ライフサイエンスコーパス: TGF

1 TGF-beta has been implicated as a major pathogenic facto

2 TGF-beta is a multifunctional cytokine affecting many ce

3 TGF-beta is pro-metastatic for malignant cancer cells.

4 TGF-beta is pro-metastatic for the late-stage breast can

5 TGF-beta is regulated at the level of activation, but ho

6 TGF-beta is synthesized as a proprotein that dimerizes i

7 TGF-beta pre-treatment amplified the effects of BK on Rh

8 TGF-beta signaling components were expressed in most HCC

9 TGF-beta signaling has been associated with the tumorige

10 TGF-beta signaling maintains CD103 expression, promotes

11 TGF-beta signaling mediated by pSMAD2, bone morphogeneti

12 TGF-beta-induced beta-catenin also regulates NR4A1 expre

13 TGF-beta1 also increased levels of inflammatory cytokine

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

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

16 TGF-beta1-dependent cardiomyocyte depolarization resulte

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

18 yet tolerogenic phenotype, expressing IL-10, TGF-beta, IL-27, and aldehyde dehydrogenase 1A2 but not

19 okines in the serum (TNF-alpha, IL-6, IL-12, TGF-beta, and VEGF) were down regulated by DMDD.

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

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

22 ts independently of the GLP-1/Notch or DAF-7/TGF-beta pathways but together with the DAF-2/insulin IG

23 xtracellular matrix protein and delivering a TGF-beta mAb resulted in a relatively focal uptake in th

24 that a pharmacological compound that abates TGF-beta signalling and enhances ERK5 signalling may be

25 , podocyte injury, fibronectin accumulation, TGF-beta expression, and, most notably, age-related impa

26 n cancers and that oncogenic K-RAS activates TGF-beta signaling to promote tumor invasion and metasta

27 cell types, suggesting a possible activation TGF-beta receptor signaling in tumor cells in response t

28 Vector carrying shRNA against TGF-beta, though did not inhibit HBV replication alone,

29 ression of transforming growth factor-alpha (TGF-alpha), established by the presence of pleural and p

30 ion and neuronal differentiation by altering TGF-beta signaling.

31 y this enigmatic family of membrane-anchored TGF-beta family signaling regulators and link membrane a

32 genase 1A2 but not IL-12 or IL-35; IL-10 and TGF-beta together drove their suppression of TH2 cell pr

33 c levels of type 2 and regulatory (IL-10 and TGF-beta) cytokines.

34 actions and required production of IL-10 and TGF-beta.

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

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

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

38 In conclusion, activin and TGF-beta are strongly connected signaling pathways that

39 ased mRNA levels of TGF-beta1, TGF-beta2 and TGF-beta3.

40 multiple inhibitors of Wnt/beta-catenin and TGF-beta pathways, leading to their overactivation.

41 n is essential for vascular development, and TGF-beta signaling plays a critical role in this process

42 The combination of nonlytic IL-2/Fc and TGF-beta/Fc had a synergistic effect to promote engraftm

43 onizes pro-inflammatory actions of FGF23 and TGF-beta.

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

45 ation of bone marrow-derived fibroblasts and TGF-beta expression.

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

47 ion of CTLA4 (3 fold), Foxp3 (1.4 folds) and TGF-beta (1.62) in aorta.

48 tion-induced reduction of bone formation and TGF-beta gene expression, we measured mRNA levels of TGF

49 ction, and increased expression of Foxp3 and TGF-beta.

50 at the combination of shRNAs against HBV and TGF-beta could be developed into a viable treatment for

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

52 knockdown inhibited EMT, cell migration, and TGF-beta signaling.

53 reg in the pathogenic development of MMD and TGF-beta in Treg induced VEGF.

54 identified an interaction between moesin and TGF-beta receptor II (TbetaRII) that allows moesin to co

55 d mediates the regulation of PHF8 by MYC and TGF-beta signaling.

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

57 f transcriptional regulation during Ras- and TGF-beta-induced EMT that involves alterations of access

58 Blockade of JAK2/STAT3 and TGF-beta signaling by specific inhibitors significantly

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

60 dings demonstrate that the absence of apical TGF-beta signaling in normal epithelia is primarily a re

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

62 and induced by COPD-related stimuli, such as TGF-beta, cigarette smoke (CS), and cellular senescence.

63 antly reduced Col-1 secretion and attenuated TGF-beta induced increment in Col-1 localization at cell

64 In vitro, treatment with NE attenuated TGF-beta-induced accumulation of fibrotic markers.

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

66 instability or KRAS mutations; (ii) CRIS-B: TGF-beta pathway activity, epithelial-mesenchymal transi

67 wth factor, transforming growth factor beta (TGF-beta), is thought to play a pivotal role.

68 The transforming growth factor-beta (TGF-beta) network of ligands and intracellular signaling

69 Transforming growth factor-beta (TGF-beta) plays an important role in the development and

70 tivation of transforming growth factor-beta (TGF-beta) signaling pathway is a common feature of hepat

71 al role for transforming growth factor-beta (TGF-beta) signals in safe-guarding specific Treg cell fu

72 mber of the transforming growth factor-beta (TGF-beta) superfamily and has been implicated in various

73 ABSTRACT: Transforming growth factor-beta (TGF-beta), RhoA/Rho-kinase and Src-family kinases (SrcFK

74 Transforming growth factor-beta (TGF-beta), serine proteinases such as trypsin, and prote

75 induced by transforming growth factor-beta (TGF-beta), we identified the TF musculin (MSC) as being

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

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

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

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

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

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

82 nd found decreased mRNA levels of TGF-beta1, TGF-beta2 and TGF-beta3.

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

84 ear export of the receptor and thereby block TGF-beta-induced migration and EMT.

85 Enforced KLF4 expression blocked TGF-beta signal transduction and inhibited cell migratio

86 lternative therapeutic modality for blocking TGF-beta signaling in humans.

87 the inactive state through regulation of BMP/TGF-beta signaling.

88 a superfamily pathways that can inhibit both TGF-beta and activin signals while enhancing bone morpho

89 gands mimics the hypertrophy seen with broad TGF-beta blockers, while avoiding the adverse effects du

90 Smad transcription factors activated by TGF-beta or by BMP receptors form trimeric complexes wit

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

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

93 e spectrum of biological signals mediated by TGF-beta superfamily members.

94 MFs were stimulated by TGF-beta, cancer cell-CM or cancer cells, with or withou

95 a molecular switch that controls the cardiac TGF-beta axis and its early transcriptional effects that

96 ted by these mRNAs include Wnt/beta-catenin, TGF-beta, and stem cell signaling.

97 we report a novel finding that, in TM cells, TGF-beta-induced increase in collagen expression is asso

98 ls on the other hand, exhibited constitutive TGF-beta signaling and were less tumorigenic.

99 The switch converting TGF-beta from a tumor-suppressor to tumor-promoter has n

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

101 Levels of anti-inflammatory cytokine TGF-beta remained practically unaffected in ImI treated

102 The master cytokine TGF-beta mediates tissue fibrosis associated with inflam

103 a group, while dexamethasone (DEX) decreased TGF-beta group mRNA levels in normal mice.

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

105 on was found to be a novel pathway of direct TGF-beta-dependent Treg-cell suppression of mast cell ac

106 nesins, KIF5A was notably upregulated during TGF-beta induced mesothelial-mesenchymal transition (Mes

107 neurogenesis and the TGF-beta pathway (i.e. TGF-beta; SMAD-2, -3, and -7; and SMURF-2) in the rat hi

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

109 fine the relative contribution of endogenous TGF-beta proteins to the negative regulation of muscle m

110 Herein, we describe an engineered TGF-beta monomer, lacking the heel helix, a structural m

111 ivity as wild-type (WT) Arkadia in enhancing TGF-beta signaling responses, while W972R does not.

112 en transferred into mice bearing established TGF-beta-OVA-expressing thymomas, produce high amounts o

113 3 ligase complex, thereby limiting excessive TGF-beta response.

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

115 ) T cells, independent of Foxp3 or exogenous TGF-beta.

116 eposition, collagen 1 and 3 mRNA expression, TGF-beta production, and activation of alternatively act

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

118 ed production of transforming growth factor (TGF) beta and interleukin (IL)-8.

119 T) is induced by transforming growth factor (TGF)-beta and facilitates tumor progression.

120 Transforming growth factor (TGF)-beta cytokines signal via a complex network of path

121 yzed the role of transforming growth factor (TGF)-beta signaling for CNV formation by generating a se

122 ncentrate on the transforming growth factor (TGF)-beta/bone morphogenetic protein (BMP) pathway, whic

123 own to stimulate transforming growth factor (TGF)-beta1 to -beta3 translation in vitro and in vivo.

124 is increased by transforming growth factor (TGF)-beta1, and ADAM10-mediated sEphrin-B2 generation is

125 ctors, including transforming growth factor (TGF)-beta1, in human granulosa cells, and their expressi

126 platform for: i) transforming growth factor (TGF)-beta1-induced spatial differentiation of fibroblast

127 nalling, and the transforming growth factor (TGF)beta family.

128 latory cytokine fusion proteins of IL-10/Fc, TGF-beta/Fc, or IL-2/Fc would enhance allogeneic bone ma

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

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

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

132 for binding the other receptor required for TGF-beta signaling, the TGF-beta type II receptor (Tbeta

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

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

135 Neutralization of HLA-G, TGF-beta, and IL-10 partially restored T cell alloprolif

136 involvement of tolerogenic molecules (HLA-G, TGF-beta, and IL-10) were tested on a mixed lymphocyte r

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

138 In CF-HBEC, TGF-beta increased KL secretion and upregulated FGF rece

139 egulated at the level of activation, but how TGF-beta is activated in this disease is unknown.

140 We review how TGF-beta family member signaling is altered during devel

141 However, TGF-beta induced apoptosis in normal and benign but not

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

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

144 Taken together, these observations identify TGF-beta2 as the crucial mediator of NPC immunomodulatio

145 their cognate ligands to type I and type II TGF-beta receptors, indicating that Cripto-1 and Cryptic

146 se changes could be attributed to changes in TGF-beta and matrix metalloproteinase-9, the downstream

147 h prevented Smad3 from binding to SBE DNA in TGF-beta-responsive SMC gene promoters, resulting in sup

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

149 sels become dependent on a small increase in TGF-beta signaling via activin receptor-like kinase 5 to

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

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

152 trate altered activity of RhoA and increased TGF-beta signaling and ENaC activity.

153 advanced stages of these cancers, increased TGF-beta expression is linked to high metastasis and poo

154 The increased TGF-beta signaling may protect against rapid retinopathy

155 We found that carbofuran increases TGF-beta signaling (i.e. increased phosphorylated SMAD-2

156 a rationale to pursue a means of increasing TGF-beta signaling as a potential therapy for Parkinson'

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

158 ring progressive kidney injury by inhibiting TGF-beta type 1 receptor.

159 Conversely, depletion of BRD7 inhibits TGF-beta responses.

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

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

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

163 Despite increases in KL, TGF-beta also increased IL-8 secretion via activation of

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

165 provide a new avenue to probe and manipulate TGF-beta signaling and may inform similar modifications

166 rotein levels of fibrosis signaling mediator TGF-beta remained the same and the second messenger, Sma

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

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

169 red an lncRNA-based mechanism that modulates TGF-beta/Smad3 signaling during SMC differentiation.

170 etained the same overall structure of native TGF-beta monomers and bound TbetaRII in an identical man

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

172 t and indirect fibroproliferative actions of TGF-beta.

173 Activation of TGF-beta receptors and p38 MAPK increased glycogen synth

174 pressed in most HCC cells, and activation of TGF-beta signaling promoted cell migration and invasion.

175 Addition of TGF-beta to GF(-) increased RASF attachment (12.7-fold)

176 The addition of TGF-beta/Fc (5- or 10-day treatment) or nonlytic IL-2/Fc

177 Co-administration of TGF-beta shRNA and HBV dual-shRNA decreased HBV DNA, HBV

178 r (BMPR) axis: the anti-proliferative arm of TGF-beta super family of receptors.

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

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

181 eous stroke because of myeloid deficiency of TGF-beta (transforming growth factor-beta) signaling.

182 models with induced conditional deletion of TGF-beta signaling in the entire eye, the retinal pigmen

183 Although the specific deletion of TGF-beta signaling in the RPE caused no obvious changes,

184 Moreover, intrathecal delivery of TGF-beta2 during the effector phase of EAE ameliorated d

185 malformations are related to deregulation of TGF-beta/BMP signaling.

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

187 phorylated SMAD2/3, a downstream effector of TGF-beta Furthermore, in the PD parietal arterioles, C1q

188 rlying cell- and process-specific effects of TGF-beta are poorly understood.

189 n this study, we investigated the effects of TGF-beta on IL-33-mediated mast cell activation.

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

191 nuclear export results in nuclear export of TGF-beta-induced beta-catenin, which then undergoes prot

192 wound healing though increased expression of TGF beta leading to enhanced formation of granulation ti

193 al inflammation, including the expression of TGF-beta, NFkappaB, MCP-1, IL-1, IL-6, ICAM-1, VCAM-1 an

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

195 esin plays any role during the generation of TGF-beta-induced Tregs (iTregs) is unknown.

196 However, the importance of TGF-beta-Smad2/3 signaling in fibroblast-mediated cardia

197 Despite the known importance of TGF-betas in promoting disease progression, no inhibitor

198 bone formation is a result of inhibition of TGF-beta gene expression.

199 cription and, consequently, in inhibition of TGF-beta/Smad3-mediated SMC differentiation.

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 ubjects' fibroblasts showed a lower level of TGF-beta2 and significantly increased the epithelial cel

203 ced inflammation, lower expression levels of TGF-beta and proteases associated with tissue remodeling

204 nervation-induced decrease in mRNA levels of TGF-beta group, while dexamethasone (DEX) decreased TGF-

205 gene expression, we measured mRNA levels of TGF-beta in denervation mouse bone and found decreased m

206 , while cancer cells produced high levels of TGF-beta.

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

208 el predicted that simultaneous modulation of TGF-beta and matrix metalloproteinases would be more eff

209 le of Th1 differentiation in the presence of TGF-beta, suggesting a novel approach to adoptive cell t

210 ally relevant for force-dependent release of TGF-beta from latency.

211 To investigate the role of TGF-beta and IL-6 in myofibroblasts (MFs) - lung cancer

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

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

214 n PTC samples from patients, upregulation of TGF-beta, p27, p65 and cyclin D1 mRNA were significantly

215 inhibition of CD8(+) T cells is dependent on TGF-beta and PD-L1.

216 inhibition of CD4(+) T cells is dependent on TGF-beta, whereas inhibition of CD8(+) T cells is depend

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

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

219 CC may contribute to activation of oncogenic TGF-beta signaling and subsequent tumor progression.

220 data indicate that KLF4 suppresses oncogenic TGF-beta signaling by activation of Smad7 transcription,

221 ary epithelial cells stimulated by IL-17A or TGF-beta2 was also inhibited by 124.1% and 69.9%, respec

222 nd may inform similar modifications of other TGF-beta family members.

223 lysis (Molecular Mechanisms of Cancer, p53-, TGF-beta-, MAPK- and Wnt-signaling).

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

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

226 inhibition or knockout bone marrow prevents TGF-beta activation and protects against PH development.

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

228 interface stabilize a specific integrin/pro-TGF-beta orientation that defines the pathway through th

229 owth factor (GF) domain in each monomer, pro-TGF-beta is secreted and stored in latent complexes.

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 of HIV-Tat and cocaine on the proliferative TGF-beta signaling cascade.

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

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

235 Cripto-1 and Cryptic recognize and regulate TGF-beta family ligands, are less clear.

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

237 udy, we show that STAT3 negatively regulates TGF-beta signaling via ERBB2-interacting protein (ERBIN)

238 t mice exhibited changes in genes regulating TGF-beta/BMP/FGF signaling, as well as in genes controll

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

240 However, to produce cell-specific responses, TGF-beta pathways are heavily regulated by secondary fac

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

242 Tumor-secreted TGF-beta and granulocyte-macrophage CSF (GM-CSF) enhance

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

244 Following the activation of SMADs, TGF-beta also induces a second phase of STAT phosphoryla

245 exosomal miR-19a in activation of the STAT3-TGF-beta pathway in HSC.

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

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

248 ion of SMAD3 or CCT6A efficiently suppresses TGF-beta-mediated metastasis.

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

250 We find that TGF-beta signaling is operative in mouse primary keratin

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

252 eta in murine bronchiolitis obliterans; that TGF-beta and the C' cascade present signaling interactio

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

254 We further show that TGF-beta and ALK1 are required in IL-37 induced pro-angi

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

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

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

258 sment, provides new evidence suggesting that TGF-alpha overexpression produces impairment in diaphrag

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

260 Beta-catenin/Tcf and the TGF-beta bone morphogenetic protein (BMP) provide critic

261 of proteins involved in neurogenesis and the TGF-beta pathway (i.e. TGF-beta; SMAD-2, -3, and -7; and

262 in, the neuropeptide receptor NPR-1, and the TGF-beta peptide DAF-7 each have stage-specific effects

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

264 a structural motif essential for binding the TGF-beta type I receptor (TbetaRI) but dispensable for b

265 In mice, the TGF-beta superfamily is implicated in the regulation of

266 /CD24- cells, constitutive activation of the TGF-beta axis was both necessary and sufficient to reduc

267 iation factor-15 (GDF-15) is a member of the TGF-beta cytokine superfamily that is widely expressed a

268 dicative of 'imprinting' by cytokines of the TGF-beta family.

269 Endoglin is part of the TGF-beta receptor complex and has a crucial role in fibr

270 onses and attenuated the upregulation of the TGF-beta signaling pathway and alpha1-antitrypsin protei

271 ive of receptors for a distinct class of the TGF-beta superfamily ligands.

272 protein (KCP) is a secreted regulator of the TGF-beta superfamily pathways that can inhibit both TGF-

273 n and contribute to the understanding of the TGF-beta-mediated fibrogenic response.

274 related to loss-of-function mutation of the TGF-beta/BMP receptor complex and the second to increase

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

276 ministration of the bispecific DVD-Ig or the TGF-beta mAb (1-10 mg/kg) but not the FnEDA mAb attenuat

277 the prodomain, apply force, and release the TGF-beta growth factor.

278 These findings demonstrate that shifting the TGF-beta superfamily signaling with a secreted protein c

279 eceptor required for TGF-beta signaling, the TGF-beta type II receptor (TbetaRII), as an alternative

280 Our study demontrated that the TGF-beta and IL-6/JAK2/STAT3 signaling pathways form a p

281 molecule that mediates IL-37 binding to the TGF-beta receptor complex.

282 -37 induces pro-angiogenic responses through TGF-beta, which may act as the bridging molecule that me

283 Thus, TGF-beta-induced nuclear export of NR4A1 in TNBC cells p

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

285 ptor signaling in tumor cells in response to TGF-beta from the TME.

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

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

288 second to increased signaling sensitivity to TGF-beta/BMP.

289 arly tumor development in many cancer types, TGF-beta acts as a tumor suppressor, whereas in the adva

290 -6 and MF-CM activated STAT3 and upregulated TGF-beta in cancer cells.

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

292 is that mediate stellate cell activation via TGF-beta.

293 ed that IL-17A induces epithelial injury via TGF-beta in murine bronchiolitis obliterans; that TGF-be

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

295 ogressive kidney disease in association with TGF-beta overexpression, administration of SRT3025 atten

296 sm compared with recipients conditioned with TGF-beta/MR1/Rapa/100 cGy.

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

298 hromatin regions in EpRas cells treated with TGF-beta.

299 ioned medium (MF-CM) or MFs, with or without TGF-beta signaling inhibitor - SB431542 and/or JAK2/STAT

300 scription factor pathways (for example, Wnt, TGF-beta, mir200, ZEB1, OVOL2, p63 and p300) and transla