ライフサイエンスコーパス: TGF-beta1

1 TGF-beta1 (transforming growth factor-beta1) importantly

2 TGF-beta1 also increased levels of inflammatory cytokine

3 TGF-beta1 also suppressed the combined effects of IL-33

4 TGF-beta1 and aryl hydrocarbon receptor activation enhan

5 TGF-beta1 and BMP-2 decreased IL-34 expression in the sy

6 TGF-beta1 and Smad3 signals achieved this effect via the

7 TGF-beta1 as well as aryl hydrocarbon receptor activatio

8 TGF-beta1 inhibited IL-33-mediated Akt and ERK phosphory

9 TGF-beta1 is enriched in the tumor microenvironment and

10 TGF-beta1 is involved in many pathological conditions, i

11 TGF-beta1 mRNA levels are increased in mouse models of i

12 TGF-beta1 profoundly alters the electrophysiological phe

13 TGF-beta1 serum concentration significantly decreased in

14 TGF-beta1 signaling is a critical driver of collagen acc

15 TGF-beta1 was identified as the primary upstream regulat

16 TGF-beta1(+) cell counts decreased in responders at the

17 TGF-beta1-dependent cardiomyocyte depolarization resulte

18 ation and transforming growth factor-beta 1 (TGF-beta1) expression/secretion were evaluated.

19 Transforming growth factor beta-1 (TGF-beta1) induces FAK activation in a time and dose dep

20 ge of linearity between 2.5 and 1000pgmL(-1) TGF-beta1; detection limit of 0.95pgmL(-1)) improve nota

21 NA expression of liver IL-6, IL-17A, IL-17F, TGF-beta1, alpha-SMA, TGR5, NTCP, OATP1a1, and ileum ASB

22 HC-HA/PTX3 on cell migration (EGF + FGF-2 + TGF-beta1) and collagen gel contraction (TGF-beta1).

23 uman kidney tubular epithelial cells (HK-2), TGF-beta1 treatment induced fibrotic changes, including

24 sion of IL-17, TNF-alpha, IL-6, IL-4, IL-21, TGF-beta1 and IFN-gamma were significantly increased in

25 IL-34, TGF-beta1, and BMP-2 productions were measured in patien

26 IL-34, TGF-beta1, and BMP-2 were expressed in synovial fluids f

27 A TGF-beta1 receptor inhibitor, Rho-associated protein kin

28 whether modulating TGF-beta1 activity with a TGF-beta1-specific, humanized, neutralizing monoclonal a

29 xpression, in the presence of Gln, abrogated TGF-beta1-induced expression of profibrotic markers.

30 in Akt1-overexpressing macrophages abrogated TGF-beta1 expression and fibroblast differentiation.

31 RGD-binding integrins were shown to activate TGF-beta1 in several non-T cell types.

32 P in non-Treg T cells does not induce active TGF-beta1 production.

33 tent, inactive form of TGF-beta1 into active TGF-beta1.

34 In contrast, measurable active TGF-beta1 and phospho-Smad2/3 were not induced by mechan

35 ibition did not affect the release of active TGF-beta1.

36 ed using transient gene expression of active TGF-beta1.

37 imulated, human B lymphocytes produce active TGF-beta1 from surface GARP/latent TGF-beta1 complexes w

38 sponded to tensile force by releasing active TGF-beta1 from latent stores with subsequent increase in

39 cell-autonomous effect in response to added TGF-beta1 or BMP7.

40 In addition, TGF-beta1 and BMP-2 antagonized tumor necrosis factor al

41 In addition, TGF-beta1 may stimulate hepcidin mRNA expression in muri

42 BLM injection and in mouse macrophages after TGF-beta1 treatment, respectively.

43 N-gamma genes, a similar level of TNF-alpha, TGF-beta1, and platelet-derived growth factor alpha gene

44 MAD3 for degradation, resulting in amplified TGF-beta1/SMAD3 signaling and miR-140 downregulation-dep

45 icantly lower levels of BDNF (P = 0.005) and TGF-beta1 (P = 0.02).

46 Also, cytokines such as IL-10 and TGF-beta1 significantly reduce cytokine secretion by ILC

47 enhanced the production of IL-4, IL-17, and TGF-beta1 by these lymphocytes in contrast to normal con

48 idence interval [95% CI], 9.7% to 18.2%) and TGF-beta1 mAb treatments (20% [95% CI, 15.3% to 24.3%],

49 a significant correlation between IL-34 and TGF-beta1 expressions.

50 Levels of both IL-34 and TGF-beta1 were thus correlated with the total leukocyte

51 e with various cytokines, including IL-4 and TGF-beta1, suggesting that differentiation can result in

52 Cytokines IL-4, IL-5, TNF-alpha, and TGF-beta1, and serum from patients with asthma increased

53 Cytokines IL-4, IL-5, TNF-alpha, and TGF-beta1, and serum from patients with asthma were sele

54 We identified GM-CSF and TGF-beta1 as key cytokines to generate langerin(high)-ex

55 ndings suggest that targeting the FGFBP1 and TGF-beta1 signaling axis holds promise for slowing age-

56 proliferation, HSC activation/fibrosis, and TGF-beta1 expression/secretion were decreased.

57 ed with attenuation of the hyperglycemia and TGF-beta1-induced enhanced ROS production, increased exp

58 We conclude that HCV activates NFkappaB and TGF-beta1 through ROS production and induction of JNK an

59 ROS, ER stress, NFkappaB, and TGF-beta1 signaling were blocked by JNK specific siRNA.

60 hology, and decreased urinary NAG, NGAL, and TGF-beta1 in db/db mice.

61 e KRAS-variant, p16 positivity, outcome, and TGF-beta1 levels was evaluated.

62 riments in PDAC cells revealed that PAR2 and TGF-beta1 synergy may involve TGF-beta1 induction of enz

63 blasts restored both their proliferation and TGF-beta1 production.

64 oop, cause a downregulation of sialidase and TGF-beta1 accumulation.

65 ulated by 2 parallel pathways, MYOCD/SRF and TGF-beta1/SMAD, via distinct binding elements within the

66 ed the first VSMC-enriched and MYOCD/SRF and TGF-beta1/SMAD-dependent TSPAN family member, whose expr

67 of HGF/Met, Janus kinase 2 (JAK2)/STAT3 and TGF-beta1 signaling by specific inhibitors inhibited BMF

68 inflammatory effects of oxidative stress and TGF-beta1 on endothelial cells by restoring redox balanc

69 sociated with increased oxidative stress and TGF-beta1 signaling and also was related to the effects

70 tic conditions including stiff substrata and TGF-beta1, and analyzed in terms of morphology, stiffnes

71 itionally, MA-35 concurrently showed an anti-TGF-beta1 effect by inhibiting Smad3 phosphorylation, re

72 to produce IL-6, which was inhibited by anti-TGF-beta1 neutralizing antibody.

73 humanized, neutralizing monoclonal antibody (TGF-beta1 mAb) is safe and more effective than placebo i

74 hese effects were functionally important, as TGF-beta1 injection suppressed IL-33-induced systemic cy

75 Kaempferol significantly attenuated TGF-beta1-mediated profibrotic pathways in vitro and in

76 s (axin-2), transforming growth factor-beta (TGF-beta1) and collagens types 1 and 3, indicating that

77 s elevates transforming growth factor beta1 (TGF-beta1) and p38 mitogen-activated protein kinase (MAP

78 osis, with transforming growth factor beta1 (TGF-beta1) as one of its strongest mediators.

79 ion of the transforming growth factor beta1 (TGF-beta1) cytokine considered as a reliable biomarker i

80 Increased transforming growth factor beta1 (TGF-beta1) in mammary adipose tissue in obese mice activ

81 Transforming growth factor beta1 (TGF-beta1) is a master cytokine in many biological proce

82 lood-based transforming growth factor beta1 (TGF-beta1).

83 ivation of transforming growth factor-beta1 (TGF-beta1) and Cxcl12 pathways in mice expressing Jak2(V

84 rs such as transforming growth factor-beta1 (TGF-beta1) and mechanical influences such as local tissu

85 gnaling of transforming growth factor-beta1 (TGF-beta1) and tumor necrosis factor-alpha (TNF-alpha) p

86 izing anti-transforming growth factor-beta1 (TGF-beta1) antibody and siRNA-mediated knockdown of TGF-

87 ion of the transforming growth factor-beta1 (TGF-beta1) in skeletal muscles and at their NMJs.

88 Transforming growth factor-beta1 (TGF-beta1) may stimulate ATP release from the urothelium

89 duction of transforming growth factor-beta1 (TGF-beta1), collagen deposition, and inhibition of matri

90 aorta) of transforming growth factor-beta1 (TGF-beta1), connective tissue growth factor, matrix meta

91 duction of transforming growth factor-beta1 (TGF-beta1).

92 ate latent transforming growth factor-beta1 (TGF-beta1).

93 Elevated levels of bioactive TGF-beta1 are associated with asymmetric fate choice in

94 ion, HSPCs express high amounts of bioactive TGF-beta1 protein, which is associated with high levels

95 odies against alphaV or beta8 subunits block TGF-beta1 activation in vitro.

96 Thus, PPARgamma ligands, by blocking TGF-beta1-induced p38 MAPK phosphorylation, prevent incr

97 ents to understand the induction of PAI-1 by TGF-beta1, the relationship between PAI-1 and esophageal

98 P-4 mediates upregulation of angiogenesis by TGF-beta1.

99 The stimulation of GLS1 expression by TGF-beta1 was dependent on both SMAD3 and p38 mitogen-ac

100 r induction of Runx transcription factors by TGF-beta1.

101 to be the only TSPAN family gene induced by TGF-beta1 and MYOCD, and reduced by SRF deficiency in VS

102 smooth muscle is independently regulated by TGF-beta1/SMAD and myocardin/serum response factor.

103 the CCN1 matricellular protein and canonical TGF-beta1/SMAD3 signaling that promotes lung fibrosis.

104 2 + TGF-beta1) and collagen gel contraction (TGF-beta1).

105 In contrast, TGF-beta1 efficiently converted human acinar cells to du

106 ocyte-cardiomyocyte gap junctional coupling, TGF-beta1 depolarized cardiomyocytes coupled to myofibro

107 The fibrosis-associated cytokine TGF-beta1 upregulates sialidases in human airway epithel

108 oteinases (MMPs), and pro-fibrotic cytokine, TGF-beta1, and enzymes, tissue inhibitors of MMPs (TIMPs

109 Results suggest that astrocyte-derived TGF-beta1 is part of an endogenous mechanism that protec

110 acrine activity of regulatory T cell-derived TGF-beta1 contributes to immunosuppression and can be in

111 ed immunosensor was validated by determining TGF-beta1 in real saliva samples.

112 tor-like kinase 1 (ALK1) and ALK5 downstream TGF-beta1 and BMP-2.

113 miR-199a-3p, collagen I, and vimentin during TGF-beta1 treatment.

114 Elevated TGF-beta1 levels in patients with the KRAS-variant sugge

115 knockout mouse models also exhibit elevated TGF-beta1/p38 MAPK signaling and induction of fibrotic g

116 the KRAS-variant had significantly elevated TGF-beta1 plasma levels (median, 23 376.49 vs 18 476.52

117 icity), proliferation (EGF + FGF-2) and EMT (TGF-beta1).

118 suppression in renal cells further enhanced TGF-beta1-induced SMAD3 phosphorylation and fibrotic gen

119 The matricellular protein CCN1 enhances TGF-beta1/SMAD3-dependent profibrotic signaling in fibro

120 Finally, exogenous TGF-beta1 to -beta3, each restituted the normal scar phe

121 t is still elusive, however, to which extent TGF-beta1 alters the electrophysiological phenotype of m

122 cells induces accumulation of extracellular TGF-beta1, forming what appears to be a sialidase - TGF-

123 Mechanistically, the profibrotic factor TGF-beta1 induced hypermethylation and repression of ery

124 ransforming growth factor (TGF)-beta family, TGF-beta1 and bone morphogenetic protein (BMP)-2, in syn

125 immobilization of the specific antibody for TGF-beta1 using Mix&Go polymer.

126 andwich type immunoassay was implemented for TGF-beta1 with signal amplification using V-Phe-SWCNT(-H

127 changes were confirmed at protein level for TGF-beta1 and ENG.

128 rcinoma (PDAC) PAR2 protein is necessary for TGF-beta1-dependent cell motility.

129 diated sEphrin-B2 generation is required for TGF-beta1-induced myofibroblast activation.

130 n but only indirectly required via Runx2 for TGF-beta1-induced selectin ligand induction on murine CD

131 iant testing, and 376 had plasma samples for TGF-beta1 measurement.

132 rs for VSMC differentiation, we screened for TGF-beta1 and MYOCD/serum response factor (SRF)-regulate

133 ase in collagen production that results from TGF-beta1 stimulation was ameliorated by the allosteric

134 tokine has limited the development of global TGF-beta1 signaling inhibitors as therapeutic agents.

135 Recombinant human TGF-beta1 (rhTGF-beta1) prevented denervation-induced re

136 This work identifies TGF-beta1 and BMP-2 as potent inhibitors of IL-34 expres

137 ial-mesenchymal transition without immediate TGF-beta1 receptor (TbetaR) kinase inhibition.

138 Bone marrow-derived mast cells cultured in TGF-beta1, beta2, or beta3 showed reduced IL-33-mediated

139 d inhibits the formation of stress fibers in TGF-beta1 treated HSCs.

140 ed to mechanical force showed an increase in TGF-beta1 activation and induction of phospho-Smad2/3 in

141 entration of glutamate was also increased in TGF-beta1-differentiated myofibroblasts compared with co

142 phases of ICH in vivo and found increases in TGF-beta1 pathway activation during the resolution phase

143 marate, malate, and citrate were observed in TGF-beta1-differentiated myofibroblasts.

144 on in ovaries, accompanied by a reduction in TGF-beta1 expression in granulosa cells.

145 tivation, and induces apoptotic signaling in TGF-beta1 treated HSCs.

146 controlled primarily by cytokines, including TGF-beta1, and requires p38alpha MAPK, but transcription

147 Although Akt1 increased TGF-beta1 expression, mitophagy inhibition in Akt1-overe

148 athway in which GSDMB induces 5-LO to induce TGF-beta1 in bronchial epithelium.

149 HCV has been shown to induce TGF-beta1 through the generation of reactive oxygen spec

150 GSDMB induces TGF-beta1 expression via induction of 5-LO, because knoc

151 mice (intratracheal bleomycin and inducible TGF-beta1).

152 pic screens for small molecules that inhibit TGF-beta1-induced epithelial-mesenchymal transition with

153 Furthermore, MA-35 inhibited TGF-beta1-induced H3K4me1 histone modification of the fi

154 lly activated MMP-2 expression and inhibited TGF-beta1-induced Smad2 and Smad3 phosphorylation.

155 thelial cells overexpressing GSDMB inhibited TGF-beta1 expression.

156 n of CAFs and tumor cells with either intact TGF-beta1 expression or devoid of TGF-beta1 in vivo show

157 d in the presence of tumor cells with intact TGF-beta1, showed a significant increase in proliferatio

158 Of interest, TGF-beta1 treatment enhanced TRPV4 activation in a PI3K-

159 that PAR2 and TGF-beta1 synergy may involve TGF-beta1 induction of enzymes that cause autocrine clea

160 2 loss on hepatic fibrogenesis that involves TGF-beta1 activation.

161 he transforming growth factor beta isoforms, TGF-beta1, -beta2, and -beta3, are small secreted homodi

162 ll types use surface GARP to activate latent TGF-beta1 was not known.

163 ng membrane protein GARP, which binds latent TGF-beta1.

164 t alphaV and beta8 interact with GARP/latent TGF-beta1 complexes in human Tregs.

165 ce active TGF-beta1 from surface GARP/latent TGF-beta1 complexes with isotype switching to IgA produc

166 een the integrin alphaVbeta8 and GARP/latent TGF-beta1 complexes.

167 brane protein that binds and presents latent TGF-beta1 on the surface of Tregs stimulated through the

168 Upon correction of VD levels, TGF-beta1 and TIMP-1 levels were decreased, and the MMP2

169 he immunosensor for the determination of low TGF-beta1 concentrations in real samples was evaluated b

170 primarily cytoplasmic deacetylase, mediates TGF-beta1-induced EMT in human lung cancer cells.

171 able polymer microspheres (TRI microspheres; TGF-beta1, Rapamycin (Rapa), and IL-2).

172 linearity extending between 15 and 3000pg/mL TGF-beta1 which is adequate for the determination of the

173 by suppressing the HIF-1alpha/calpains/MMP2/TGF-beta1 pathway.

174 d, phase 2 study assessed whether modulating TGF-beta1 activity with a TGF-beta1-specific, humanized,

175 Moreover, TGF-beta1 overexpression in cancer cells was co-related

176 Moreover, TGF-beta1 treatment following ICH decreased microglial I

177 Notably, TGF-beta1 prevented hippocampal dendritic spine loss and

178 Notably, TGF-beta1 reduced hippocampal dendritic spine loss and m

179 beta1 is known to be crucial, the ability of TGF-beta1 to increase expression of both DNMT1 and DNMT3

180 on and progression by targeted abrogation of TGF-beta1 expression in metastatic cells in situ.

181 Absence of TGF-beta1 in tumor cells also failed to result in myofib

182 expression leads to increased activation of TGF-beta1 signaling as well as increased myofibroblast d

183 ow conduction and ectopic activity, block of TGF-beta1 signaling completely abolished both arrhythmog

184 gression of renal fibrosis, dual blockade of TGF-beta1 and TNF-alpha is desired as its therapeutic ap

185 roxyphenolic compounds as potent blockers of TGF-beta1 responses (IC50 50 nM), Snail1 expression, an

186 ed in chromatin remodeling in the control of TGF-beta1 gene transcription.

187 P plays a crucial role in the development of TGF-beta1-mediated acute lung injury by promoting pulmon

188 her intact TGF-beta1 expression or devoid of TGF-beta1 in vivo showed a significant increase in tumor

189 rylation, resulting in the downregulation of TGF-beta1-induced fibrotic gene expression.

190 fails to repress the inflammatory effect of TGF-beta1 which is suppressed upon TAK1 inhibition.

191 The present study examined the effects of TGF-beta1 crosstalk in TME and its role in mediating tum

192 nse to TGF-beta1 and mediates the effects of TGF-beta1 on angiogenesis.

193 tent with our previously reported effects of TGF-beta1 on IgE-mediated activation, demonstrate that T

194 uced NF-kappaB activation and enhancement of TGF-beta1.

195 There was increased expression of TGF-beta1 and TGF-beta1R.

196 Enhanced expression of TGF-beta1 mRNA and cytokine was evidenced in the livers

197 s by converting the latent, inactive form of TGF-beta1 into active TGF-beta1.

198 t, genetic and pharmacological inhibition of TGF-beta1/Smad3 signals suppressed endogenous glucose pr

199 TGFBRII-Fc is an inhibitor of TGF-beta1 and TGF-beta3, but not TGF-beta2, signaling.

200 Injections of an inhibitor of TGF-beta1 signaling SB-431542 also decreased the weights

201 Knockdown of TGF-beta1 expression in the tumor cells negatively affec

202 a1) antibody and siRNA-mediated knockdown of TGF-beta1, previously identified as an important synapto

203 Levels of TGF-beta1 were increased with GP+RAP/alpha-syn immunizat

204 ouse bone and found decreased mRNA levels of TGF-beta1, TGF-beta2 and TGF-beta3.

205 oblasts to the latency-associated peptide of TGF-beta1 and prevented activation of the latent TGF-bet

206 etric immunosensor for the quantification of TGF-beta1, a cytokine proposed as a biomarker for patien

207 protein 2 (FHL2) is a critical regulator of TGF-beta1 expression.

208 es 90 days after ICH, confirming the role of TGF-beta1 in functional recovery from ICH.

209 ese findings underscore an important role of TGF-beta1/Smad3 signaling in hepatic gluconeogenesis, bo

210 d a significant increase in the secretion of TGF-beta1 ligand along with enhanced protein expression

211 -beta1 promoter, whereas the upregulation of TGF-beta1 gene transcription correlates with reduced occ

212 reases in DNMT1 and DNMT3a were dependent on TGF-beta1 activation of focal adhesion kinase and PI3K/A

213 monstrate the repressive function of FHL2 on TGF-beta1 expression and contribute to the understanding

214 s for Alzheimer's disease, mainly focused on TGF-beta1 and astrocytes.

215 R2-APs, PAR2 mutation and PAR2 inhibitors on TGF-beta1-induced migration, reporter gene activity, and

216 acquired a robust myofibroblast phenotype on TGF-beta1 stimulation.

217 ith PAR2-AP alone failed to enhance basal or TGF-beta1-induced C-terminal phosphorylation of Smad3, S

218 EMD or TGF-beta1 provoked a significant increase of IL-11 and P

219 uximab may help these patients by overcoming TGF-beta1-induced suppression of antitumor immunity.

220 In BAVnon-dil patients, TGF-beta1 and MMP-2 gene expression increased significan

221 response and outcome, p16 status, and plasma TGF-beta1 levels was tested.

222 that patients with early increases in plasma TGF-beta1 concentrations had better outcomes 90 days aft

223 Importantly, endogenous CCN1 potentiates TGF-beta1-induced SMAD3 activation and induction of prof

224 Depletion of extracellular Gln prevented TGF-beta1-induced myofibroblast differentiation.

225 wn-regulation by short hairpin RNA prevented TGF-beta1-mediated disruption of the cortical actin stru

226 relates with the inability of Mn(2+) and pro-TGF-beta1 to stabilize the open conformation of the alph

227 e we show how integrin alphaVbeta6 binds pro-TGF-beta1 in an orientation biologically relevant for fo

228 nd increases affinity of alphaVbeta6 for pro-TGF-beta1 25- to 55-fold, it increases alphaVbeta8 affin

229 Furin cleaves and promotes activation of pro-TGF-beta1 and pro-TGF-beta2, and TGF-beta2 in turn incre

230 We have determined a structure of pro-TGF-beta1 with the proprotein convertase cleavage site m

231 nsforming growth factor-beta1 precursor (pro-TGF-beta1), integrins bind to the prodomain, apply force

232 pro-activin A share features seen in the pro-TGF-beta1 and pro-BMP-9 structures, but reveal a new oli

233 nded-closed conformation, and binding to pro-TGF-beta1 does not stabilize the open conformation of it

234 mine alphaVbeta8 for atypical binding to pro-TGF-beta1.

235 ding ERK and AKT, as well as the profibrotic TGF-beta1/SMAD pathway.

236 hancing the effect of EtOH on IL-15, RANTES, TGF-beta1, and TNF-alpha cytokines while restoring MCP-2

237 ion or knockdown of ROCK1 expectedly reduced TGF-beta1 induced fibrotic responses.

238 vitro analysis revealed that MSLN regulates TGF-beta1-inducible activation of WT PFs by disrupting t

239 A) microparticles were engineered to release TGF-beta1, Rapamycin, and IL-2, to locally sustain a mic

240 f genes important to both airway remodeling [TGF-beta1, 5-lipoxygenase (5-LO)] and airway-hyperrespon

241 ith exogenous glutamate or alpha-KG restored TGF-beta1-induced expression of profibrotic markers in G

242 Transcriptome analysis revealed TGF-beta1-dependent changes in 29 of 63 ion channel/pump

243 hypoxia-inducible factor-1alpha and reversed TGF-beta1-induced metabolic reprogramming.

244 ssessed through ELISA and the ratio of serum TGF-beta1/ENG (T/E) was evaluated.

245 a1, forming what appears to be a sialidase - TGF-beta1 - sialidase positive feedback loop.

246 Specifically, TGF-beta1 signaling suppressed the LKB1-AMPK axis, there

247 rmal fibroblasts showed that P311 stimulated TGF-beta1 to -beta3 translation, a process that involved

248 -Gq-calcium signaling arm failed to suppress TGF-beta1-induced cell migration, reporter gene activity

249 (PMCs) showed that CTGF blockade suppressed TGF-beta1-induced fibroblast proliferation and myofibrob

250 We then confirmed that TGF-beta1 treatment modulated inflammatory profiles of m

251 on IgE-mediated activation, demonstrate that TGF-beta1 can provide broad inhibitory signals to activa

252 These results demonstrate that TGF-beta1 increases expression of DNMT1 and DNMT3a throu

253 studies with young T cells demonstrated that TGF-beta1 in the aged environment can drive increased re

254 We have previously found that TGF-beta1 can suppress IgE-mediated mast cell activation

255 Given that TGF-beta1 and myocardin (MYOCD) are potent activators fo

256 use models of iron overload, indicating that TGF-beta1 may contribute to hepcidin synthesis under the

257 rat ventricular myofibroblasts revealed that TGF-beta1, applied for 24 to 48 hours at clinically rele

258 These results show that TGF-beta1 activation on the surface of human Tregs impli

259 al vein endothelial cells, we here show that TGF-beta1 aggravates oxidative stress-mediated inflammat

260 The results show that TGF-beta1 induces local fibroblast-to-myofibroblast diff

261 Taken together, our data show that TGF-beta1 modulates microglia-mediated neuroinflammation

262 a) in the markers between groups showed that TGF-beta1 and TIMP-1 levels were significantly decreased

263 All in all, our results suggest that TGF-beta1 stimulation increases active beta-catenin conc

264 romotes functional recovery, suggesting that TGF-beta1 may be a therapeutic target for acute brain in

265 cyte crosstalk in vitro, which suggests that TGF-beta1 may play a potentially important role in arrhy

266 scriptional coactivators TAZ and YAP and the TGF-beta1 (TGFbeta) effector Smad3 regulate a common set

267 oride, a GSK3 inhibitor, also attenuated the TGF-beta1-induced increase in alpha-SMA, COL1, and FN ex

268 Smad7, as an inhibitory smad in the TGF-beta1 signaling pathway, was decreased in the myofib

269 Expression changes of the TGF-beta1 active dimer and ENG were analyzed also by Wes

270 sion of FHL2 abrogates the activation of the TGF-beta1 promoter, whereas the upregulation of TGF-beta

271 e site mutated to mimic the structure of the TGF-beta1 proprotein.

272 using mice with conditional deletions of the TGF-beta1-responsive transcription factors Smad2, Smad3,

273 ates recruitment of RNA polymerase II on the TGF-beta1 promoter, suggesting that FHL2 may be involved

274 Here we demonstrate that the TGF-beta1/Smad3 signaling pathway promotes hepatic gluco

275 We detected association of FHL2 with the TGF-beta1 promoter, which showed higher activity in Fhl2

276 rol short hairpin RNA had no effect on these TGF-beta1-induced responses.

277 Thus, TGF-beta1 mAb added to renin-angiotensin system inhibito

278 e protein-to-creatinine ratio >/=800 mg/g to TGF-beta1 mAb (2-, 10-, or 50-mg monthly subcutaneous do

279 (ECM) protein, is upregulated in response to TGF-beta1 and mediates the effects of TGF-beta1 on angio

280 selectin ligands on CD4 cells in response to TGF-beta1 requires Smad4 plus either Smad2 or Smad3.

281 tic reprogramming that occurs in response to TGF-beta1 stimulation and direct contact with stiff subs

282 elated transcription factor 3 in response to TGF-beta1, thereby allowing LC differentiation marked by

283 d EC and angiogenesis in vivo in response to TGF-beta1.

284 (COL1), and fibronectin (FN) in response to TGF-beta1.

285 tes induction of angiogenesis in response to TGF-beta1.

286 In Tregs, TGF-beta1 activation requires GARP, a transmembrane prot

287 The serum levels of 25-hydroxy VD, TGF-beta1, TIMP-1, MMP2 and MMP9 were measured at baseli

288 timulated abnormal collagen accumulation via TGF-beta1/Smad2/3 pathway.

289 GF, bFGF, and SDF-1, which was not seen when TGF-beta1 expression was abrogated in tumor cells.

290 the bone marrow of Jak2(V617F) mice, whereas TGF-beta1 or Cxcl12 stimulation induces collagen deposit

291 d DNMT3a demonstrates a novel means by which TGF-beta1 may regulate DNA methylation in these cells.

292 g development and differentiation, for which TGF-beta1 is known to be crucial, the ability of TGF-bet

293 omycin exposure-a lung injury model in which TGF-beta1 plays a critical role.

294 CV-induced ER stress and UPR activation with TGF-beta1 production has not been fully characterized.

295 This was associated with TGF-beta1-induced expression of the glutaminase (GLS) is

296 ngiogenesis markers in animals injected with TGF-beta1, and these effects did not occur in Thbs4(-/-)

297 NHLFs that are induced by interactions with TGF-beta1 or stiff hydrogels are accompanied by the accu

298 In cardiac fibroblasts stimulated with TGF-beta1, phenotypic switches of cardiac fibroblasts to

299 f is not required for PAR2 to synergize with TGF-beta1 to promote cell motility.

300 Treatment of podocytes in vitro with TGF-beta1 resulted in increased expression of Notch-1, E