ライフサイエンスコーパス: TGFbeta

1 induced by transforming growth factor beta (TGFbeta).

2 tivation of transforming growth factor-beta (TGFbeta).

3 liferative versus prometastatic functions of TGFbeta.

4 ically reduced cell migration in response to TGFbeta.

5 the responsiveness of these cells to EGF and TGFbeta.

6 cluding CXCR4, CXCR7, MMP12, MMP13, IL-6 and TGFbeta.

7 t of MSCs was dependent on their response to TGFbeta.

8 are resistant to the suppressive effects of TGFbeta.

9 at clearing established tumors that secrete TGFbeta.

10 inhibition was rescued by treating TEC with TGFbeta.

11 ess sensitive to the pro-fibrotic effects of TGFbeta.

12 nosuppressive tumor microenvironment such as TGFbeta.

13 o induction of fiber cell differentiation by TGFbeta.

14 tumour metastasis, was markedly inhibited by TGFbeta.

15 y regulated by the cell cycle rather than by TGFbeta.

16 t terminate cytosolic signal transduction by TGFbeta.

17 g that mediates antiproliferative effects of TGFbeta.

18 ting that P-Rex1 is a downstream mediator of TGFbeta-1 signaling.

19 , up-regulates their stability, and promotes TGFbeta-1-induced expression of profibrotic proteins, su

20 WT mice, and its genetic deletion attenuated TGFbeta-1-stimulated lung fibroblast migration, Rac1 act

21 ctivated by transforming growth factor beta (TGFbeta)-activated kinase 1 (TAK1; MAP3K7), which is ass

22 Lys-63-ubiquitination activates the TGFbeta-activated kinase (Tak1), which feeds back to pho

23 We find that TGFbeta activates the transcription factor ZEB1 to repre

24 es and positively correlated with markers of TGFbeta activation in colon cancer.

25 alphav integrin blockade also reduces TGFbeta activation in primary human skeletal muscle and

26 revealing IGSF1 as an important regulator of TGFbeta/Activin pathways in the pituitary.

27 In addition, DMF abrogated TGFbeta/Akt1 mediated inhibitory phosphorylation of glyc

28 Here we show that TGFbeta also promotes genomic instability in the form of

29 by constitutively-activated EGFR may rely on TGFbeta and a possible relationship between TGFbeta and

30 expected cross-pathway inhibition in between TGFbeta and BMP, despite the fact that both use (or coul

31 are (TGFbeta and Wnt/beta-catenin) or share (TGFbeta and bone morphogenetic protein (BMP)) core signa

32 marrow niche signals (SCF, IL-1beta, G-CSF, TGFbeta and CXCL4) and activation of an inducible Irf8 a

33 Inhibition of TGFbeta and CXCR7 or activation of BMP and CXCR4 signall

34 TGFbeta and a possible relationship between TGFbeta and EGFR signalling may prevent EMT progression

35 Therefore, TGFbeta and growth pathways interact in postmitotic cell

36 n important aspect of the cross-talk between TGFbeta and Hippo signaling, showing that TGFbeta induce

37 pression or lack thereof was associated with TGFbeta and IL-6 production respectively.

38 elief of SMURF2 autoinhibition is induced by TGFbeta and is mediated by the inhibitory SMAD, SMAD7.

39 The DR group showed high levels of TGFbeta and low levels of C3 and TNFalpha in the kidneys

40 EMT indicating a partial divergence between TGFbeta and MEK/ERK in early carcinogenesis.

41 TGFbeta and MYC drive central features of basal breast c

42 ER+ dependent interaction between TGFbeta and NFkappaB was further shown to be associated

43 nsiveness of HaCaT and HECV cells to EGF and TGFbeta and resulted in a dysregulation of phospho-prote

44 Previously, we showed that daf-7 TGFbeta and tph-1 tryptophan hydroxylase expression in s

45 nts of crosstalk, which either do not share (TGFbeta and Wnt/beta-catenin) or share (TGFbeta and bone

46 le signaling pathways, including Prlr/Stat5, TGFbeta and Wnt/beta-catenin.

47 nd a surprising absence of crosstalk between TGFbeta and Wnt/beta-catenin.

48 eam node of transforming growth factor beta (TGFbeta) and bone morphogenetic protein (BMP) pathways.

49 cluding the transforming growth factor beta (TGFbeta) and epithelial growth factor (EGF).

50 Transforming growth factor beta (TGFbeta) and fibroblast growth factor (FGF) signaling pa

51 ed with elevated transforming growth factor (TGFbeta) and its signaling protein Smad3, known contribu

52 enes that are activated by TLR ligands, IL4, TGFbeta, and damage-associated molecular patterns (DAMPS

53 ible for up-regulating TANGO1 in response to TGFbeta, and this mechanism is mediated by the transcrip

54 pro-fibrotic stimulus, which was reduced by TGFbeta antibody or the anti-fibrotic nintedanib.

55 gn and well-differentiated pancreatic cells, TGFbeta appears to promote the progression of advanced c

56 abnormally thin epidermis, and we identified TGFbeta as a negatively regulated target of estrogen sig

57 lts define the oncogenic effects of the GARP-TGFbeta axis in the tumor microenvironment and suggest m

58 hat Klotho inhibition of the profibrotic Wnt/TGFbeta axis underlies its anti-fibrotic effect in aging

59 chically influence the cell population, with TGFbeta being most dominant followed by IL-6 and IL-4.

60 These analyses reveal the complexity of TGFbeta-BMP signaling and illuminate potential therapeut

61 components important in organogenesis (Wnt, TGFbeta/ BMP, FGF, Notch, SHH, Erbb) were differentially

62 We find that TGFbeta/BMP/SMAD pathway signaling is strongly activated

63 Mechanistic investigations revealed that TGFbeta bound to its receptors (TGFBR), which promoted t

64 In both contexts, senescence depends on TGFbeta but is independent of ERK/MAPK activation.

65 g cells, EPO induced the secretion of active TGFbeta by antigen-presenting cells, which in turn conve

66 w KLF10 opposes the prometastatic effects of TGFbeta by limiting its ability to induce epithelial-to-

67 We show here for the first time that TGFbeta can induce purified primary lens epithelial cell

68 tend the so-called TGFbeta paradox, in which TGFbeta can induce two disparate cell fates, to a new ep

69 signature showed a functional convergence on TGFbeta canonical signalling.

70 Neuronal DAF-7/TGFbeta causes a DAF-1/TGFbetaR signaling cascade in the

71 inally, we report that ITGA1 is required for TGFbeta/collagen-induced EMT and metastasis.

72 2 and prevented EMT independent of exogenous TGFbeta, consistent with most observations identifying p

73 study reveals a critical mechanism by which TGFbeta controls TH17 cell differentiation and uncovers

74 ial gene expression signature; expression of TGFbeta correlated with expression of EMT-related genes,

75 ectively, our results illuminate a Kindlin-2/TGFbeta/CSF-1 signaling axis employed by breast cancer c

76 bers of the transforming growth factor beta (TGFbeta) cytokine family have long been associated with

77 efining PTP4A1 as a molecule of interest for TGFbeta-dependent fibrosis, our study provides informati

78 TAT3 signaling is hyperactivated in SSc in a TGFbeta-dependent manner.

79 o be caused by a more proximal deficiency in TGFbeta-dependent signaling in Kindlin-2-deficient cells

80 creates an effective barrier against further TGFbeta-dependent tumor progression by preventing genomi

81 TGFbeta did not act by promoting nuclear MRTF translocat

82 Importantly, this work revealed that TGFbeta did not induce EMT in PC9 cells, but rather TGFb

83 mpared with controls, dogs treated with pUBC-TGFbeta-DN-RII demonstrated an attenuated increase in co

84 more fractionated and less organized in pUBc-TGFbeta-DN-RII versus pUBc-LacZ dogs.

85 Concurrently, TGFbeta drives Notch1-mediated EMT to generate tumor ini

86 stage, signaling pathways including Wnt and TGFbeta during early regrowth, and negative regulation o

87 coactivators TAZ and YAP and the TGF-beta1 (TGFbeta) effector Smad3 regulate a common set of genes,

88 Moreover, TGFbeta elevated TAZ mRNA in a p38-dependent manner.

89 Here we reveal that TGFbeta enables TH17 cell differentiation by reversing S

90 Yet, the mechanism by which TGFbeta enables TH17 cell differentiation remains elusiv

91 against DNA double strand breaks induced by TGFbeta expressed in the tumor microenvironment.

92 rotein 3 (Foxp3), TH2 and TH17 cytokine, and Tgfbeta expression in mesenteric lymph node (MLN) CD4(+)

93 beta family signaling by selectively binding TGFbeta family ligands and sequestering them.

94 Follistatin (FST) regulates TGFbeta family signaling by selectively binding TGFbeta

95 TGFbeta family signaling in the uterus is critical for e

96 g highlighted the important contributions of TGFbeta family signaling to normal development, adult ho

97 Inhibition of TGFbeta family signaling, a known negative regulator of

98 so inhibits the activation of p38, prevented TGFbeta from inducing epithelial-myofibroblast transitio

99 shing a molecular basis for the dichotomy of TGFbeta function during tumor progression.

100 ating the above findings, tumors harboring a TGFbeta gene expression signature and RUNX3 loss exhibit

101 Thus, autophagy antagonises TGFbeta gene expression.

102 sion with extracellular matrix organization, TGFbeta genes, epithelial-to-mesenchymal transition (EMT

103 ine closure by mediating the response to the TGFbeta gradient.

104 Although TGFbeta has been strongly implicated in lens cell fibros

105 d transcripts that are involved in WNT, HGF, TGFbeta, IGF, BMP, FGF and estrogen signaling.

106 ontribute to the growth inhibitory effect of TGFbeta in hepatocarcinoma cells.

107 , our findings suggest that the abundance of TGFbeta in the tumor microenvironment may in fact engage

108 neutralize the effects of immunosuppressive TGFbeta in the tumor microenvironment while empowering t

109 tolerance by enriching and activating latent TGFbeta in the tumor microenvironment.

110 effects of transforming growth factor-beta (TGFbeta) in SSc skin fibroblasts.

111 We showed that TGFbeta induced an interaction between Smad4 and putativ

112 We show that this occurs via TGFbeta-induced activation of CD73 and the associated in

113 ess TGFbeta signaling, and RNF11 may promote TGFbeta-induced cell migration.

114 Therefore, TGFbeta-induced disruption of SKI reverses SKI-SMAD4-med

115 regulation on TGFbeta treatment and prevents TGFbeta-induced EMT and invasion of cancer cells.

116 s establish that KLF10 functions to suppress TGFbeta-induced EMT, establishing a molecular basis for

117 SCLC cells resulted in a marked reduction of TGFbeta-induced EMT, migration, and invasion in vitro, a

118 on of the pro-growth signal CDK2 and ablated TGFbeta-induced EMT.

119 ulatory T cell (Treg) is in part mediated by TGFbeta-induced inhibition of inositol trisphosphate (IP

120 Rho kinases (ROCKs) play multiple roles in TGFbeta-induced myofibroblast activation that could be t

121 ks TGFbeta signaling, matrix remodeling, and TGFbeta-induced myofibroblast differentiation.

122 nIN cells, pERK was not necessary for either TGFbeta-induced pSMAD2 phosphorylation or CDK2 repressio

123 fibrotic pirferidone), or Akt suppressed the TGFbeta-induced TAZ expression.

124 , as MRTF silencing/inhibition abolished the TGFbeta-induced TAZ expression.

125 etic inhibition of Smad3 did not prevent the TGFbeta-induced TAZ up-regulation, indicating that this

126 ERK phosphorylation in duct cells mitigated TGFbeta-induced upregulation of growth suppressive pSMAD

127 In cancer cells, pERK had no effect on TGFbeta-induced upregulation of pSMAD2 and p21, suggesti

128 ential IL-15 or antigen exposure followed by TGFbeta induces liver-adapted TRM, including their signa

129 Here, we show that TGFbeta induces robust TAZ but not YAP protein expressio

130 en TGFbeta and Hippo signaling, showing that TGFbeta induces TAZ via a Smad3-independent, p38- and MR

131 exposure to transforming growth factor beta (TGFbeta) induces partial EMT and enables sliding on narr

132 We have previously demonstrated that TGFbeta Inducible Early Gene-1 (TIEG1), also known as KL

133 ination of senescent cells through temporary TGFbeta inhibition leads to developmental defects.

134 did not induce EMT in PC9 cells, but rather TGFbeta-inhibition induced an EMT-intermediate.

135 bination of trastuzumab, pertuzumab, and the TGFbeta inhibitor expressed epithelial markers and were

136 bination of trastuzumab, pertuzumab, and the TGFbeta inhibitor than in mice given single agents or a

137 into the HCA model to predict the effect of TGFbeta inhibitor treatment on disease evolution.

138 ive central features of basal breast cancer: TGFbeta is an autocrine and paracrine signaling factor t

139 Mechanistically, we established that TGFbeta is required for D-ECM production but dispensable

140 TGFbeta is the most abundantly secreted cytokine in the

141 The requirement for TGFbeta is two fold and sequential: autocrine via Tgfbet

142 Transforming growth factor beta (TGFbeta) is important in maintaining self-tolerance and

143 Transforming growth factor beta (TGFbeta) is instrumental in TH17 cell differentiation by

144 ry factors, transforming growth factor beta (TGFbeta) is regarded as a key determinant of malignancy.

145 Furthermore, exogenous TGFbeta led to rapid and sustained TGFBR1-dependent ERK

146 Signaling driven by TGFbeta ligand Activin and constitutively active recepto

147 olecules in transforming growth factor beta (TGFbeta) ligand pathways that have been found to have a

148 Cultivating RS-hAFSCs in ET conditions with TGFbeta may therefore increase their therapeutic potenti

149 TGFbeta-mediated activation of autophagy has recently be

150 a Type II receptor sensitizing PDAC cells to TGFbeta-mediated activation of p38 and SMAD signals.

151 Mechanistically, GRM3 antagonizes TGFbeta-mediated activation of protein kinase A and inhi

152 present study, we define a novel process of TGFbeta-mediated autophagy in cancer cell lines of vario

153 initially facilitates and later antagonizes TGFbeta-mediated cell cycle arrest, yet remains critical

154 in protecting from chronic liver disease and TGFbeta-mediated fibrosis remains unclear.

155 II receptor in colon cancer cells, enhancing TGFbeta-mediated growth inhibition and stress-induced ap

156 However, a key aspect of this cross-talk, TGFbeta-mediated regulation of TAZ or YAP expression, re

157 of T cells to produce IL-2, which overcomes TGFbeta-mediated suppression.

158 transition in epithelial-derived carcinomas, TGFbeta-mediated therapy-resistance in melanoma, treatme

159 ein stability and knockdown of GRM3 enhances TGFbeta-mediated tumor suppressor function.

160 TGFbeta member Vg1 is implicated in mesoderm formation b

161 kidney-derived EPO reduced the expression of TGFbeta mRNA and abrogated kidney allograft acceptance.

162 s and decreased Il13 and Il17a and increased Tgfbeta mRNA expression in the jejunum; numbers of CD103

163 However, TGFbeta neutralizes SMAD4-mediated suppression without a

164 r a ROCK-inhibitor to diminish the effect of TGFbeta on TM was demonstrated.

165 Human mammary cells treated with TGFbeta or undergoing EMT upregulated CD73 cell-surface

166 s for PCO, our findings extend the so-called TGFbeta paradox, in which TGFbeta can induce two dispara

167 We also report that TGFbeta partially activates STAT3 and show that inhibiti

168 By precisely varying FGF, BMP, WNT, and TGFbeta pathway activity in a minimal, chemically define

169 ppressed phosphorylation of Smad proteins in TGFbeta pathway and inhibited key responsive protein, P4

170 DNA methylation of the gene regions encoding TGFbeta pathway components were detected in NSCLC sample

171 Here we show that treatment with TGFbeta pathway inhibitor SB431542 together with ascorbi

172 factor appears to regulate components of the TGFbeta pathway specifically in pale R7.

173 at these proteins were regulated through the TGFbeta pathway, indicated that they may be important fo

174 To better understand dysregulation of the TGFbeta pathway, we first generated mouse models of neop

175 The transforming growth factor beta (TGFbeta) pathway plays critical roles during cancer cell

176 Elevation of the EGFR, RAS and TGFbeta pathways was observed in one subtype whereas the

177 athways, i.e., the nuclear-factor-kappaB and TGFbeta pathways.

178 ecisive for the expansion of hAFSCs and that TGFbeta present in ET conditions causes the phenotype of

179 The Amon TGFbeta processing factor appears to regulate components

180 with healthy macrophages, in contrast to the TGFbeta produced in response to healthy AC.

181 Exogenous TGFbeta promotes EMT in a unique pathway of PRMT5-MEP50

182 TGFbeta promotes invasion and crosstalks with Eph signal

183 nd along with enhanced protein expression of TGFbeta Receptor (TGFbetaR)-1, TGFbetaR-2 and phosphoryl

184 actin-binding protein transgelin (TAGLN) and TGFbeta receptor (TGFbetaR).

185 inhibitors began to secrete ligands for the TGFbeta receptor and underwent EMT.

186 ated mouse models of neoplastic disease with TGFbeta receptor deficiencies.

187 Here, we dissected the roles of TGFbeta receptor II (TGFBR2) and BMP receptor II (BMPR2)

188 d uncover a novel mechanism by which loss of TGFbeta receptor II (Tgfbr2) mediates invasion and metas

189 , followed by 10 days of incubation with the TGFbeta receptor inhibitor in the presence of trastuzuma

190 ll invasion by directly targeting ADAM9, the TGFbeta receptor TGFBR2 and the EMT inducers ZEB1, ZEB2,

191 Inhibition of type I TGFbeta receptors ALK1/2/3/6 responsible for phosphoryla

192 Inhibition of type I TGFbeta receptors ALK1/2/3/6 responsible for phosphoryla

193 SPO1 stimulation, LGR5 formed complexes with TGFbeta receptors.

194 es signals derived from tumor cells, such as TGFbeta; reciprocally, in fibroblasts, Snail1 organizes

195 lls through which crosstalk between MSCs and TGFbeta regulates tumour metastasis.

196 matical modelling to analyse the role of the TGFbeta-related molecules BMP4 and Vg1/GDF1 in positioni

197 to potentiate an epigenetic mechanism of the TGFbeta response.

198 provide a mechanism to explain the unleashed TGFbeta responses in metastatic cancer cells.

199 in down-regulated gene expression of several TGFbeta-responsive genes, dampened cell proliferation, a

200 , a peptide antagonist of TSP1 activation of TGFbeta, reversed the increased expression of fibrotic m

201 ta reveal the miR-182-mediated disruption of TGFbeta self-restraint and provide a mechanism to explai

202 romote chromatin remodeling and activate the TGFbeta, Shh and Wnt signaling pathways.

203 ed bone remodelling and reduced TNFalpha and TGFbeta sigalling.

204 er and identifies LGR5 as a new modulator of TGFbeta signaling able to suppress colon cancer metastas

205 bitory interneurons, which was contingent on TGFbeta signaling activation.

206 el cooperation between cancer cell-extrinsic TGFbeta signaling and cancer cell-intrinsic RUNX3 inacti

207 Knockdown of LGR5 attenuated downstream TGFbeta signaling and increased cell proliferation, surv

208 We identify ELMO1 as a novel target of TGFbeta signaling and show that restoration of Tgfbr2 re

209 ives the invasiveness of NSCLC, highlighting TGFbeta signaling as a candidate therapeutic target in t

210 ression results, we found that inhibition of TGFbeta signaling blocked OS regeneration.

211 Agents that block TGFbeta signaling can increase the anti-tumor efficacies

212 R-spondin 1 (RSPO1)/LGR5 directly activates TGFbeta signaling cooperatively with TGFbeta type II rec

213 uncovers a novel cross-talk between LGR5 and TGFbeta signaling in colon cancer and identifies LGR5 as

214 upport activation of the COL1A2 enhancer and TGFbeta signaling in fibroblasts.

215 PTP4A1 promotes TGFbeta signaling in human fibroblasts through enhanceme

216 ere induced by the serum protein albumin via TGFbeta signaling in primary astrocytes.

217 ose homolog PTP4A2 are critical promoters of TGFbeta signaling in primary dermal fibroblasts and of b

218 addition, Jagged1 overexpression upregulates Tgfbeta signaling in prostate stromal cells and promotes

219 Second, Akt-CA activates Tgfbeta signaling in retinal explants, which is a negati

220 maintained by estrogen-induced repression of TGFbeta signaling in the local fibroblasts.

221 In addition, TGFbeta signaling increases GRM3 protein stability and k

222 tion-dependent alteration to the HMOX1/THBS1/TGFbeta signaling pathway by iAs.

223 pound Minnelide revealed deregulation of the TGFbeta signaling pathway in CAF, resulting in an appare

224 Previously, we found that the TGFbeta signaling pathway links the environment and prol

225 ase 1 (FIEL1), which potently stimulates the TGFbeta signaling pathway through the site-specific ubiq

226 lation of BAMBI, a negative regulator of the TGFbeta signaling pathway.

227 regulatory role for embryonic myosin in the TGFbeta signaling pathway.

228 th downregulation of the MAPK, PI3K/Akt, and TGFbeta signaling pathways and a loss of epithelial-mese

229 catenin or SMAD3 to induce oncogenic WNT and TGFbeta signaling pathways, respectively.

230 regulation of cell migration and the BMP and TGFbeta signaling pathways.

231 Here, we show that DAF-7/TGFbeta signaling promotes expression of lag-2 in the DT

232 TGFbeta signaling regulates LEC proliferation and differ

233 nals, yet may also contribute to detrimental TGFbeta signaling such as EMT.

234 Mechanistic investigations revealed that TGFbeta signaling through SMAD2/SMAD3 was necessary for

235 The delivery of an inhibitor of TGFbeta signaling to PD-1-expressing cells extends the s

236 g partners for SMURF2 can sustain or repress TGFbeta signaling, and RNF11 may promote TGFbeta-induced

237 otypic RDEB skin cultures with inhibitors of TGFbeta signaling, lysyl oxidase, or integrin beta1-medi

238 d show that inhibiting STAT3 potently blocks TGFbeta signaling, matrix remodeling, and TGFbeta-induce

239 with the MYH3 missense mutations had reduced TGFbeta signaling, revealing a regulatory role for embry

240 s, and this program interacts with deficient TGFbeta signaling, thereby accelerating the transformati

241 to trastuzumab and pertuzumab by activating TGFbeta signaling, which induces EMT.

242 al for the pathological, EMT-inducing arm of TGFbeta signaling.

243 of Hect E3 ligases previously implicated in TGFbeta signaling.

244 d mesenchymal character induced by localized TGFbeta signaling.

245 mice, suggesting induction of the downstream TGFbeta signaling.

246 ter response to the environment and to DAF-7/TGFbeta signaling.

247 lates treated with SB431542, an inhibitor of TGFbeta signaling.

248 SRF signaling responds to YAP-TEAD-dependent TGFbeta signaling.

249 n mediating transforming growth factor beta (TGFbeta) signaling and has been shown to function as a t

250 ed impaired transforming growth factor beta (TGFbeta) signaling in cultured cyclin-dependent kinase i

251 mbryos, the transforming growth factor beta (TGFbeta) signaling is elevated due to enhanced transcrip

252 ependent on transforming growth factor beta (TGFbeta) signaling.

253 nhibitor of transforming growth factor beta (TGFbeta) signaling.

254 We hypothesized that TGFbeta signalling controls expression of the miRNA gene

255 ferentiate into TH17 cells in the absence of TGFbeta signalling in a RORgammat-dependent manner.

256 Here the authors show that ERG balances TGFbeta signalling through the SMAD1 and SMAD3 pathways,

257 Western analysis revealed that TGFbeta signalling via Smad2/3/4 occurred differently be

258 Transforming growth factor beta (TGFbeta) signalling is essential for VBW closure, but th

259 While TGFbeta signals are anti-proliferative in benign and wel

260 and also revealed novel mechanisms by which TGFbeta signals are transduced.

261 at ERK is a key factor in growth suppressive TGFbeta signals, yet may also contribute to detrimental

262 represses transcriptional activation by the TGFbeta-SMAD gene regulatory pathway.

263 otic effect in renal fibrosis via regulating TGFbeta-Smad pathway.

264 TGFbeta-SMAD signaling exerts a contextual effect that s

265 liver homoeostasis by controlling canonical TGFbeta-SMAD signalling, driving the SMAD1 pathway while

266 with the noncanonical Hh pathway, involving TGFbeta/SMAD (transforming growth factor-beta/Sma- and M

267 that uses SB431542 (SB) compound to inhibit TGFbeta/Smad activation, and found that SB treatment pro

268 as achieved by impairing either the Stat3 or TGFbeta/Smad pathways, respectively.

269 Thus, a suppression of TGFbeta/Smad signaling in vitro is critical to maintaini

270 tion factor, KLF10, is a pivotal effector of TGFbeta/SMAD signaling that mediates antiproliferative e

271 tissues, and its action is mediated through TGFbeta/Smad3 signaling.

272 TGFbeta/Smad3 up-regulated Kruppel-like factor (KLF5) pr

273 Furthermore, TGFbeta/Smad3-stimulated KLF5 production and SMC de-diff

274 d mechanism of action of a HDACi, ITF2357 in TGFbeta-stimulated in vitro primary human cornea stromal

275 cancer invasion pathways and in response to TGFbeta stimulation and therefore orients future chemoth

276 nscriptional repressor that is degraded upon TGFbeta stimulation.

277 The ligands of the TGFbeta super family along with SMADs have also been imp

278 atterning depends on signaling from Nodal, a TGFbeta superfamily member.

279 Zebrafish Gdf3 (Dvr1) is a member of the TGFbeta superfamily of cell signaling ligands that inclu

280 Growth factors of the TGFbeta superfamily play key roles in regulating neurona

281 riptomic and proteomic profiling reveal that TGFbeta superfamily signaling pathways are preferentiall

282 gulate stem-cell pluripotency, including the TGFbeta superfamily, all of which are aberrantly elevate

283 The 10th FASEB meeting 'The TGFbeta Superfamily: Signaling in Development and Diseas

284 Resistance to TGFbeta suppression, while disadvantageous in autoimmuni

285 We show that RELB represses TGFbeta target promoters independently of DNA binding at

286 ulatory T cells, that did develop when these TGFbeta-targeting miRNAs were overexpressed, were capabl

287 eduction of CXCR7, while, in the presence of TGFbeta, this CXCL12 effect of MSCs on tumour cells is r

288 positive stem-like cells and cooperates with TGFbeta to drive gemcitabine resistance.

289 C13) binds to ALK5/TGFBR1 (type1 receptor of TGFbeta) to promote wound healing.

290 182 silencing leads to SMAD7 upregulation on TGFbeta treatment and prevents TGFbeta-induced EMT and i

291 Here, however, we show that TGFbeta treatment induces SMAD7 transcription but not it

292 Heterozygous loss of the arterial-specific TGFbeta type I receptor, activin receptor-like kinase 1

293 pression of miR302 effected silencing of the TGFbeta type II receptor and facilitated plasticity in a

294 tivates TGFbeta signaling cooperatively with TGFbeta type II receptor in colon cancer cells, enhancin

295 ge lymphoma expression, which stabilized the TGFbeta Type II receptor sensitizing PDAC cells to TGFbe

296 Furthermore, silencing of CXCL12 in TGFbeta-unresponsive MSCs restored their ability to prom

297 s for prognosis and early detection, and the TGFbeta-VAV1 axis represents a therapeutic target.

298 Pharmacological inhibition of TGFbeta-VAV1 signalling decreased the squamous/EMT-like

299 ysis revealed IL-10, IL-12, IL-13, IL-23 and TGFbeta were elevated, these were not statistically diff

300 ted injury, increased the bioavailability of TGFbeta, which promoted extracellular matrix production,