4+CD25-CD45RA+ T cells, and less so in memory CD4+CD25-CD45RA- T cells.","20880351:2, 12920022:1097, 18270368:1286",2,3,null,"T-Lymphocytes, B-Lymphocytes","positive"]
["TGFB1 -> RBP1","Expression","In both cell populations, transforming growth factor-beta 1 treatment increased CRBP-1 expression., We also demonstrate that CRBP-1 expression by fibroblasts is regulated in vitro by retinoic acid and transforming growth factor-beta1., The expression of CRBP-1 is regulated at the transcriptional level by TGF-beta and retinoic acid but not synergistically, suggesting a possible common pathway., TGF-ß1 should be capable of diffusing through the microporous membrane, subsequently modulating CRBP-1 transcription.","12004002:12, 9403724:10, 11319755:4, 12419830:1201",2,4,"Rattus norvegicus","Fibroblasts","positive"]
["TGFB1 -> S100A4","Expression","TGF-beta1 increased S100A4 expression in cultured ileal fibroblasts., In vitro experiments using human dermal microvascular endothelial cells demonstrated that TGF-beta1 induced myofibroblastic features in human dermal microvascular endothelial cells, including spindle cell morphology, reduction of CD34 expression, and induction of S100A4, alpha-smooth muscle actin, and COL1A1 expression, as well as the increased nuclear expression of phospho-Smad2., TGF-ß1 induced an increase in the expression of fibroblast-specific protein-1 and a decrease in the expression of CD31. <more data available...>","20489045:10, 19608867:2, 17974953:1193, 11967021:1076, 17562716:1290, 16571622:1253, 10504497:1057, 19506550:1180, 20592463:9, 20070253:8 <more data available...>",2,16,"Homo sapiens, Mus musculus","Fibroblasts, Endothelial Cells, Hepatocytes, Epithelial Cells","positive"]
["TGFB1 -> S100A6","Expression","The above data suggest that NF-?B activation and subsequent binding to an NF-?B-binding site correlates with the induction of S100A6 promoter activity by PDGF, transforming growth factorß, and TNF-a. [FIGURE 8.] View larger version: In this window.","18753141:1246",2,1,null,null,"positive"]
["TGFB1 -> SMAD7","Expression","TGF-beta increased Smad7 expression at both 4 and 24 hours., Lipopolysaccharide reduced whereas TGF-beta1 increased smad-7 expression., In this report, we show that TGF-beta can stabilize Smad7 mRNA and activate Smad7 transcription., The levels of Smad 7 mRNA was rapidly and transiently increased by TGF-beta., Smad7 mRNA was inhibited by TGF-beta, but augmented by coincubation with EM-A or EM703., Moreover, whereas the phorbol ester PMA alone had no effect, it potentiated the TGF-beta1-induced expression of Smad7 mRNA. <more data available...>","19374154:7, 20632282:12, 10823886:3, 9886263:3, 18600500:4, 9712726:4, 11325521:5, 11716483:0, 18704440:6, 16837618:5 <more data available...>",2,100,"Homo sapiens, Rattus norvegicus, Mus musculus, Mammalia","Fibroblasts, Mesangial Cells, Eosinophils, myofibroblasts, Podocytes, Keratinocytes, Neurons, Astrocytes, Odontoblasts, Muscle Cells <more data available...>","positive"]
["TGFB1 -> SOCS3","Expression","TGF-beta inhibits IL-6-induced SOCS3 promoter activity in T cells., These data show that TGF-beta coordinately induces LIF and SOCS3 to promote prosurvival signaling., Furthermore, TGF-beta rapidly induces sustained SOCS-3 expression in macrophage/osteoclast precursors., In this study, we demonstrate that LPS-induced endogenous TGF-beta1 contributes to the inducible SOCS3 expression in macrophages., This suggests that TGF-beta-induced expression of SOCS3 may represent a crucial mechanism by which TGF-beta antagonizes specific anti-osteoclastic JAK/STAT signals, priming precursors for resorption rather than inflammatory functions. <more data available...>","19535626:4, 20181800:8, 12646633:7, 17920684:3, 13679037:8, 18031698:1059",2,6,null,"T-Lymphocytes, Osteoclasts, Macrophages","positive"]
["TGFB1 -> SOX9","Expression","Moreover, exogenous TGF-beta can induce Sox9 expression in the mandibular arch., In contrast, TGF-beta-stimulated COL2A1, aggrecan, and SOX-9 mRNA levels were abrogated by IL-1beta., In addition, up-regulation of Fibronectin and suppression of Sox9 expression by TGF-beta1 was also found to be mediated by CTGF., Transforming growth factor-beta treatment increased MAPK activity and Sox-9, aggrecan, and collagen type II gene expression., TGF-beta1 increased the Sox9 messenger ribonucleic acid expression to 180% compared to control group in intervertebral disc tissue. <more data available...>","18684439:6, 17604656:13, 17111364:7, 15564911:11, 20157375:7, 20590658:6, 19096623:9, 18496879:5, 16575901:3, 17525254:5 <more data available...>",2,21,"Bos taurus, Rattus norvegicus, Homo sapiens","Chondrocytes, Mesenchymal Stem Cells, Mesangial Cells, Hepatic Stellate Cells, chondroblasts","positive"]
["TGFB1 -> SRGN","Expression","Metabolic labeling experiments reveal that TGF-beta induces selectively the expression of proteoglycan-I, whereas the level of proteoglycan-II remains unaltered., A transforming growth factorß response element was identified in the promoter of the a1(I) collagen gene, and transforming growth factorß1 increased the stability of mRNA for a1(I) collagen in confluent cultures of fibroblasts.42 Also, transforming growth factorß2 knockout mice have a reduced corneal stroma layer compared with normal mice, which indicates that transforming growth factorß2 plays an important role in embryonic corneal development, which shares some key process with corneal wound healing.53 In addition to its effects on collagen synthesis, transforming growth factorß1 increases the synthesis of the chondroitin sulfate proteoglycan core protein and the mass of the glycosaminoglycan side chains.54 Besides its direct effects on extracellular matrix gene expression, transforming growth factorßs also could have indirect effects on corneal scar formation by altering the levels of the proteases that degrade matrix proteins and their inhibitors.","1863601:2, 11095603:1224",2,2,"Homo sapiens","Fibroblasts","positive"]
["TGFB1 -> STAT1","Expression","IFN-gamma down-regulates TGF-beta1-induced IgA expression through Stat1 and p300 signaling.","20016942:100",2,1,null,null,"positive"]
["TGFB1 -> SYNPO","Expression","Anti-TGF-ß antibody 2G7 blocked synaptopodin expression and inhibited the redistribution of zona occludens-1 (Figure 1D).","16207831:1114",2,1,null,"Podocytes","positive"]
["TGFB1 -> TF","Expression","However, in quiescent, well-differentiated cells, TGF-beta repressed the mitogenic responses to both nutrients alone (by 90%) and to nutrients plus the exogenous stimulatory factors epidermal growth factor (E), insulin (I), and transferrin (T) (by 55-65%)., TGF-beta(1) and bFGF upregulate transferrin gene expression of cultured lens epithelial cells remarkably, can reduce lenticular oxidative damaging process in which transferrin participates and play an important role in the pathological mechanism of cataract formation after extracapsular cataract extraction.","1701348:3, 11835825:8",2,2,null,"Epithelial Cells","positive"]
["TGFB1 -> TGFB2","Expression","TGF-beta1 stimulated TGF-beta2 production (p < 0.01 relative to control)., In contrast, incubation with TGF-beta1 increased fibronectin, procollagen, vascular endothelial growth factor (VEGF), and TGF-beta2 protein production (P < .05)., In the present study, we show that hypoxia-induced TGF-beta2 gene expression is dependent on thrombospondin-1-mediated bioactivation of latent TGF-beta., As previously reported for the mouse fibroblast cell line AKR-2B, the expression of TGF-beta 2 mRNA transcripts of 5.4, 4.7, 3.7 and 3.0 kb was decreased after a 24 hr treatment with 5 ng/ml of TGF-beta 1, TGF-beta 2 or TGF-beta 3. <more data available...>","12772773:7, 12546137:6, 18090870:8, 12411310:2, 1389225:1, 20573232:7, 17651146:7, 17332363:1164, 10886500:1308, 9492075:1234 <more data available...>",2,25,"Homo sapiens, Mus musculus, Rattus norvegicus, Bos taurus","Fibroblasts, Endothelial Cells, Lymphocytes, Null, Epithelial Cells, Stromal Cells","positive"]
["TGFB1 -> TGFBR1","Expression","In contrast, both TGF-beta and Ang II increased TGF-beta receptor I mRNA to about 260% or 180% of controls (P<0.05)., Interestingly, TGF-beta1 differentially stimulated or inhibited the expression of TbetaR-I and TbetaR-II mRNA in the gliomas., Furthermore, this truncated Smad4 functioned as a dominant negative form in TGF-beta1-mediated reporter activity and TGF-beta1 receptor expression., TGF-beta1 treatment increased the expression of TGF-beta1, TbetaR-I and TbetaR-II in mesenchymal cells in the cambium layer at 7 days in culture. <more data available...>","10426193:8, 10048979:3, 12860278:5, 12038632:8, 10861501:5, 9490005:3, 9516449:3, 15577613:5, 19091788:9, 19038005:5 <more data available...>",2,53,"Homo sapiens, Mus musculus","Fibroblasts, Osteoclasts, renal tubular epithelial cells, Macrophages, Endothelial Cells, Osteoblasts, Granulosa Cells, basal cells, Epithelial Cells, Chondrocytes <more data available...>","positive"]
["TGFB1 -> TGFBR2","Expression","These data indicate that TGFB1-insensitivity in LbetaT2 cells results from a deficiency in Tgfbr2 expression., Dysregulated TGF-beta signalling may result from mutations in TGFBR1 and TGFBR2 genes, thus resulting in degenerative changes in the vessel wall., Expression of the transforming growth factor-beta type II receptor (TGF-beta RII) is highly regulated and is a critical determinant of the cellular response to TGF-beta., TGF-beta1 treatment increased the expression of TGF-beta1, TbetaR-I and TbetaR-II in mesenchymal cells in the cambium layer at 7 days in culture. <more data available...>","16384533:13, 18550062:2, 11179682:0, 12038632:8, 10861501:5, 9167190:2, 9516449:3, 11290556:6, 12198207:11, 19088080:4 <more data available...>",2,24,"Homo sapiens, Rattus norvegicus","Epithelial Cells, Fibroblasts, Endothelial Cells, Muscle Cells, T-Lymphocytes, Myeloid Cells","positive"]
["TGFB1 -> TGM2","Expression","TGase 2 mRNA expression was up-regulated as the result of TGF-beta treatment in competitive RT-PCR., Transforming growth factor-beta and interleukin -1beta induced Factor XIIIa and tTGase expression in cartilage and meniscal organ cultures., This study suggests that in the isolated perfused rat kidney and in the absence of other exogenous growth factors, TGF-beta1 selectively increases the synthesis of extracellular matrix and tissue transglutaminase without changes that would result in the reduction of extracellular matrix degradation. <more data available...>","16044258:6, 11438463:3, 10505687:11, 17460246:6, 12874459:1070, 10892867:1253, 9582307:1045, 9114053:1188, 18235007:1172, 14555988:1123 <more data available...>",2,25,"Homo sapiens, Rattus norvegicus","Fibroblasts, Keratinocytes, Epithelial Cells","positive"]
["TGFB1 -> THBS2","Expression","Using this assay, we observed that thrombospondin-1 and CISP/thrombospondin-2 syntheses were respectively stimulated threefold and twofold by a 24-h treatment with 2 ng/ml TGF beta 1., After 96 h of treatment, TSP-1 and TSP-2 mRNA levels were significantly increased (p < 0.05) by TGFbeta1 treatment, which also inhibited HP75 cell growth., Further, p38 MAPK mediated induction of collagen I and TSP-2 expression by TGF-beta1 was still achieved in the presence of dexamethasone, showing that dexamethasone does not block p38 while it delays Smad2 phosphorylation and antagonizes stimulation of a Smad3/Smad4 dependent TGF-beta reporter construct. <more data available...>","7698241:4, 15347840:5, 15905080:5, 15616224:1300",2,4,"Homo sapiens, Bos taurus","Hepatic Stellate Cells","positive"]
["TGFB1 -> VEGFA","Expression","Retinoic acid enhanced the TGF-beta-increased levels of VEGF mRNA., TGF beta-1 significantly (P < .05) increased production of VEGF., TGF-beta and hypoxia synergistically induced VEGF mRNA expression., Receptor restoration also changed the levels of VEGF mRNA induced by TGF-beta(1)., Transforming growth factor -beta is a potent stimulator of VEGF expression in vitro., T(3) enhanced the TGF-beta-induced increase in the levels of mRNA for VEGF., Actinomycin D inhibited the TGF-beta1-induced peak in VEGF mRNA, whereas cycloheximide did not. <more data available...>","12801520:9, 9416408:8, 11678207:6, 12399125:6, 11115468:2, 12706291:5, 10516092:5, 8603372:2, 15347840:4, 11779736:13 <more data available...>",2,100,"Homo sapiens, Rattus norvegicus, Mus musculus, Bos taurus","Osteoblasts, mesothelial cells, Fibroblasts, Hepatic Stellate Cells, Blood Platelets, Myocytes, Smooth Muscle, Epithelial Cells, Mesenchymal Stem Cells, Monocytes, Endothelial Cells <more data available...>","positive"]
["TGFB1 -> VIM","Expression","Translation of SMAD2 mRNA as well as TGF-ß-induced cell motility and vimentin expression was regulated by MNK1 signaling., Furthermore, induction of vimentin expression by TGF-beta1 and hypoxia was evaluated in gastric cancer cells., Here, we suggest a mechanism to explain how TGFbeta1 contributes to the up-regulation of vimentin expression while blocking myogenesis., Western blotting analysis showed that TGF-beta1 decreased cytokeratin and increased vimentin levels, while DMSO decreased both cytokeratin and vimentin. <more data available...>","21406405:7, 20358301:4, 17270292:2, 10580588:7, 20727350:6, 20671927:3, 20958047:7, 19213777:6, 21418395:5, 1879463:2 <more data available...>",2,61,"Mus musculus, Rattus norvegicus, Homo sapiens","Stromal Cells, Fibroblasts, mesothelial cells, Epithelial Cells, Hepatocytes, myofibroblasts","positive"]
["TGFB2 -> CLU","Expression","Transforming growth factor-ß2 increased SA-ß-Gal activity, lipid peroxidation, and the mRNA expressions of Apo J, SM22, and SPARC., Apo J mRNA expression was maximally increased by 2.5 ± 0.5-fold after transforming growth factor-ß1 and by 3.5 ± 0.2-fold after transforming growth factor-ß2 treatment (Fig. 5A) .","20554622:9, 19171648:1210",2,2,null,null,"positive"]
["TGFB2 -> HSPB1","Expression","Both H(2)O(2) and TGF-beta2 increased the Hsp27 expression.","18552392:9",2,1,null,null,"positive"]
["TGFB2 -> INPP5D","Expression","During glucocorticoid conditioning of bone marrow Mf, TGF-ß1 and TGF-ß2 mRNA and protein expression were found to increase in parallel to SHIP1 expression.","17947710:1361",2,1,null,null,"positive"]
["TGFB2 -> ITGB2","Expression","TGF-ß-neutralizing Antibody Abrogates all-trans-retinoic acid- and TGF-ß2-induced MUC4 Expression in CD18/HPAF-SF Cells.","10938282:1204",2,1,null,null,"positive"]
["TGFB2 -> PTGS2","Expression","We found that TGF-beta2 and FGF-2 oppositely affect bovine corneal endothelial cell proliferation and TGF-beta2 can override the stimulating effects of FGF-2 by increasing COX-2 expression in these cells.","16963022:7",2,1,"Bos taurus","Endothelial Cells","positive"]
["TGFB2 -> PTK2","Expression","By immunofluorescence staining and western blotting, we observed that TGF-beta2 markedly enhanced the expression of integrin beta1 and the Tyr-phosphorylation of focal adhesion kinase (FAK).","17960115:9",2,1,null,"Epithelial Cells","positive"]
["TGFB2 -> SMAD7","Expression","The addition of transforming growth factorß2 to siSmad4-transfected cells induced a significant increase in Smad7 gene expression (210% ± 12%) compared with that in the unstimulated siSmad4 group.","19516008:1195",2,1,null,null,"positive"]
["TGFB2 -> TGFB1","Expression","TGF beta 2 had similar effects on Osteopontin gene expression as TGF beta 1., Immunolocalization showed that exogenous TGF-beta(2) stimulates increased expression of endogenous TGF-beta(1)., Transforming growth factor-beta 2 treatment of trabecular cells also increased their expression of the TGF-beta 1 gene., Moreover, injection of TGF-beta 2 stimulated synthesis of TGF-beta 1 in chondrocytes and osteoblasts within the newly induced bone and cartilage, suggesting positive autoregulation of TGF-beta., Active TGF beta downregulated its mRNA-expression: after 6 days TGF beta(1)-mRNA was reduced to 55.1+/-11.0%, TGF beta(2)-mRNA to 30.1+/-16.5%, and TGF beta(3)-mRNA to 0.3+/-0.4% in 20% FCS-cultures as compared to their expression in freshly isolated cells (n=4, P<0.05). <more data available...>","3166460:11, 17163882:7, 8977496:11, 2351696:4, 10640441:6, 16301614:1276, 20952520:1119, 12429716:1168, 12911534:1234, 17502504:1165 <more data available...>",2,19,"Homo sapiens","Chondrocytes, Myocytes, Cardiac, T-Lymphocytes, Fibroblasts, Neutrophils, B-Lymphocytes","positive"]
["TGFB2 -> TGM2","Expression","Treatment of subconjunctival fibroblasts with TGF-beta2 caused an increase in activation and expression of tTgase., TGF-beta 2 treatment upregulated the expression of Col1 alpha 1, Col4 alpha 2, fibronectin, CTGF, TGM2, and TSP-1 mRNA and protein in cultured astrocytes., Increased levels of TGF-beta2 in the aqueous humor may lead to an increase of tTgase expression and activity in the human trabecular meshwork, causing an increase of irreversibly cross-linked extracellular matrix proteins., TGF-beta2 markedly induced expression of cell-surface tissue transglutaminase on retinal pigment epithelial cells and increased attachment and migration on fibronectin and collagen type I. <more data available...>","17460246:5, 15671284:4, 10892867:13, 14985317:7, 16936095:1247, 14691167:1041",2,6,null,"Fibroblasts, Astrocytes, Epithelial Cells","positive"]
["TGFB2 -> THBS2","Expression","Among members of the TGF beta family, TGF beta 1 and TGF beta 2 and to a lesser extent activin could stimulate thrombospondin-1 and CISP/thrombospondin-2 synthesis, whereas inhibin and Müllerian inhibiting substance were inactive.","7698241:7",2,1,null,null,"positive"]
["TGFB2 -> VEGFA","Expression","Intrapleural injection of TGF-beta(2) induced a dose-dependent increase in VEGF production., Stimulation of VEGF expression by TGF-beta2 was blocked by cycloheximide, suggesting that de novo protein synthesis is required., The thrombin-induced calcium mobilization may play an important permissive role in maximizing TGF-beta2-induced VEGF expression in RPE cells., Exogenous TGFbeta2 stimulates VEGF production in a dose-dependent fashion (0-400pg/ml) through a MAPK-dependent pathway, but also inhibits capillary network formation. <more data available...>","11779736:5, 17331500:4, 17525207:9, 16414296:7, 10830293:1292, 16162788:1177",2,6,"Homo sapiens","Monocytes, mesothelial cells","positive"]
["TGFBR1 -> CSF1R","Expression","TGF-ß1-induced expression of c-fms in EM42 cells and epithelial cells is inhibited by TGFBR I antagonists and p38 inhibitor.","19505996:1179",2,1,null,"Epithelial Cells","positive"]
["TGFBR1 -> PTGS2","Expression","Interestingly, administering a TßR-I antagonist to quiescent 4T1 cells significantly reduced their expression of Cox-2 messenger RNA and protein (Figure 1F).","18725385:1117",2,1,null,"fibroblastoids","positive"]
["TGFBR1 -> TGFB1","Expression","This persistence was because of autocrine synthesis of TGF-beta1, which was inhibited by both anti-TGF-beta1 antibody and the ALK5 inhibitor SB431542., Based on these findings, we hypothesize that the interaction between c-Ski and TßRI might interfere with nuclear translocation of the R-Smad/Smad4 complex, thereby attenuating TGF-ß signaling., These results show that constitutively reduced Tgfbr1-mediated TGF-beta signaling significantly enhances colorectal cancer development and results in increased tumor cell proliferation. <more data available...>","19193641:6, 20959473:4, 19147584:4, 19535626:7, 19432813:7",2,5,"Homo sapiens","myofibroblasts, T-Lymphocytes, Mesenchymal Stem Cells","positive"]
["TGFBR2 -> PTGS2","Expression","The reduced expression of TbetaRII, increased expression of COX-2, and the ability to form colonies in Matrigel were all reversible upon withdrawal of exogenous TGF-beta1 for the RIE-Tr cells., MDA-MB-231 cells overexpressing dominant-negative TGFbeta type II receptors showed decreased bone metastases and reduced osteoclastic bone resorption with impaired COX-2 expression.","10023661:11, 16489006:7",2,2,null,"Osteoclasts","positive"]
["TGFBR2 -> VEGFA","Expression","VEGF expression was stimulated by ALK5, TßRII, and SMAD2, and inhibited by BMP-9 via ALK1, BMPRII, and SMAD1.","19506300:1238",2,1,null,null,"positive"]
["TGM2 -> ABCA1","Expression","retinoic acid-stimulated expression of ABCA1 was attenuated in TG2-/- bone marrow macrophages in vitro., Transglutaminase-2 deficiency in bone marrow cells, shown to impair apoptotic cell phagocytosis and macrophage ABCA1 expression in vitro, did not significantly alter necrotic core formation in low-density lipoprotein receptor-deficient mice and led to a small increase in lesion size,33 which suggests only a modest role in vivo compared with Mfge8.","16410462:1175, 17420351:1220",2,2,null,"Macrophages","positive"]
["TGM2 -> CYBB","Expression","Inhibition of cross-linking activity of TG2 by monodansylcadaverin in these cells led to diminished nitroblue tetrazolium positivity, production of less superoxide anion, and decreased expression of GP91PHOX, the membrane-associated subunit of NADPH oxidase.","16763214:3",2,1,null,null,"positive"]
["TGM2 -> TGFB1","Expression","In addition, TG2 also activates transforming growth factor-beta (TGF-beta)., Particularly relevant is the finding that both TGF-beta and IL-12 regulations were significantly altered in the absence of TG2., Free Gd3+ ions may also activate tissue transglutaminase, which in turn activates transforming growth factor beta (TGF-beta) produced by dendritic cells., Increased TG2 expression in these fibroblasts led to NF-kappaB activation, resulting in the increased expression of transforming growth factor beta(1). <more data available...>","18688035:2, 15905580:8, 19886227:11, 19657147:2, 18558621:6, 12810961:2, 18523305:1259, 15199098:1330, 11686302:1320",2,9,null,"Macrophages, Dendritic Cells, Fibroblasts, Mesangial Cells","positive"]
["TGM2 -> ZEB2","Expression","Slug, Zeb1, and Zeb2 mRNA levels were increased in OV90-TG2 compared with control cells.","19951993:1247, 19951995:1247",2,2,null,null,"positive"]
["TLR2 -> CCL3","Expression","lower m.w. hyaluronan-induced MIP-1a expression requires the TLR2 receptor., B, Optimum MIP-1a and RANTES production in response to PorB is dependent on the expression of TLR2., In some experiments, TLR2 stimulation appeared to preferentially induce the transcripts of specific chemokines, such as IL-8 and MIP-1a., Compared with wild-type mice, lesion-induced levels of CCL3, CCL4, CXCL2, and CXCL10 mRNA were significantly reduced in the absence of TLR2 signaling (Fig. 2B)., In contrast, TLR2 activation by Tc52 resulted in IL-8, MCP-1, and MIP-1a production, whereas no secretion of TNF-a occurred. <more data available...>","16818787:1208, 17709538:1252, 11477091:1180, 17151286:1198, 12055254:1319, 19155492:1344, 15819701:1276, 11477091:181, 19155492:345",2,9,"Homo sapiens","Macrophages, Peritoneal, Macrophages, Monocytes","positive"]
["TLR2 -> CD80","Expression","In summary, anti-TLR2 blocked the lipopeptide-induced increase in CD80 median fluorescence intensity and the increase in the percentage of cells positive for CD80., TLR2 and TLR4 differentially regulate B7-1 resulting in distinct cytokine responses to the mycoplasma superantigen MAM as well as to disease induced by Mycoplasma arthritidis., The TLR2 agonist Pam3Cys significantly stimulated the maturation of DCs by enhancing the surface expression of CD11c, MHC class I, MHC class II, CD40, CD80, and CD86., The synthetic hBD-3-induced shift in CD80 expression was partially inhibited by GD2.F4 or by TLR2.5 (mean percent inhibition ± SEM, 53 ± 6%, n = 4; and 57 ± 6%, n = 4, respectively). <more data available...>","11160304:1193, 16469054:100, 19109203:1127, 18006661:1115, 12704121:1267, 19923446:1185",2,6,"Homo sapiens","Dendritic Cells, Monocytes","positive"]
["TLR2 -> CD86","Expression","Systemic administration of ligands for TLR2 or -4 in human artery-artery-severe combined immunodeficient chimeras drives differentiation of adventitial DCs into chemokine-producing effector cells with high-level expression of both CD83 and CD86 and mediates T-cell regulatory function through release of interleukin 18., Toll-like receptor2-mediated enrichment of CD86 and MHC class II expression by polysaccharide A-stimulated bone marrow-derived DCs., There may be some differences in the Toll-like receptor2-mediated signaling pathway between cytokine production and CD83/CD86 expression. <more data available...>","16461802:6, 17178920:1159, 11160323:1246, 19109203:1127, 18462086:1175, 19930041:1428, 18217947:1256, 19297478:1234, 19923446:1185, 11823477:142 <more data available...>",2,19,"Homo sapiens","T-Lymphocytes, Dendritic Cells, Macrophages, B-Lymphocytes","positive"]
["TLR2 -> CEBPB","Expression","The TLR2 agonist Pam(3)CSK(4) was also shown to induce ASK1 Ser967 dephosphorylation, JNK and c-jun phosphorylation, C/EBPbeta activation, and COX-2 expression in RAW 264.7 macrophages., Signaling by the TLR2 agonist LpqH induced expression of C/EBPß and its binding to CIITA promoter I and promoter IV., The mycobacterial lipoprotein and Toll-like receptor2 agonist LpqH induces expression of the transcription factor C/EBPß, which can act as a transcriptional activator or repressor, depending on the promoter and stimulus. <more data available...>","20200402:8, 17982082:1418, 19629181:1341, 19454718:1183, 19629181:342, 19454718:184",2,6,null,"Macrophages","positive"]
["TLR2 -> CEBPD","Expression","Toll-like receptor2 stimulation also induces C/EBPd expression and binding to the CIITA promoter [31]., TLR2 signaling by LpqH induced expression of liver inhibitory protein and C/EBPd and enhanced expression of LAP at time points that correlated kinetically with the onset of inhibition of IFN-?-induced CIITA expression.","19629181:1348, 17982082:1080, 19629181:349",2,3,null,"Macrophages","positive"]
["TLR2 -> DUSP1","Expression","Anti-TLR2 antibodies, as well as specific ERK and p38 MAPK inhibitors, decreased MKP-1 transcription in lipomannan-stimulated cells.","18201568:3",2,1,null,"Macrophages","positive"]
["TLR2 -> HSPB1","Expression","TLR1/2 ligand palmitoyl-3-cysteine-serine-lysine-4 (Pam3CSK4) induces activation of PKDs via a PKC-independent manner, and Pam3CSK4-induced expression of heat shock protein 27 and MCP-1, as well as activation of PKDs, is inhibited by Gö6976, but not by broad-spectrum PKC inhibitors, in mouse bone marrow-derived mast cells (26).","19414785:1064, 19414785:65",2,2,"Mus musculus","Mast Cells","positive"]
["TLR2 -> ITGAX","Expression","The TLR2 agonist Pam3Cys significantly stimulated the maturation of DCs by enhancing the surface expression of CD11c, MHC class I, MHC class II, CD40, CD80, and CD86.","19109203:1127, 19109203:128",2,2,null,"Dendritic Cells","positive"]
["TLR2 -> ITGB2","Expression","Peptidoglycan (TLR2 ligand), flagellin (TLR5 ligand), and Imiquimod R837 (TLR7 ligand) could significantly upregulate cell surface expression of intercellular adhesion molecule (ICAM)-1 and CD18, and induce the release of IL-1beta, IL-6, IL-8, growth-related oncogene -alpha, and superoxides of eosinophils., It therefore appears that fimbriae influence TLR2-dependent cellular activation through interactions with at least two functionally associated pattern recognition receptors , CD14 and CD11b/CD18., Based on earlier findings that P. gingivalis fimbriae bind CD14 and stimulate TLR2/PI3K-mediated inside-out signaling for CD11b/CD18 activation (11, 27), we now show that activation of this pathway leads to increased monocyte adhesion to fibrinogen, ICAM-1, and endothelial cells.","17332440:5, 16988241:1069, 16751412:1065",2,3,"Mus musculus","Eosinophils, Macrophages, Endothelial Cells","positive"]
["TLR2 -> LCN2","Expression","LCN2 expression is increased in response to activation of TLR2 and TLR4 signaling by bacterial peptides (42)., Also, our in vitro experiments suggest that toll-like receptor2 and toll-like receptor4 activation and in particular IL-1ß, strongly induce NGAL/lipocalin-2 expression in neonatal cardiomyocytes.","18317594:1267, 19329498:1186",2,2,null,"Keratinocytes, Myocytes, Cardiac","positive"]
["TLR2 -> PTGS2","Expression","Furthermore, costimulation with the TLR2 ligand Pam3Cys also led to enhanced COX-2 mRNA., Administration of TLR2 neutralizing antibody effectively inhibited peptidoglycan-induced iNOS and COX-2 expression., Finally, adenylate cyclase toxin and TLR2 or TLR4 act synergistically to increase COX-2 expression., Interestingly, histamine synergistically activated Toll-like receptor2-mediated Cox-2 expression and PGE(2) production., PGN-induced COX-2 promoter luciferase activity was prevented by selective inhibition of TLR2 and c-Jun in RAW 264.7 macrophages. <more data available...>","14966191:6, 20451669:4, 17927697:7, 20040740:4, 20200402:9, 15636756:4, 14966134:4, 20828867:8, 20558725:9, 16407295:8 <more data available...>",2,34,"Mus musculus, Homo sapiens","Microglia, Macrophages, Fibroblasts, PBMCs, Epithelial Cells","positive"]
["TLR2 -> STAT3","Expression","TLR2 activation triggers STAT3 and Smad3 activation., TLR2 activation sequentially stimulates NF-?B, STAT3 and Smad3 activation., In addition, blockade of TLR2 abrogated peptidoglycan-SA-induced STAT3 and Smad3 activation. [thumbnail] ., Secondly, HSP60 activation of TLR2 mediates the expression and phosphorylation of Stat3 in tumor cells., These finding indicated that peptidoglycan-SA-stimulated TLR2 activation increased NF-?B, STAT3 and Smad3 activities depending on a time pattern., Moreover, targeting TLR2 in the host or in the melanoma cells markedly inhibited the B16 cell-induced phosphorylation of Stat3 (Fig. 3F). <more data available...>","20520770:250, 20520770:260, 20520770:255, 19654875:266, 20520770:318, 19654875:200, 20520770:319, 19654875:159, 19654875:164",2,9,null,"B-Lymphocytes","positive"]
["TLR2 -> VEGFA","Expression","The free fatty acids-induced VEGF expression was mostly mediated by TLR2., These studies demonstrated that TLR2 signaling through the PI3K-Akt pathway is necessary for lipoteichoic acid-induced VEGF expression in pulp cells., These data indicate that TLR2 may be essential to mesenchymal stem cell-mediated myocardial recovery and VEGF production., TNF-alpha and TLR-2, -3 and -4 agonists induced the expression of vascular endothelial growth factor, which was partially abolished by the blockage of HIF-1 alpha with CTM. <more data available...>","18641052:5, 19767581:4, 20173040:13, 19744167:9, 16981238:10, 17182109:10",2,6,"Homo sapiens","Adipocytes, Odontoblasts, Mesenchymal Stem Cells, Chondrocytes, Fibroblasts","positive"]
["TNFRSF1A -> AQP4","Expression","TNFR1-dependent increase in aquaporin -4 mRNA and protein expression was observed with a concomitant increase in water content, in brain (18% increase in C57Bl6 mice treated with lipopolysaccharide versus those treated with saline), similar to cerebral edema observed in sepsis.","17884256:3",2,1,null,null,"positive"]
["TNFRSF1A -> CD83","Expression","The CD83 promoter is also activated by chimeric latent membrane protein 1-CD40, latent membrane protein 1-TNFR1, and latent membrane protein 1-TNFR2.","12857898:1232",2,1,null,null,"positive"]
["TNFRSF1A -> VEGFA","Expression","Further analysis showed that induction of EPOR and VEGF expression in primary cortical neurons after glucose deprivation largely depended on TNFRI and was further up-regulated by TNF., Activation of TNFR1 increased the expression of vascular endothelial growth factor, p21(WAF1/CIP1), and manganese superoxide dismutase in MCF7 breast cancer cells, and increased the expression of CCl2/MCP-1 and IL-1beta in THP-1 macrophages., IL-6 and VEGF production are cooperatively regulated by activated TNF receptors as well as the activating stimulus. <more data available...>","18413601:5, 18606683:8, 17640973:1152, 18824767:1116",2,4,null,"Neurons, Macrophages","positive"]
["TREM2 -> CD86","Expression","In addition, TREM-2 induces upregulation of some T cell stimulatory molecules, such as MHC class II, CD40, and CD86., TREM2/DAP12 engagement in DCs leads to upregulation of CCR7, CD40, CD86, and DC survival but not IL-12 nor TNF-alpha production., Ligation of triggering receptor expressed on myeloid cells-2 induced increased cell surface expression of CD40, CD86, and MHC class II but Ag-capturing mechanisms were not down-regulated (53)., KARAP/DAP12-TREM2 triggering on human dendritic cells promotes incomplete maturation process, i.e., dendritic cells up-regulation of CCR7, CD40, CD86, and MHC class II molecules, but not TNF-alpha nor IL-12 production (32). <more data available...>","11602640:1310, 11828015:1087, 14978127:1314, 15128777:1290, 14978127:315, 15128777:291",2,6,"Homo sapiens","T-Lymphocytes, Antigen-Presenting Cells, Monocytes, Dendritic Cells","positive"]
["UCP2 -> BCL2L1","Expression","Furthermore, UCP2 overexpression in HCT116 cells resulted in decreased cleavage and activation of the key apoptosis effector caspase-3, increased abundance of the antiapoptotic Bcl-XL protein, and less expression of PUMA-a (Fig. 2A, bottom right), an essential proapoptotic protein targeted by the tumor suppressor p53 (19, 20).","18413749:1201",2,1,null,null,"positive"]
["VEGFA -> ADAMTS1","Expression","These results indicate that VEGF significantly induces ADAMTS1 expression in endothelial cells in a PKC-dependent fashion.","16936124:9",2,1,null,"Endothelial Cells","positive"]
["VEGFA -> ANGPT1","Expression","VEGF increased the amount of angiopoietin1, but not Ang2, protein secreted into the medium., Both hypoxia and VEGF (10 ng/ml) treatment significantly increased angiopoietin-1 mRNA expression., Since VEGF blockade opposed the effect of angiotensin II on cell proliferation, it is hypothesised that VEGF mediates the angiotensin II-dependent effect in concert with the changes in angiopoietin expression., C, time course of Angiopoietin-1, Ang2, and Tie2 mRNA expression stimulated by VEGF in Bovine aortic endothelial cells. <more data available...>","11381069:9, 12686170:5, 18390690:8, 10336473:1140, 12649156:1241, 14672554:1300, 20881939:1266, 11289054:1240, 21179479:1334, 16176970:1075 <more data available...>",2,11,"Bos taurus, Homo sapiens","Epithelial Cells, Pericytes, Endothelial Cells, Adipocytes","positive"]
["VEGFA -> AQP4","Expression","VEGF administration highly upregulated AQP4 mRNA and protein in the ventral midbrain., VEGF alone significantly increased the extravasation of Evans blue and up-regulated the levels of AQP4 protein expression in the injured spinal cord issue, but the levels of AQP1 expression were not significantly changed.","18022290:5, 21092735:2",2,2,null,null,"positive"]
["VEGFA -> BCL2","Expression","VEGF increases Bcl-2 expression by 33% over cells cultured in standard media., The expression of bcl-2 in HL-60 cells was upregulated by VEGF., The expression and localization of the survival factor bcl-2 was dependent on VEGF., In contrast, VEGF-induced tube formations and Bcl-2 expression were significantly decreased at the end of this period., VEGF decreases active caspase 3 levels and increases expression of the anti-apoptotic protein Bcl-2., TSP1 also attenuated VEGF-mediated Bcl-2 expression in endothelial cells in vitro and angiogenesis in vivo. <more data available...>","11877669:6, 16584583:8, 16428272:9, 14633857:4, 20430442:4, 10859480:4, 11461089:2, 11380405:2, 17015762:6, 17251059:10 <more data available...>",2,67,"Homo sapiens, Bos taurus","Neurons, Endothelial Cells, synoviocytes, Myocytes, Cardiac, Fibroblasts, somatic cells","positive"]
["VEGFA -> CCL3","Expression","VEGF and TNFalpha secreted from primary tumors signal through circulatory system to stimulate lung endothelial cells and macrophages to enhance production of S100A8 and A9 as well as MIP-1alpha, which in turn stimulate primary tumor cells as well as macrophages in bone marrow to migrate over to the lungs presumably via local chemokine gradient., However, VEGF can also increase expression of intercellular adhesion molecule-1 (ICAM-1) and macrophage inflammatory protein 1a (MIP1a) in endothelial and brain parenchymal cells (27) and increase the permeability of the brain-blood barrier (28, 29).","19329882:3, 18263734:1059",2,2,null,"Macrophages","positive"]
["VEGFA -> CCND1","Expression","VEGF stimulated both cyclin D1 synthesis and Cdk4 kinase activity, inhibited by PD 98059 and dominant negative JNK-1., In cultures of human umbilical vein endothelial cells , VEGF augmented cyclin D1 expression and cell growth., VEGF and expression of constituitively active JNK each stimulated the synthesis of cyclin D1 and increased the activity of the cyclin-dependent kinase-4, which was inhibited 55% by ANP., The main purposes of this study were to investigate the regulation of polysaccharides isolated from A. cinnamomea on vascular endothelial growth factor (VEGF)-induced cyclin D1 expression and down stream signaling pathway that may correlate with their anti-angiogenc effects in endothelial cells . <more data available...>","9756915:9, 16899623:8, 11250939:5, 15850596:0, 12235165:1196, 12439750:1163, 14744780:1303, 11815623:1228, 16899588:1062, 12907650:1275 <more data available...>",2,15,"Homo sapiens, Bos taurus","Endothelial Cells, Epithelial Cells","positive"]
["VEGFA -> CTSL1","Expression","Our results demonstrate the transcriptional upregulation of cathepsin L expression by VEGF.","17574778:1",2,1,null,null,"positive"]
["VEGFA -> CTSS","Expression","Remaining to be determined are the signaling mechanism(s) by which VEGF-A up-regulates cathepsin and down-regulates cysteine protease inhibitor expression and activity in venules transitioning into mother vessels, and the mechanisms by which the cathepsin-cysteine protease inhibitor balance is subsequently restored as mother vessels evolve into daughter vessels., GAPDH serves as a control. (B,C) Human recombinant VEGF (10 ng/ml) up-regulates cathepsin S mRNA and protein in Human umbilical vein endothelial cells when assessed by RT-PCR and western blot using GAPDH and tubulin as respective controls (D) Human recombinant VEGF (10 ng/ml) stimulates Cathepsin S-like activity, as assessed by the cleavage of fluorigenic substrate, Cbz-Val-Val-Arg-AMC, by 37% in Human umbilical vein endothelial cells cell lysates. (E,F) To demonstrate the effect of hypoxia on Cathepsin S up-regulation total RNA and protein was isolated from Human umbilical vein endothelial cells endothelial cells (grown in normal or hypoxic conditions) and examined by RT-PCR and western blot.","19435903:1281, 20824056:1214",2,2,"Homo sapiens","Endothelial Cells","positive"]
["VEGFA -> CXCL10","Expression","Collectively, these findings indicate that VEGF-induced augmentation of IP-10 expression is a major mechanism underlying its proinflammatory function., Vascular endothelial growth factor induces IP-10 chemokine expression., It is reported that VEGF may also play a major role to augment the expression of IP-10 in T cells (Feldman et al, 2002)., As shown in Figure 3C, an anti-VEGF antibody significantly decreased the secretion of TNFa and IL-1ß in hypoxia, while significantly restoring CXCL10 production., Moreover, we observed that a combination of VEGF with IFN-? resulted in a synergistic induction of endothelial cell IP-10 mRNA and protein expression, but not Mig expression (Figure 4, c-e, and not shown). <more data available...>","16493069:8, 11890674:100, 17505511:1164, 18694997:1165, 14660742:1195, 20220052:1213",2,6,"Mesocricetus auratus","T-Lymphocytes, Dendritic Cells, Endothelial Cells","positive"]
["VEGFA -> DUSP1","Expression","VEGF-A and VEGF-E maximally induced MKP-1 expression in ECs; however, the other VEGF subtypes had no effect., vascular endothelial growth factor enhances transcription of DUSP1 and DUSP5 genes in ECs.., Real-time polymerase chain reaction analysis showed a reduction in basal and VEGF-induced MKP-1 mRNA.","18003751:2, 19741200:1148, 19020052:1218",2,3,"Homo sapiens","Endothelial Cells","positive"]
["VEGFA -> FLI1","Expression","We also found that ETV-1, Fli-1, ERG, MMP-1, -3, -7, -8, -9, -10, -13, and -19 expression is up-regulated more than 1.5-fold in human umbilical vein endothelial cells after 2 h of VEGF treatment.","20432469:5",2,1,"Homo sapiens","Endothelial Cells","positive"]
["VEGFA -> HBEGF","Expression","HB-EGF mRNA was induced by 8-fold after 2 h of VEGF stimulation, and it returned to base line within 6 h., Induction of HB-EGF expression by vascular endothelial growth factor (VEGF) released from ECs led to the suggestion that HB-EGF may participate in recruitment of mesenchymal cells that form the medial and adventitial layers of arteries and veins during embryonic development,14 a process with similarities to arteriogenesis in the adult.","9468491:2, 15994441:1059",2,2,"Homo sapiens","Endothelial Cells","positive"]
["VEGFA -> ID1","Expression","Vascular endothelial growth factor (VEGF) and TGFbeta induced the expression of Id1 and Id3 in HUVECs., Inhibitor of DNA binding-1 was localized predominantly in the cytoplasm, and was rapidly upregulated by stimulation with serum and vascular endothelial growth factor., Thus, VEGF-induced activation of Id1 and Id3 may be a critical molecular event required to promote mobilization of bone marrow precursors., endothelial progenitor cells mobilization promotes an up-regulation of Id1 and Id3, induced by the raised plasma VEGF-A (Benezra et al., 2001[Go]). <more data available...>","15494533:3, 19701608:5, 11840325:1178, 15602010:1443, 11840326:1188, 20065063:1248, 17426247:1247",2,7,null,"Endothelial Cells, Fibroblasts","positive"]
["VEGFA -> ID3","Expression","Stimulation of FTC133 cells with exogenous VEGF enhanced inhibitor of DNA binding-3 expression, which could be abrogated by the KDR-specific inhibitor ZM323881, suggesting that VEGF regulation of inhibitor of DNA binding-3 is KDR dependent., Surface expression of ICAM-1 (c), E-selectin (d), and av integrin (e) was measured in mock transfectants with or without stimulation with VEGF (20 ng/ml), and ID1 and ID3 small hairpin RNA double transfectants stimulated with VEGF., It has been reported that VEGF may up-regulate inhibitor of DNA binding-3 expression (26), an angiogenic gene believed to play a critical role in cell proliferation (19) and precursor endothelial cell recruitment (20).","16926250:7, 15494533:1197, 16394085:1259",2,3,null,"Endothelial Cells","positive"]
["VEGFA -> INHBA","Expression","On the other hand, VEGF increased the production of activin A.","15117880:8",2,1,"Bos taurus","Endothelial Cells","positive"]
["VEGFA -> INPP5D","Expression","A previous report found that VEGF-A can induce SHIP expression in endothelial cells,15 and thus SHIP expression, or function, could be induced in niche cells to limit effector functions of bone marrow niche cells., It has been previously shown that SHIP-1 mRNA is upregulated in human umbilical vein endothelial cells in response to vascular endothelial growth factor A, and SHIP-1 protein abundance increases in the endothelium of the ovary during angiogenesis.32 However, the present work is the first to demonstrate a function for SHIP-1 in endothelium, and it identifies the phosphatase as an important modulator of endothelial cell Akt, which is critically involved in the regulation of vascular homeostasis and angiogenesis in numerous paradigms.33 Although the other isoform of SHIP, SHIP-2, is widely expressed in various tissues,9-11 SHIP-2 was not detected in bovine aortic endothelial cells.","19074735:1280, 19423845:1215",2,2,"Homo sapiens","Endothelial Cells","positive"]
["VEGFA -> ITGB2","Expression","Flow cytometric analysis of several adhesion molecules at the polymorphonuclear neutrophil surface showed that all VEGF isoforms slightly upregulated beta1- and beta2-integrins and PECAM, and downregulated L-selectin; all these molecules are activation markers., Both VEGF and PlGF induced expression of CD11a and CD18 on monocytes within the same range, indicating that the preparations of PlGF and VEGF were of comparable activity., VEGF enhanced the expression of alpha1beta1 and alpha2beta2 integrins, and neutralizing antibodies to alphavbeta1 integrins blocked growth factor-induced neovascularization (18-20). <more data available...>","14968118:5, 12600898:1154, 12844492:1061, 15242977:1050",2,4,null,"Neutrophils, Monocytes","positive"]
["VEGFA -> MCL1","Expression","Northern blotting and immunoblotting analyses revealed that the expression level of MCL1, a member of the BCL2 family, was increased by VEGF., We further found that vascular endothelial growth factor (VEGF) is a novel regulator of Mcl-1 expression in prostate cancer cells., VEGF can inhibit the apoptosis of HL-60 cells possibly through increasing the expressions of Bcl-2 and Mcl-1 mRNA and protein, which may represent one of the mechanisms responsible for human acute leukemia., We have also reported that transcription of the MCL1 gene is up-regulated by VEGF stimulation (25) . <more data available...>","9850095:3, 20085644:4, 17178043:9, 10667597:1219, 15217829:1125, 11705851:1162, 14996703:1152, 19234191:1059, 12612065:1035, 16518413:1159 <more data available...>",2,11,"Bos taurus","hematopoietic cells, Myeloid Cells, B-Lymphocytes, thymocytes, Plasma Cells, Endothelial Cells","positive"]
["VEGFA -> PDPN","Expression","In vitro, endogenous and VEGF-A-induced VEGFR-3 and podoplanin expression by human microvascular endothelial cells was reduced by siRNA to NFATc1, to levels comparable to reductions seen with siRNA to Prox-1.","19233265:8",2,1,"Homo sapiens","Endothelial Cells","positive"]
["VEGFA -> PLAT","Expression","Co-added bFGF and VEGF increased t-plasminogen activator mRNA levels and enzyme activity in both cell types in a synergistic manner., At equimolar concentrations (0.5 nM), VEGF was a more potent inducer of t-PA mRNA than bFGF, while bFGF was a more potent inducer of u-PA and PAI-1 mRNAs., VEGF-A induces hypertrophy and loss of barrier function in pre-existing vessels, and induces angiogenic sprouting, characterized by marked expression of VEGFR-3 and lack of expression of tPA and Tie-2 in endothelial cells, and lack of alpha-SMA in pericytes. <more data available...>","11522025:3, 1755866:2, 14688216:9, 9378778:4, 7507853:3, 15602010:1797, 11443212:1237, 7730348:1214, 12805403:1163, 10523040:1203 <more data available...>",2,13,"Bos taurus, Homo sapiens","Endothelial Cells, Monocytes","positive"]
["VEGFA -> PTGS2","Expression","Furthermore, aspirin and sodium salicylate inhibited COX-2 expression stimulated by VEGF., Yet the signaling pathways by which VEGF modulates COX-2 gene expression are still less well defined., Treatment of HMEC-1 with VEGF resulted in a dose- and time-dependent up-regulation of COX-2 mRNA and protein levels., IGFBP7 attenuated VEGF-enhanced cyclooxygenase -2 and VEGF mRNA expression, and prostaglandin E(2) secretion., Consistent with this, we show that the induction of Cox-2 gene expression by VEGF requires nuclear factor of activated T cells activation. <more data available...>","14521608:9, 16336951:2, 12107271:1, 19374835:3, 11238591:2, 12881220:9, 20032081:10, 21273371:5, 18093816:7, 16651031:4 <more data available...>",2,44,"Homo sapiens, Rattus norvegicus, Bos taurus","Endothelial Cells, Muscle Cells, Luteal Cells, B-Lymphocytes, Mesangial Cells, Myocytes, Cardiac","positive"]
["VEGFA -> S1PR3","Expression","We show that the VEGF stimulates the expression of Edg3/S1P3 (S1P3) and that expression of this Gi-protein-coupled receptor is both sufficient and necessary for the expression of Akt3., Secondly, VEGF regulates S1P1 and S1P3 expression (Igarashi et al. 2003, Hughes et al. 2005, Fieber et al. 2006)., S1P3 expression was induced by 3-fold at P16 (4 days of hypoxia; **P < 0.03). (C) Ang-2 and VEGF mRNA in the course of hypoxia (n = 3)., Substantial cross-talk exists between Sphingosine 1-phosphate and VEGF, such that Sphingosine 1-phosphate transactivates VEGF-2 receptor (56) and VEGF up-regulates both S1P3 (57) and S1P1 receptor expression associated with an enhanced intracellular signaling response to Sphingosine 1-phosphate (58).","16527273:5, 18509004:1060, 17710232:1081, 18055454:1357",2,4,null,"Endothelial Cells","positive"]
["VEGFA -> SOCS3","Expression","Thus, consistent with published reports (33,34), light-induced VEGF may activate STAT3 and induce SOCS3 expression.","18356406:1189",2,1,"Mus musculus",null,"positive"]
["VEGFA -> SYNPO","Expression","Both anti-VEGF antibodies and sFlt-1 significantly reduced the expression of synaptopodin that, similar to nephrin, was restored in rescue experiments when 32.5 pM of VEGF was delivered 5 min after infusion of either anti-VEGF antibodies or sFlt-1. [Figure 6] View larger version (74K): [in this window] [in a new window] [Download PowerPoint slide] .","17255128:1146",2,1,null,null,"positive"]
["VIM -> AXL","Expression","In conclusion, our data show that vimentin functionally contributes to Epithelial-to-mesenchymal transition and is required for induction of Axl expression.","21057535:9",2,1,null,null,"positive"]
["ZEB2 -> VIM","Expression","Inversely, inhibition of Smad interacting protein-1 expression by RNAi strategies in BT-549 cells and MCF10A cells decreased vimentin expression., Further studies identified that Smad interacting protein 1 overexpression inhibits expression of E-cadherin and enhances expression of mesenchymal proteins such as fibronectin and vimentin., At the same time, ZEB2 has been shown to directly activate the Vimentin promoter by an unknown mechanism (Bindels et al. 2006), causing Vimentin to be expressed., There is increased expression of transcription factors, such as Snail, Slug, Twist, E47, ZEB1, and ZEB2, which leads to increased expression of N-cadherin and vimentin and concomitant decrease of E-cadherin and cytokeratins, proteins essential for establishment of cell-cell adhesion (4, 6-8).","16568083:5, 19806322:7, 18381893:1282, 18381457:1072",2,4,null,null,"positive"]

{"sheet":"Reduced network","index":8,"n_rows":39,"n_cols":8,"rows_kept":39,"flags":["formulas_cached_only"]}
["CD14 -> CD68","Expression","human microglia cell line clone 3 cells are typical microglia, as suggested by the constitutive expression of Iba-1 and CD14, and IFN-gamma-induced expression of CD11b, CD68 and MHCII.","20375612:3",2,1,null,"positive"]
["CD14 -> CD86","Expression","In contrast, immature dendritic cells cultured in G4 plus human pancreatic RNase or eosinophil-derived neurotoxin for 48 h, although still CD14-, up-regulated the surface expression of CD83, CD86, and HLA-DR, indicating that human pancreatic RNase and eosinophil-derived neurotoxin treatment induced phenotypic maturation of DCs (Fig. 7A).","15528350:1252",2,1,null,"positive"]
["CD14 -> ITGAX","Expression","Treatment of U937 cells with PMA markedly increased CD14, CD11a, CD11b and CD18 antigen expression, and slightly increased CD11c expression., In particular, those for CD11c and tumor necrosis factor a (TNFa) were markedly increased, and there were lesser, but significant, increases in Spp1, CD14, CD45, CCL9, Toll-like receptor 4 (TLR4), and interleukin-1B (IL-1ß) (Fig. 6G,H).","1689274:1, 18160655:1251",2,2,null,"positive"]
["CEBPA -> CSF1","Expression","For example, when expressed alone, RUNX1, C/EBPa, and PU.1 are poor activators of the M-CSF promoter.","15988004:1056",2,1,null,"positive"]
["CEBPA -> PROS1","Expression","Reporter gene analysis suggests that members of the CCAAT/enhancer binding protein (C/EBP) family of transcription factors are potent activators of protein S gene transcription in HepG2 cells.","17061980:6",2,1,null,"positive"]
["CEBPD -> CEBPA","Expression","Previous investigations indicated that transcription of the C/EBPalpha gene is sequentially activated during differentiation, initially by C/EBPbeta and C/EBPdelta and later by C/EBPalpha (autoactivation)., Nuclear expression of the 36-kilodalton C/EBP delta protein increases immediately after birth, followed first by increases in the 38-kilodalton C/EBP beta protein expression and then by increases in the 42-kilodalton C/EBP alpha protein expression., These data demonstrate that Myc specifically inhibits the terminal stages of the adipogenic program and suggest that Myc may act by blocking C/EBPbeta- and C/EBPdelta-directed activation of C/EBPalpha and PPARgamma2 expression, although the precise molecular mechanism is not understood. <more data available...>","10373535:1, 7910803:4, 10623469:4, 18703634:1194, 18930917:1043, 18653467:1203, 12138207:1046, 12186946:1140, 16154099:1059, 17273556:1253 <more data available...>",2,43,null,"positive"]
["CEBPD -> SOCS3","Expression","The doxycycline-dependent expression of C/EBP-d neither increased Spi-2 and Socs3 transcripts nor interfered with their induction by IL6RIL6 (Fig. 5B).","14600146:227",2,1,null,"positive"]
["CSF1 -> C3","Expression","Macrophage colony-stimulating factor (M-CSF) enhances complement component C3 production by human monocytes/macrophages.","8477063:100",2,1,null,"positive"]
["CSF1 -> CD14","Expression","It has been demonstrated that the expression of CD16 and CD14 is regulated by macrophage colony stimulating factor (M-CSF) and GM-CSF., M-CSF was also shown by flowcytometric analysis to influence the expression of CD14, a receptor for LPS, which might render monocytes more sensitive to LPS., Daily administration of macrophage colony stimulating factor (M-CSF) to the mice resulted in increased levels of MSR-A expression and reduced levels of CD14 as well as several cytokine expressions, leading to shortening of the inflammatory process. <more data available...>","12153694:6, 8877404:9, 10594845:5, 9566797:4, 15256426:1265",2,5,null,"positive"]
["CSF1 -> CEBPA","Expression","Ectopic expression of THOC5 mimicked M-CSF mediated cell maturation and enhanced protein expression of the myeloid transcription factors C/EBPbeta, C/EBPalpha, Pu-1 and also GAB2 (a PI-3 Kinase and macrophage development regulator)., M-CSF and G-CSF use separate pathways to activate ERK and modify C/EBPa .","19015024:4, 19587381:1161",2,2,null,"positive"]
["CSF1 -> CSF1R","Expression","However, after 48 h, M-CSF significantly stimulated c-Fms expression., IL-10 together with M-CSF increased the expression of M-CSF receptors., This treatment completely prevented M-CSF-induced c-Fms expression in a dose-dependent manner but had little effect on TNFa-induced c-Fms up-regulation (Fig. 5D)., Incubation with CSF-1 down-regulated CSF-1R expression and was associated with proliferation of mononuclear cells with decreased CSF-1R binding., We demonstrated that one mechanism by which this occurs is PU.1 down-regulation by the negative control of NFI-A on M-CSFR levels (Fig. 7) because M-CSF induces PU.1 expression through M-CSFR in the hematopoietic myeloid-osteoclast lineage (1-3). <more data available...>","16461346:213, 8978307:46, 16461346:221, 19819976:310, 19059913:261, 19628784:169",2,6,null,"positive"]
["CSF1 -> CYBB","Expression","Consistent with this, we find that expression of gp91phox and p67phox protein is also increased by M-CSF differentiation in Western blots of cell lysate proteins (Fig. 1C)., Of interest to the current studies, HoxA9 overexpression in murine myeloid cells does not impair granulocyte-colony stimulating factor- or macrophage-colony stimulating factor-induced expression of gp91Phox, a phagocyte respiratory burst oxidase protein (4).","16210632:1196, 15681849:71",2,2,null,"positive"]
["CSF1 -> ITGB2","Expression","The levels of CD11a and CD18 expression on granulocytes were significantly enhanced by administration of M-CSF.","11789672:6",2,1,null,"positive"]
["CSF1 -> LGALS3","Expression","Macrophage colony-stimulating factor (M-CSF), which is present at increased levels in MRL/lpr mice, but not in MRL/Mp- +/+ mice, induced the expression of Mac-2 antigen and Fas antigen on spleen adherent cells of MRL/Mp- +/+ mice.","8870694:4",2,1,null,"positive"]
["CSF1 -> TLR2","Expression","CSF-1 also down-regulated expression of TLR1, TLR2, and TLR6, but not the LPS receptor, TLR4, or TLR5., TLR-2 expression on monocytes was enhanced by macrophage colony-stimulating factor (M-CSF) and interleukin-10 (IL-10), but was reduced by transforming growth factor beta1, while CD16 expression was inducible by these cytokines., Toll-like receptor 2 and 4 surface expressions on human monocytes are modulated by interferon-gamma and macrophage colony-stimulating factor.","11751985:7, 15146415:10, 11672593:100",2,3,null,"positive"]
["CSF1 -> TREM2","Expression","Addition of macrophage colony stimulating factor (M-CSF) to LN cell culture allowed the proliferation and expression of TREM2 in LN cells, and the addition of neutralizing anti-M-CSF antibodies suppressed the proliferation of LN cells despite the expression of TREM2., Whereas Humphery et al. recently reported that TREM-2 expression is induced during in vitro osteoclastogenesis induced by culture bone marrow-derived macrophages with macrophage CSF (MCSF) and the receptor activator of NF-?B ligand (4), we find that differentiation of macrophages in MCSF alone leads to expression of TREM-2. [Figure 3] View larger version (33K): [in this window] [in a new window] .","20345919:4, 16951310:1159",2,2,null,"positive"]
["CSF1R -> PTPN6","Expression","Traumatic injury to the central nervous system activates microglia and strongly increases expression of SHP-1, which physically associates with and is activated by c-Fms in these cells (17).","12361947:312",2,1,null,"positive"]
["GFAP -> APOD","Expression","ApoD levels increased by 35% in the peri-infarct area after 10 and 30 days after pMCAO, mainly in neuron-specific nuclear protein (NeuN) positive neurons and glial fibrillary acidic protein (GFAP) positive astrocytes.","20083089:4",2,1,null,"positive"]
["GFAP -> VIM","Expression","As for GFAP, increased lesion-induced up-regulation of vimentin expression is also already apparent at 1 dpl, with knock-out animals showing higher expression than wild-type animals (Fig. 5b).","12843240:1209",2,1,null,"positive"]
["ITGAX -> CD86","Expression","We found that the expression level of co-stimulatory molecules, CD40, CD54, CD80, CD86 and CD11b, were elevated evidently, except CD11c, I-A(d) and H-2K(d)., As reported previously (24), bone marrow-derived macrophage-derived dendritic cells expressed high levels of CD11c, CD86, and I-Ab, and LPS up-regulated the expression of CD86 and I-Ab.","20499643:4, 19336404:170",2,2,null,"positive"]
["ITGB2 -> TLR2","Expression","The anti-CD18 monoclonal antibody markedly reduced TLR2 expression in endothelial cells as induced by polymorphonuclear neutrophils.","14561708:1314",2,1,null,"positive"]
["LCN2 -> GFAP","Expression","Third, the LCN2-induced GFAP expression was blocked by a nitric oxide synthase inhibitor NG-monomethyl-L-arginine (Fig. 8F,G)., Because LCN2 also induced GFAP expression in astrocytes in our study (Fig. 6), we next attempted to determine whether NO is involved in the LCN2 actions in astrocytes., Rho/ROCK pathway appeared to play a pivotal role in regard to LCN2 actions on astrocyte morphology, based on the following results: (1) a ROCK inhibitor, Y27632, partly blocked LCN2-induced morphological changes (Fig. 9A,B); (2) Y27632 also inhibited the LCN2-induced GFAP expression (Fig. 9C,D); and (3) LCN2 induced Rho activation in astrocytes (Fig. 9E). <more data available...>","19129400:366, 19129400:358, 19129400:384, 19129400:439",2,4,null,"positive"]
["PTPN6 -> CYBB","Expression","Consistent with this, SHP1 inhibition increases gp91PHOX and p67PHOXmRNA in undifferentiated U937 cells., In undifferentiated U937 cells, we found that overexpression of CS453-SHP1 increases gp91PHOX and p67PHOX mRNA abundance relative to control vector transfectants (Fig.2 C).","11483597:208, 11483597:223",2,2,null,"positive"]
["PTPN6 -> ITGB2","Expression","Surface expression of ß2 integrins is increased on motheaten polymorphonuclear leukocytes .","11067945:1301",2,1,null,"positive"]
["STAT3 -> CD14","Expression","STAT3 inhibitor pretreatment could also down-regulate high CD14 and CD16 expression by BxPC-3 conditioned medium treatment.","17545630:1248",2,1,null,"positive"]
["STAT3 -> CD9","Expression","Furthermore, activation of STAT3 induced the expression of CD9, indicating the LIF/STAT3 pathway is critical for maintaining CD9 expression., In a previous study, the addition of leukemia inhibitory factor or STAT3 activation induced CD9 expression in embryonic stem cells [13], which indicates that the leukemia inhibitory factor/STAT3 pathway is critical for maintaining CD9 expression.","11950938:5, 12954725:1222",2,2,null,"positive"]
["STAT3 -> CEBPA","Expression","Gene expression profile and quantitative PCR analysis of G-CSF-stimulated cell lines revealed that the expression of C/EBPalpha was up-regulated by the activation of Stat3., Treatment of freshly isolated adult rat hepatocytes with 10-100 mM ethanol rapidly (< 3 min) inhibits interleukin-6 (IL-6)-induced STAT3 activation, tyrosine and serine phosphorylation and IL-6-induced CCAAT enhancer binding protein (C/EBP) alpha and beta mRNA expression., One is that activated Stat3 binds to the promoter region of C/EBPa and induces the transcription of C/EBPa. <more data available...>","15664994:3, 10486586:2, 15664994:261, 15664994:66, 15664994:47, 15664994:255, 15664994:266",2,7,null,"positive"]
["STAT3 -> CXCL10","Expression","Inhibitors of p38 mitogen-activated protein kinase, c-Jun N-terminal kinase (JNK), phosphatidylinositol-3-OH kinase and signal transducer and activator of transcription 3 decreased OSM-induced CXCL10 production.","19616927:6",2,1,null,"positive"]
["STAT3 -> HPGD","Expression","Activation of signal transducer and activator of transcription3 may augment potently the androgen bound receptor signaling and contribute to synergistic induction of 15-PGDH expression by combined treatments with IL-6 and dihydrotestosterone.","14749354:1215",2,1,null,"positive"]
["STAT3 -> OSMR","Expression","STAT3 activation further enhances OSMR expression, thereby establishing a positive-feedback loop., We found that Stat3flx/flx/NIC tumors expressed lower levels of both cebpd and osmr, two genes that are induced by Stat3 (28, 29)., We show that OSMR expression is dependent on LIF-induced STAT3 and that the subsequent OSMR-mediated signal inhibits the phosphorylation of STAT5 and coordinately activates signal transducer and activator of transcription3-dependent apoptosis in the involuting mammary gland.","20348953:1139, 19690134:1181, 18927239:1084",2,3,null,"positive"]
["STAT3 -> VIM","Expression","Specific inhibition of STAT3 activation by Janus kinase2-specific inhibitor AG490 blocked STAT3 phosphorylation, cell motility, induction of N-cadherin and vimentin expression and IL6 production., Stat3 can enhance transcription of the vimentin gene.","19088723:9, 14712222:1097",2,2,null,"positive"]
["TLR2 -> CD86","Expression","TLR2 is essential for neisserial porin up-regulation of B7-2 and class II MHC in B cells ., Anti-TLR2 blocked increases in the CD86 median fluorescence intensity, but not the percentage of cells positive for CD86., There may be some differences in the Toll-like receptor2-mediated signaling pathway between cytokine production and CD83/CD86 expression., This indicates that the up-regulation of B7-2 and class II MHC surface expression was dependent on the normal expression of TLR2 on the B cell., They also showed that, in human Immature dendritic cells, cytokine production and CD83/CD86 expression were independently induced by M161Ag through TLR2. <more data available...>","11823477:142, 11160304:195, 11160323:247, 11823477:146, 11160323:191, 19109203:128, 11316801:237, 19109203:149, 11160304:179, 11823477:182",2,10,null,"positive"]
["TLR2 -> CEBPD","Expression","TLR2 signaling by LpqH induced expression of liver inhibitory protein and C/EBPd and enhanced expression of LAP at time points that correlated kinetically with the onset of inhibition of IFN-?-induced CIITA expression., Toll-like receptor2 stimulation also induces C/EBPd expression and binding to the CIITA promoter [31].","17982082:1080, 19629181:349",2,2,null,"positive"]
["TLR2 -> HSPB1","Expression","TLR1/2 ligand palmitoyl-3-cysteine-serine-lysine-4 (Pam3CSK4) induces activation of PKDs via a PKC-independent manner, and Pam3CSK4-induced expression of heat shock protein 27 and MCP-1, as well as activation of PKDs, is inhibited by Gö6976, but not by broad-spectrum PKC inhibitors, in mouse bone marrow-derived mast cells (26).","19414785:65",2,1,null,"positive"]
["TLR2 -> ITGAX","Expression","The TLR2 agonist Pam3Cys significantly stimulated the maturation of DCs by enhancing the surface expression of CD11c, MHC class I, MHC class II, CD40, CD80, and CD86.","19109203:128",2,1,null,"positive"]
["TLR2 -> ITGB2","Expression","Peptidoglycan (TLR2 ligand), flagellin (TLR5 ligand), and Imiquimod R837 (TLR7 ligand) could significantly upregulate cell surface expression of intercellular adhesion molecule (ICAM)-1 and CD18, and induce the release of IL-1beta, IL-6, IL-8, growth-related oncogene -alpha, and superoxides of eosinophils.","17332440:5",2,1,null,"positive"]
["TLR2 -> LCN2","Expression","LCN2 expression is increased in response to activation of TLR2 and TLR4 signaling by bacterial peptides (42).","18317594:1267",2,1,null,"positive"]
["TLR2 -> STAT3","Expression","TLR2 activation triggers STAT3 and Smad3 activation., TLR2 activation sequentially stimulates NF-?B, STAT3 and Smad3 activation., In addition, blockade of TLR2 abrogated peptidoglycan-SA-induced STAT3 and Smad3 activation. [thumbnail] ., Secondly, HSP60 activation of TLR2 mediates the expression and phosphorylation of Stat3 in tumor cells., These finding indicated that peptidoglycan-SA-stimulated TLR2 activation increased NF-?B, STAT3 and Smad3 activities depending on a time pattern., Moreover, targeting TLR2 in the host or in the melanoma cells markedly inhibited the B16 cell-induced phosphorylation of Stat3 (Fig. 3F). <more data available...>","20520770:250, 20520770:260, 20520770:255, 19654875:266, 20520770:318, 19654875:200, 20520770:319, 19654875:159, 19654875:164",2,9,null,"positive"]
["TREM2 -> CD86","Expression","Ligation of triggering receptor expressed on myeloid cells-2 induced increased cell surface expression of CD40, CD86, and MHC class II but Ag-capturing mechanisms were not down-regulated (53)., KARAP/DAP12-TREM2 triggering on human Dendritic cells promotes incomplete maturation process, i.e., Dendritic cells up-regulation of CCR7, CD40, CD86, and MHC class II molecules, but not TNF-alpha nor IL-12 production (32).","14978127:315, 15128777:291",2,2,null,"positive"]

{"sheet":"Networks centrality analysis","index":9,"n_rows":119,"n_cols":8,"rows_kept":119,"flags":["formulas_cached_only"]}
[null,"Betweenness centrality original network",null,null,"Betweenness centrality reduced network",null,null,"Betweenness centrality expanded network"]
["A2M",0,null,"APOD",0,null,"A2M",0]
["ABCA1",0,null,"C3",0,null,"ABCA1",0]
["ADAMTS1",0,null,"CD14",12.5,null,"ADAMTS1",0]
["AIF1",5.5,null,"CD68",0,null,"AIF1",2.9]
["ALOX5AP",0,null,"CD86",0,null,"ALOX5AP",0]
["APOD",0,null,"CD9",0,null,"ANGPT1",39.535]
["B2M",63,null,"CEBPA",68,null,"APOD",0]
["C3",0,null,"CEBPD",22.5,null,"AQP4",165.068]
["CASP1",0,null,"CSF1",79,null,"AXL",230.2]
["CCND1",31,null,"CSF1R",6,null,"B2M",41.686]
["CD14",52.73,null,"CXCL10",0,null,"BCL2",628.594]
["CD68",0,null,"CYBB",0,null,"BCL2A1",0]
["CD83",0,null,"GFAP",10,null,"BCL2L1",1061.926]
["CD86",0,null,"HPGD",0,null,"C3",0]
["CD9",0,null,"HSPB1",0,null,"CASP1",3.21]
["CEBPA",356,null,"ITGAX",0,null,"CAT",5]
["CEBPD",133.57,null,"ITGB2",47,null,"CCL3",282.545]
["CLU",0,null,"LCN2",16,null,"CCND1",392.224]
["CSF1",674.53,null,"LGALS3",0,null,"CD14",113.22]
["CSF1R",20,null,"OSMR",0,null,"CD44",924.268]
["Ctla2a",0,null,"PROS1",0,null,"CD68",0]
["CX3CR1",0,null,"PTPN6",25,null,"CD80",161.784]
["CXCL10",9.67,null,"SOCS3",0,null,"CD83",1.7000000000000002]
["CYBB",0,null,"STAT3",58.5,null,"CD86",344.11]
["FCGR2B",0,null,"TLR2",112.5,null,"CD9",0]
["FLI1",6,null,"TREM2",1,null,"CEBPA",354.18]
["GFAP",37,null,"VIM",0,null,"CEBPB",432.14]
["GUSB",0,{"$nulls":4},"CEBPD",350.066]
["HLA-E",0,{"$nulls":4},"CLU",2.996]
["HPGD",0,{"$nulls":4},"CP",0]
["HSPB1",0,{"$nulls":4},"CSF1",988.465]
["HSPB8",0,{"$nulls":4},"CSF1R",92.782]
["ID3",0,{"$nulls":4},"Ctla2a",0]
["IFI27",0,{"$nulls":4},"CTSL1",40.5]
["IFIT3",0,{"$nulls":4},"CTSS",40.5]
["IL13RA1",0,{"$nulls":4},"CX3CR1",0]
["INPP5D",0,{"$nulls":4},"CXCL10",94.777]
["ISG15",0,{"$nulls":4},"CYBB",80.513]
["ITGAX",5,{"$nulls":4},"DUSP1",532.608]
["ITGB2",149.52,{"$nulls":4},"FCGR2B",0]
["ITGB5",0,{"$nulls":4},"FCGR3A",44]
["LCN2",16.33,{"$nulls":4},"FGF9",177.567]
["LGALS3",353.87,{"$nulls":4},"FLI1",35.317]
["LXN",0,{"$nulls":4},"GFAP",560.961]
["MCL1",0,{"$nulls":4},"GUSB",0]
["MET",0,{"$nulls":4},"HBEGF",168.93]
["NCF1",44,{"$nulls":4},"HLA-DQB1",0]
["NFATC1",48,{"$nulls":4},"HPGD",0]
["OSMR",0,{"$nulls":4},"HSPB1",9.019]
["P2RX7",11,{"$nulls":4},"HSPB8",0]
["PDPN",0,{"$nulls":4},"ID1",187.55]
["PROS1",0,{"$nulls":4},"ID3",0]
["PTGS1",0,{"$nulls":4},"IFI27",0]
["PTPN6",72,{"$nulls":4},"IFIT1",20.917]
["RBP1",0,{"$nulls":4},"IFIT2",62.748]
["S100A4",0,{"$nulls":4},"IFIT3",0]
["SBNO2",0,{"$nulls":4},"IL13RA1",0]
["SERPING1",0,{"$nulls":4},"INHBA",650.267]
["SOCS3",0,{"$nulls":4},"INPP5D",0]
["SOX9",24,{"$nulls":4},"ISG15",24.783]
["SRGN",0,{"$nulls":4},"ITGAX",11.428]
["STAT1",113.33,{"$nulls":4},"ITGB2",276.74]
["STAT3",268.23,{"$nulls":4},"ITGB5",0]
["SYNPO",0,{"$nulls":4},"LCN2",16]
["TF",0,{"$nulls":4},"LGALS1",25.155]
["TGFB1",1042.87,{"$nulls":4},"LGALS3",337.962]
["TGFBR1",0,{"$nulls":4},"LST1",3]
["TGFBR2",0,{"$nulls":4},"LXN",0]
["TGM2",0,{"$nulls":4},"MAFB",1.6680000000000001]
["THBS2",0,{"$nulls":4},"MCL1",0]
["TLR2",436.37,{"$nulls":4},"MET",244.374]
["TNFRSF1A",0,{"$nulls":4},"MT2A",0]
["TREM2",1.53,{"$nulls":4},"NCF1",31.717]
["VIM",0,{"$nulls":4},"NFATC1",9.257]
[{"$nulls":6},"NR3C1",131.252]
[{"$nulls":6},"OSMR",10.283]
[{"$nulls":6},"P2RX7",17.957]
[{"$nulls":6},"P2RY6",1.182]
[{"$nulls":6},"PDPN",0]
[{"$nulls":6},"PLAT",0]
[{"$nulls":6},"PPARD",244.374]
[{"$nulls":6},"PRL",220.869]
[{"$nulls":6},"PROS1",0]
[{"$nulls":6},"PSMB8",0]
[{"$nulls":6},"PTGS1",290.29]
[{"$nulls":6},"PTGS2",2052.175]
[{"$nulls":6},"PTK2",1.83]
[{"$nulls":6},"PTPN6",9.028]
[{"$nulls":6},"PTPRC",0.996]
[{"$nulls":6},"RBP1",0]
[{"$nulls":6},"S100A4",119.952]
[{"$nulls":6},"S100A6",0]
[{"$nulls":6},"S1PR3",0]
[{"$nulls":6},"SBNO2",0]
[{"$nulls":6},"SERPINA3",0]
[{"$nulls":6},"SERPING1",0]
[{"$nulls":6},"SLC14A1",0]
[{"$nulls":6},"SMAD7",174.15]
[{"$nulls":6},"SOCS3",346.939]
[{"$nulls":6},"SOX9",246.458]
[{"$nulls":6},"SRGN",0]
[{"$nulls":6},"STAT1",412.833]
[{"$nulls":6},"STAT3",222.061]
[{"$nulls":6},"SYNPO",0]
[{"$nulls":6},"TF",11.327]
[{"$nulls":6},"TGFB1",3933.911]
[{"$nulls":6},"TGFB2",663.781]
[{"$nulls":6},"TGFBR1",0]
[{"$nulls":6},"TGFBR2",79.328]
[{"$nulls":6},"TGM2",92.376]
[{"$nulls":6},"THBS2",0]
[{"$nulls":6},"TLR2",783.062]
[{"$nulls":6},"TNFRSF1A",3.917]
[{"$nulls":6},"TREM2",0]
[{"$nulls":6},"UCP2",0]
[{"$nulls":6},"VEGFA",3165.611]
[{"$nulls":6},"VIM",195.2]
[{"$nulls":6},"ZEB2",1]