ライフサイエンスコーパス: TGF-beta receptor

1 gical blockade of the ALK-5 component of the TGF-beta receptor.

2 ody or locally by using a soluble, defective TGF-beta receptor.

3 egulates its availability for binding to the TGF-beta receptor.

4 nhibition of activin-like kinase-5, a type I TGF-beta receptor.

5 ALK-1 and to a lesser extent by the type II TGF-beta receptor.

6 me fusion to signal transduction through the TGF-beta receptor.

7 be activated via a pathway that bypasses the TGF-beta receptor.

8 betaglycan, is the most abundantly expressed TGF-beta receptor.

9 d through the TGF-beta3 ligand that binds to TGF-beta receptors.

10 ansforming growth factor-beta (TGF-beta) and TGF-beta receptors.

11 d monolayers that present peptide ligands to TGF-beta receptors.

12 s compensating for the reduced expression of TGF-beta receptors.

13 all molecules inhibit the kinase activity of TGF-beta receptors.

14 AF homology domain physically interacts with TGF-beta receptors.

15 y forming membrane invaginations that enfold TGF-beta receptors.

16 often associated with the functional loss of TGF-beta receptors.

17 mutations in the genes encoding type I or II TGF-beta receptors.

18 nits of the transforming growth factor beta (TGF-beta) receptor.

19 on within the graft drives stenosis and that TGF-beta receptor 1 (TGF-betaR1) inhibition can prevent

20 transforming growth factor beta (TGF-beta), TGF-beta receptor 1 (TGF-betaR1), connective tissue grow

21 nteracts closely with PDGF receptor beta and TGF-beta receptor 1 at the cell membrane, suggesting tha

22 TGF-beta receptor 1 inhibition prevents stenosis of tiss

23 and C2C12 myotubes treated with TGF-beta, a TGF-beta receptor 1 pharmacological inhibitor, adenoviru

24 icity and DRG neuronal hyperexcitability via TGF-beta receptor 1-mediated noncanonical signaling.

25 ition of SMAD2/3 signaling via targeting the TGF-beta receptor 1.

26 en ILEI, the PS1-protease, TGF-beta, and the TGF-beta receptor 1.

27 teracts with TGF-beta1 to augment fibroblast TGF-beta receptors 1 and 2 expression and TGF-beta-induc

28 We demonstrated that TGF-beta receptor 2 (TGF-betaR2) and SNAIL2 are direct t

29 on of BEC in severe asthma through targeting TGF-beta receptor 2 mRNA.

30 -19a increased SMAD3 phosphorylation through TGF-beta receptor 2 signaling and abrogated BEC prolifer

31 2 causes upregulation of Fzd2, Ifi27l2a, and TGF-beta receptor 2.

32 ether TGF-beta signaling in hepatocytes, via TGF-beta receptor-2 (Tgfbr2), promotes HCC and liver fib

33 to malignant progression and is mediated by TGF-beta receptor activation in HMEC.

34 the same cells that, conversely, the type I TGF-beta receptor activin receptor-like kinase 5 is disp

35 h (SM16, a selective inhibitor of the type 1 TGF-beta receptor activin receptor-like kinase 5, orally

36 Suppression of TGF-beta receptor activity or ablation of SMAD3 or SMAD4

37 eptor expression and signaling, and blocking TGF-beta receptor activity potentiates the antiprolifera

38 ays such as transforming growth factor-beta (TGF-beta) receptor activity.

39 adult neurogenesis, genetic deletion of the TGF-beta receptor ALK5 reduced the number, migration and

40 HES ligated the transforming growth factor (TGF) beta receptor and promoted Smad2/3 phosphorylation.

41 ing, and mediated by upregulation of type II TGF-beta receptor and connective tissue growth factor.

42 , we report that CEA directly interacts with TGF-beta receptor and inhibits TGF-beta signaling.

43 Klotho protein directly binds to the type-II TGF-beta receptor and inhibits TGF-beta1 binding to cell

44 lasts from mouse PDA were also responsive to TGF-beta receptor and PI3K/AKT inhibition with regard to

45 GF-beta signaling involves activation of the TGF-beta receptors and downstream signal transducers Sma

46 of TGF-beta, including binding to mammalian TGF-beta receptors and inducing mouse and human Foxp3(+)

47 gnaling complex formation that includes both TGF-beta receptors and integrins.

48 l, rapid anti-inflammatory activity of the 2 TGF-beta receptors and of TGF-beta1.

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

50 Interestingly, TGF-beta receptors and Smad-2/3 phosphorylation were up-

51 ocytic commitment or increased expression of TGF-beta receptors and SMAD3 phosphorylation.

52 eta signaling by reducing gene expression of TGF-beta receptors and Smad4, leading to increased expre

53 ation among transforming growth factor-beta (TGF-beta) receptors and its modulation by coreceptors re

54 With blockade of TGF-beta receptor, Ang II-mediated hypertrophy was conve

55 d expression of TMEPAI were inhibited by the TGF-beta receptor antagonist SB431542 and overexpression

56 The TGF-beta receptor antagonist SB431542 completely blocked

57 and it upregulated mir-200b/c as well as the TGF-beta receptor antagonist, BMP2.

58 -beta ligands, followed by the addition of a TGF-beta receptor antagonist, dramatically increased the

59 p by a pan-TGF-beta-neutralizing antibody, a TGF-beta receptor antagonist, or LTBP gene silencing res

60 TGF-beta receptor antagonists also rescued cells from do

61 and Mv1Lu cells whereas the majority of the TGF-beta receptors are localized in non-lipid-raft fract

62 4 hours post-wounding) of type I and type II TGF-beta receptors as well as unexpectedly high fibrobla

63 Here we show that expression of the TGF-beta receptor-associated protein, SARA (Smad anchor

64 , on MB gamma neurons upstream of the type-I TGF-beta receptor Baboon.

65 Although structurally similar, BMP and TGF-beta receptors bind in dramatically different modes,

66 p52ShcA competed with Smad3 for TGF-beta receptor binding, and down-regulation of ShcA e

67 suramin decreased expression of the type II TGF-beta receptor, blocked phosphorylation of the EGF an

68 TAB1 does not interact with TGF-beta receptors, but TAB1 is indispensable for TGF-be

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

70 TSC1 interacts with the TGF-beta receptor complex and Smad2/3 and is required fo

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

72 ment of the transforming growth factor-beta (TGF-beta) receptor complex activates multiple signaling

73 cribe the crystal structure of a six-element TGF-beta:receptor complex, addressing long-standing ques

74 Furthermore, p52ShcA sequestered TGF-beta receptor complexes to caveolin-associated membr

75 show that reduced expression of the type II TGF-beta receptor correlates with loss of luminal differ

76 type I activin-like receptor kinase 5 (ALK5) TGF-beta receptor coupled to Smad signal transducers.

77 growing that imbalanced activation of other TGF-beta receptors coupled with reduced activity of muta

78 n resulted in decreased Smad3 binding to the TGF-beta receptor, decreased Smad3 activation, and incre

79 recapitulate in great part the phenotype of TGF-beta receptor-deficient CD4 T cells, while SMAD4 was

80 TGF-beta receptor-deficient CD8(+) T-cells showed enhanc

81 Enhanced apoptosis of TGF-beta receptor-deficient nTreg cells was associated w

82 Compromised IL-7Ralpha expression in TGF-beta-receptor-deficient T cells was associated with

83 d the development and homeostasis defects of TGF-beta-receptor-deficient T cells.

84 hK1, Col alpha1(I), and Col alpha1(III) in a TGF-beta receptor-dependent manner.

85 lear translocation of p-Smad2 and p-Smad3 in TGF-beta receptor-dependent, but SphK1-independent, mann

86 Although TGF-beta receptors directly activate both Smads 2 and 3,

87 l-specific deletion of the gene encoding the TGF-beta receptor during chronic lymphocytic choriomenin

88 us manner, acting in cis with PDGFR-beta and TGF-beta receptors during induction/polarization and mig

89 ing mechanism expands and partially explains TGF-beta receptor dynamics and consequential signaling d

90 ociated sorting protein Disabled-2 (Dab2) in TGF-beta receptor endocytosis.

91 he roles of transforming growth factor-beta (TGF-beta) receptor endocytosis in signaling have been in

92 Moreover, loss of TRIM33 enhances TGF-beta receptor expression and signaling, and blocking

93 nity T cell receptors, and the abrogation of TGF-beta receptor expression led to failed maintenance o

94 es observed that the promoter of the type II TGF-beta receptor gene (TbetaR-II) is strongly stimulate

95 by heterozygous missense mutations in either TGF-beta receptor gene (TGFBR1 or TGFBR2), which are pre

96 Similarly, mutations in TGF-beta receptor gene family members cause craniofacial

97 r the type I (TbetaRI) or type II (TbetaRII) TGF-beta receptor has been documented in approximately 3

98 ere blocked by a transforming growth factor (TGF) beta receptor I (TGFbetaRI) kinase inhibitor.

99 was further confirmed by RNAi using specific TGF-beta receptor I (TbetaR1) siRNA duplexes.

100 (ADP-ribose) polymerase-1 (PARP-1) regulates TGF-beta receptor I (TbetaRI) and II (TbetaRII) expressi

101 rther demonstrated that VEPH1 interacts with TGF-beta receptor I (TbetaRI) and inhibits nuclear accum

102 observed that SMAD7, a negative regulator of TGF-beta receptor I (TBRI) kinase, is markedly decreased

103 TGF-beta receptor I (TGF-beta RI) expression is increase

104 ck-specific knockout mouse model by crossing TGF-beta receptor I (Tgfbr1) floxed mice with K14-CreER(

105 ad2/3, allowing Smad2/3 association with the TGF-beta receptor I and Smad anchor for receptor activat

106 esponse to TGF-beta, RASSF1A is recruited to TGF-beta receptor I and targeted for degradation by the

107 Overexpression of constitutively active TGF-beta receptor I in aged cardiac fibroblasts ameliora

108 he activin receptor-like kinase 5 pathway of TGF-beta receptor I in astrocytes.

109 ression, which is similar with the result of TGF-beta receptor I inhibitor treatment.

110 the effect of a small molecule inhibitor of TGF-beta receptor I kinase (TbetaRI), SD-208, on various

111 horylation, which was blocked by a selective TGF-beta receptor I kinase inhibitor but not by CRM197.

112 Gene expression was blocked by the TGF-beta receptor I kinase inhibitor SB431542.

113 The addition of a TGF-beta receptor I kinase inhibitor that blocks Smad-de

114 tion of SD208, a small-molecule inhibitor of TGF-beta receptor I kinase, or forced overexpression of

115 ings suggest that collagen products adsorb a TGF-beta receptor I kinase-dependent activity of EMD and

116 ing TGF-beta1 or T cell-specific deletion of TGF-beta receptor I lacked TCRalphabeta+CD8alphaalpha+ I

117 Although TGF-beta receptor I signaling was required for both Foxp

118 pression and ESM/EMF contraction depended on TGF-beta receptor I signals.

119 Inhibition of TGF-beta receptor I using SB431542 ablated TGF-beta-indu

120 taining alpha3beta1 integrins, beta-catenin, TGF-beta receptor I, E-cadherin, and phosphorylated Smad

121 Aberrant signaling via TGF-beta receptor I/activin receptor-like kinase 5 may b

122 ather, polarized basolateral presentation of TGF-beta receptors I and II deprives apically delivered

123 omplex with transforming growth factor-beta (TGF-beta) receptor I (TGF-betaRI), and activated Smad3.

124 mediator of transforming growth factor-beta (TGF-beta) receptor I kinase (TBRI) activation, is consti

125 pression of transforming growth factor-beta (TGF-beta) receptors I and II and diminished SMAD3 phosph

126 egulator of transforming growth factor-beta (TGF-beta) receptor-I kinase, is markedly reduced in MDS

127 ic protein linking IL-2 to the ectodomain of TGF-beta receptor II (also known as FIST) become resista

128 ta1-resistant cell line DB lacked functional TGF-beta receptor II (T beta RII) in contrast to the TGF

129 unction of epithelial TGF-beta signaling via TGF-beta receptor II (TbetaRII) and its contribution to

130 TPase activating protein 1 (IQGAP1) binds to TGF-beta receptor II (TbetaRII) and suppresses TbetaRII-

131 mune diabetes, here we show that ablation of TGF-beta receptor II (TbetaRII) in T cells, but not Foxp

132 we developed prostate stromal cells null for TGF-beta receptor II (TbetaRII) or engineered to express

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

134 We report that DHT decreases the level of TGF-beta receptor II (TbetaRII) through a transcriptiona

135 pressing a T cell-specific dominant-negative TGF-beta receptor II (TGF-betaRII DN) show dampened Th2

136 gnaling components demonstrated by decreased TGF-beta receptor II (TGF-betaRII) and SMAD3 expression.

137 tor pathway, mice additionally received anti-TGF-beta receptor II (TGF-betaRII) antibodies.

138 Levels of TGF-beta receptor II (TGF-betaRII) as well as Smad7 (a T

139 TGF-beta receptor II (TGF-betaRII), critically implicate

140 (activin receptor-like kinase 5 [ALK-5]) and TGF-beta receptor II (TGF-betaRII).

141 Loss of TGF-beta receptor II (TGFbetaR2) in the prostate stroma

142 Mice lacking TGF-beta receptor II (TGFbetaRII) in retinal neurons had

143 First, the Tgf-beta receptor II (Tgfbr2) was specifically removed f

144 In mice with a dominant-negative form of TGF-beta receptor II and impaired TGF-beta signaling, IL

145 Here, we show TGF-beta receptor II and TGF-beta-activated kinase 1 (TA

146 TGF-beta receptor II appears to be a receptor important

147 crease in TGF-beta ligands and an absence of TGF-beta receptor II in malignant peripheral nerve sheat

148 a tumor-reactive TCR and a dominant-negative TGF-beta receptor II induces complete and sustained tumo

149 We found that TGF-beta receptor II signaling regulates Noggin, Wnt9a,

150 iR-93 and its family members directly target TGF-beta receptor II to enhance iPSC generation.

151 cells in which a truncated dominant-negative TGF-beta receptor II was stably transfected to avoid aut

152 precipitation revealed binding of albumin to TGF-beta receptor II, and Smad2 phosphorylation confirme

153 is sensitive to whether they can initiate a TGF-beta receptor II-mediated response to counterbalance

154 dvantage of transforming growth factor-beta (TGF-beta) receptor II dominant negative (dnTGF-betaRII)

155 ells in our transforming growth factor beta (TGF-beta) receptor II dominant-negative (dnTGFbetaRII) m

156 brogated in transforming growth factor beta (TGF-beta) receptor II knockout mice indicating a role fo

157 Peripheral CD4+ and CD8+ T cells with TGF-beta-receptor II (TGF-betaRII) deficiency activated

158 Transforming growth factor (TGF)beta receptor III (TGFbetaR3), or beta-glycan, binds

159 nt differences among MEF lines in content of TGF-beta receptor III were similar to those in EGFR, alb

160 land and conditional deletion of the type II TGF-beta receptor in mammary epithelium, an increased le

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

162 tory factor, GSK3 inhibitor (CHIR99021), and TGF-beta receptor inhibitor (SB431542); retain high neur

163 contact-induced expression of TGF-beta1 and TGF-beta receptor inhibitor SB431542 inhibited contact-i

164 bination of erlotinib and SB505124, a type I TGF-beta receptor inhibitor.

165 phosphorylation in pericytes, and again, the TGF-beta-receptor inhibitor SB431542 (0.5-5muM) blocked

166 A TGF-beta-receptor inhibitor SB431542 (0.5-5muM) decrease

167 combination of therapeutic adenoviruses and TGF-beta receptor inhibitors could be an efficient antic

168 Ligand binding of the type I and II TGF-beta receptors initiate downstream signaling.

169 Finally, we cloned the tomato ortholog of TGF-beta Receptor Interacting Protein (TRIP1), which was

170 Our findings suggest that BAT3, a TGF-beta receptor-interacting protein, is capable of mod

171 fy BAT3 (HLA-B-associated transcript 3) as a TGF-beta receptor-interacting protein.

172 o the important role of caveolin-1 (CAV1) in TGF-beta receptor internalization and TGF-beta signaling

173 eta) signaling owing to its participation in TGF-beta receptor internalization.

174 TGF-beta receptor internalized through caveolin-1 lipid

175 Although the role of the types I and II TGF-beta receptors is fairly well established, the role

176 of how a MAP kinase cascade is activated by TGF-beta receptors is not clear.

177 ng type I and type II (TbetaRI and TbetaRII) TGF-beta receptors is well characterized and is essentia

178 Betaglycan, or the type III TGF-beta receptor, is a coreceptor that regulates TGF-be

179 F-beta increased hepcidin mRNA expression or TGF-beta receptor kinase activity, respectively, which i

180 r423/425 residues that are phosphorylated by TGF-beta receptor kinase and are critical for the nuclea

181 Inhibition of TGF-beta receptor kinase completely prevents induction o

182 naling in the SW480 cells, and the selective TGF-beta receptor kinase inhibitor LY364947 did not prev

183 ells remained quiescent in the presence of a TGF-beta receptor kinase inhibitor, whereas exogenous TG

184 Suppression of TGF-beta signaling, either by TGF-beta receptor kinase inhibitors or by silencing Smad

185 In addition to TGF-beta receptor kinase inhibitors, myofibroblast activ

186 In addition to TGF-beta receptor kinase inhibitors, we identified small

187 ated by pharmacological inhibition of type I TGF-beta receptor kinase, combined inhibition of MEK/Src

188 Inhibition of TGF-beta receptor kinase, knockdown of Smad4, or overexp

189 We also determined the effects of a TGF-beta-receptor kinase inhibitor (LY2109761) in CRC tu

190 unction of Smad signaling and the effects of TGF-beta-receptor kinase inhibitors have not been analyz

191 generated endothelium-specific heterozygous TGF-beta receptor knockout (TbetaRII(endo+/-)) mice to e

192 itical, and proteins that associate with the TGF-beta receptors may exert positive or negative regula

193 e imbalance of activation of BMPR2 and other TGF-beta receptors may yield future therapies for PAH.

194 sion of apically targeted type I and type II TGF-beta receptors mediated Smad3 signaling from the api

195 These results suggest that inhibiting TGF-beta receptor-mediated function in collecting ducts

196 Transforming growth factor-beta (TGF-beta) receptor oligomerization has important roles i

197 es a latent transforming growth factor beta (TGF-beta) receptor on regulatory T cells.

198 itro and ex vivo Pharmacologic inhibition of TGF-beta receptor or SMAD3 abrogates the TGF-beta-stimul

199 a signaling, including either subunit of the TGF-beta receptor or SMAD3, thereby engendering controve

200 d transcriptional activity without affecting TGF-beta receptors or Smad2, whereas overexpression of t

201 Inhibition of the TGF-beta receptor pathway abolishes the fibrinogen-induc

202 the larval germline progenitor pool, and the TGF-beta receptor pathway acts in the germline stem cell

203 he mechanism of action of sGARP involves the TGF-beta receptor pathway, mice additionally received an

204 Pharmacologic inhibition of TGF-beta receptor, PI3K, or protein kinase B (AKT) was f

205 Regulating TGF-beta receptor presentation provides an avenue to alt

206 in complex with the B-site of mouse type II TGF-beta receptor promoter DNA (mTbetaR-II(DNA)).

207 duced mammary carcinomas lacking the type II TGF-beta receptor (PyMT(mgko)) are highly metastatic com

208 secrete TGF-beta1, which in turn activates a TGF-beta receptor/RAC1/SMAD-dependent signaling pathway

209 al adaptor in mesenchymal cells required for TGF-beta receptor recycling as well as Smad2 phosphoryla

210 errin) or -independent (i.e., LacCer) cargo, TGF-beta receptor recycling was abrogated.

211 iapoptotic PI3K/AKT pathway does not require TGF-beta receptor-regulated Smad2 and Smad3.

212 Here we show that the highly homologous TGF-beta receptor-regulated Smads (R-Smads): Smad2 and S

213 the translationally controlled assembly of a TGF-beta receptor signaling complex containing alpha3bet

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

215 anti-TGF-beta antibody or use of a specific TGF-beta receptor signaling inhibitor resulted in rescue

216 d through a transforming growth factor-beta (TGF-beta) receptor signaling.

217 Here, we show that TGF-beta-receptor signaling is required during gastrulat

218 earning, and that the activity of the type I TGF-beta receptor SMA-6 in the hypodermis is needed duri

219 inhibition of any of the five intermediates (TGF-beta receptor, Smad2, EGF, EGF-R, and ERK1/2) attenu

220 stinct but cooperating pathways that involve TGF-beta receptor/Smad2 activation and EGF-mediated EGF-

221 Transforming growth factor (TGF)-beta receptors stimulate diverse signaling processe

222 g the endocytic and trafficking itinerary of TGF-beta receptor subunits.

223 in mice bearing tumors that lack the type II TGF-beta receptor, suggesting that the increase in metas

224 utations in transforming growth factor-beta (TGF-beta) receptor superfamily members underlie conditio

225 F-beta receptor (T beta RII), and the type I TGF-beta receptor (T beta RI) to regulate diverse cellul

226 e (WAP-Cre), we have now ablated the type II TGF-beta receptor (T beta RII) expression specifically w

227 TGF-beta receptor (T beta RIII), the type II TGF-beta receptor (T beta RII), and the type I TGF-beta

228 nserved cell surface receptors, the type III TGF-beta receptor (T beta RIII), the type II TGF-beta re

229 Transforming growth factor beta (TGF-beta) receptor (TbetaR) signaling contributes to nor

230 Neocortical neurons lacking the type II TGF-beta receptor (TbetaR2) fail to initiate axons durin

231 Internalization and degradation of TGF-beta receptor TbetaRI inhibits TGF-beta signaling an

232 proteins that differentially bound to type I TGF-beta receptor (TbetaRI) in nontransformed, HER2-tran

233 tically, fibulin-3 interacts with the type I TGF-beta receptor (TbetaRI) to block TGF-beta induced co

234 teral mobility and endocytosis of the type I TGF-beta receptor (TbetaRI) with TGF-beta phosphoprotein

235 endocytosis of the signal-transducing type I TGF-beta receptor (TbetaRI).

236 eventing it from interacting with the type I TGF-beta receptor (TbetaRI).

237 10), which was found to selectively activate TGF-beta receptor (TbetaRI/II)-dependent Smad3 phosphory

238 pe I and II transforming growth factor beta (TGF-beta) receptors (TbetaRI and TbetaRII, respectively)

239 omplex formation of TbetaRI with the type II TGF-beta receptor (TbetaRII) and subsequent downstream T

240 etween the cytoplasmic domain of the type II TGF-beta receptor (TbetaRII) and the FN receptor (alpha5

241 Oligomerization of ALK5 and the type II TGF-beta receptor (TbetaRII) has been thoroughly investi

242 ation of the serine/threonine kinase type II TGF-beta receptor (TbetaRII), which in turn promotes a T

243 al plasma membrane expression of the type II TGF-beta receptor (TbetaRII).

244 signaling by directly binding to the type II TGF-beta receptor (TbetaRII).

245 Here, we show that type III TGF-beta receptor (TbetaRIII or betaglycan) expression i

246 GF-beta superfamily coreceptor, the type III TGF-beta receptor (TbetaRIII or betaglycan), occurs in a

247 The type III TGF-beta receptor (TbetaRIII) is a ubiquitous co-recepto

248 We previously demonstrated that the type III TGF-beta receptor (TbetaRIII, or betaglycan) serves as a

249 he type III transforming growth factor beta (TGF-beta) receptor (TbetaRIII) is a marker that distingu

250 he type III transforming growth factor beta (TGF-beta) receptor (TbetaRIII), also known as betaglycan

251 Transforming growth factor-beta (TGF-beta) receptors (TbetaRs) are essential components f

252 o express a soluble form of the neutralizing TGF-beta receptor (TGF-beta-R).

253 ased expression of dominant-negative type II TGF-beta receptor (TGF-beta-RII-DN) in the posterior lef

254 ells in CD11c(dnR) mice, whose NK cells lack TGF-beta receptor (TGF-betaR) signaling.

255 The expression of TGF-beta receptors (TGF-R) was verified at the mRNA and

256 as a tumor factor that attracts BM-hMSCs via TGF-beta receptors (TGFbetaR) on BM-hMSCs.

257 g mouse lines with selective deletion of the TGF-beta receptors Tgfbr1/2, Smad2, or Smad3.

258 nt of the type I transforming growth factor (TGF)-beta receptor (TGFBR1), which transduces TGF-beta g

259 -penetrance HNSCC in combination with type I TGF-beta receptor (Tgfbr1) deletion.

260 t a common hypomorphic variant of the type I TGF-beta receptor, TGFBR1*6A, may account for approximat

261 cells by mutations in the gene encoding the TGF-beta receptor TGFBR2.

262 in a 1,4-dihydropyridine inducer of type II TGF-beta receptor (TGFBR2) degradation-1 (ITD-1).

263 is deleted or mutated in 55% and the type II TGF-beta receptor (Tgfbr2) gene is altered in a smaller

264 e drove expression of the accessory type III TGF-beta receptor Tgfbr3, also called betaglycan.

265 Type III TGF-beta receptor (TGFBR3) and its shed extracellular do

266 mas revealed that expression of the type III TGF-beta receptor (TGFBR3) decreases with advancing stag

267 in-9 interacts with CD44 in association with TGF-beta receptors to drive both Foxp3 and galectin-9 ex

268 n of let-7c inhibited both the expression of TGF-beta receptor type 1 and the response to TGF-beta1.

269 e TGF-beta1 signaling pathway, including the TGF-beta receptor type 1.

270 ts directly with the cytoplasmic tail of the TGF-beta receptor type I (TbetaRI) in a kinase-dependent

271 Patients with mutations in either TGF-beta receptor type I (TGFBR1) or TGF-beta receptor t

272 ith the pan anti-TGF-beta antibody (1D11) or TGF-beta receptor type I inhibitor (SB431542), kidney pe

273 The TGF-beta receptor type I kinase inhibitor SB431542 [4-(4

274 264.7, by overexpressing a dominant negative TGF-beta receptor type II (TbetaRIIDN) construct.

275 goal, they used transgenic mice in which the TGF-beta receptor type II (Tbr2) was conditionally ablat

276 th factor-beta (TGF-beta) signaling members, TGF-beta receptor type II (TBRII), Smad2, Smad4 and Smad

277 either TGF-beta receptor type I (TGFBR1) or TGF-beta receptor type II (TGFBR2), such as those with L

278 in and mRNA and TGF-beta signaling proteins (TGF-beta receptor type II and phosphorylated SMAD3) incr

279 CAN expression was regulated in CAFs through TGF-beta receptor type II and SMAD signaling.

280 Clinically, we observed a loss of TGF-beta receptor type II expression in 69% of human pro

281 An adenovirus encoding human TGF-beta receptor type II fused to the Fc region of huma

282 n of CD11c promoter-driven dominant-negative TGF-beta receptor type II in C57BL/6 mice (CD11c-DNR), c

283 by infecting two different dominant negative TGF-beta receptor type II transgenic mouse lines.

284 stinal tumor growth in mice by up-regulating TGF-beta receptor type II, reducing proliferation and pr

285 Inactivation of only the TGF-beta receptor type II, Tgfbr2, in the mouse liver (T

286 a6-null mice, as well as recombinant soluble TGF-beta receptor type II-Fc (rsTGF-betaRII-Fc) and anti

287 rf2, accompanied by an increase in levels of TGF-beta receptor type II.

288 -beta or the expression of dominant negative TGF-beta receptor type II.

289 ults in elevated expression of TGF-beta2 and TGF-beta receptor type III (TbetaRIII); activation of a

290 TGF-beta receptor type-2 (TGFBR2) is the ligand-binding

291 Although both recombinant soluble TGF-beta receptor type-II (rsTGF-beta RII-Fc) and 6.3G9

292 Endogenous BAT3 protein interacts with TGF-beta receptors type I and type II in renal mesangial

293 , along with the prodifferentiation proteins TGF-beta-receptor type II (TBRII) and embryonic liver fo

294 on of TGF-beta signaling, by deletion of the TGF-beta receptor, type II (Tgfbr2), cooperates with Trp

295 The TGF-beta receptor V (TGFBRV or LRP1) has been shown to b

296 re-lox technology, expression of the type II TGF-beta receptor was selectively knocked out in fibrobl

297 the TbetaRII gene, which encodes the type II TGF-beta receptor, was deleted via a mesodermal-specific

298 s and reflects the polarized distribution of TGF-beta receptors, which thus affects SMAD activation i

299 Muscle-derived Gbb activates the TGF-beta receptors Wishful thinking (Wit) and either Sax

300 -mediated patching/immobilization of a given TGF-beta receptor with fluorescence recovery after photo