ライフサイエンスコーパス: TGF-beta receptor

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

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

3 ion of TGFBR1 mRNA, which encodes the type I TGF-beta receptor.

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

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

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

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

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

9 -beta receptors from a pool of intracellular TGF-beta receptors.

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

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

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

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

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

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

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

17 ted, at least partially, via upregulation of TGF-beta receptors.

18 y either depleting microglia or blocking the TGF-beta receptors.

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

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

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

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

23 TGF-beta receptor 1 inhibition prevents stenosis of tiss

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

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

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

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

28 there was increased microRNA-125b/TGF-beta1/TGF-beta receptor 1/VEGF-A signaling.

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

30 nly 1/12 of Transforming Growth Factor beta (TGF-beta) Receptor-1.

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

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

33 -19a increased SMAD3 phosphorylation through TGF-beta receptor 2 signaling and abrogated BEC prolifer

34 2 causes upregulation of Fzd2, Ifi27l2a, and TGF-beta receptor 2.

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

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

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

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

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

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

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

42 ormation, we generated zebrafish lacking the TGF-beta receptor Alk5 and found a strikingly specific d

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

58 expression of several integrin subunits and TGF-beta receptors, and nuclear translocation of p-SMAD2

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

60 The TGF-beta receptor antagonist SB431542 completely blocked

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

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

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

64 TGF-beta receptor antagonists also rescued cells from do

65 4 hours post-wounding) of type I and type II TGF-beta receptors as well as unexpectedly high fibrobla

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

96 eta by directing an increase in cell surface TGF-beta receptors from a pool of intracellular TGF-beta

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

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

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

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

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

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

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

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

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

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

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

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

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

110 otility, which is effectively blocked by the TGF-beta receptor I inhibitor galunisertib (LY2157299).

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

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

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

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

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

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

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

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

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

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

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

122 heterozygous kinase-inactivating mutation in TGF-beta receptor I, we found that the effects of this m

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

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

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

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

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

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

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

130 Male and female dominant-negative TGF-beta receptor II (dnTGF-betaRII) (model of PBC) and

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

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

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

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

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

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

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

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

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

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

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

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

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

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

145 es(10,11), inducible genetic deletion of the TGF-beta receptor II (TGFBR2) in CD4(+) T cells suppress

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

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

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

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

150 iating hepatocytes (TICs) were isolated from TGF-beta receptor II floxed mice (Tgfbr2(fl/fl) ) and tr

151 Specifically, the deficiency of TGF-beta receptor II in bone marrow progenitors results

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

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

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

155 arkers, Rae-1 expression was notably low and TGF-beta receptor II was high in tx-MDSCs when compared

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

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

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

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

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

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

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

163 1, adipocytes increased the abundance of the TGF-beta receptor in melanoma cells, thereby enhancing c

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

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

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

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

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

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

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

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

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

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

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

175 -beta3 were necessary for caveolae-dependent TGF-beta receptor internalization.

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

177 TGF-beta receptor internalized through caveolin-1 lipid

178 th serial transplantation, we show that this TGF-beta receptor is critical to maintain the HSC pool.

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

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

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

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

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

184 in response, in the absence or presence of a TGF-beta receptor kinase inhibitor, revealed substantial

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

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

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

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

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

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

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

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

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

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

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

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

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

198 sterol negatively regulates the stability of TGF-beta receptors on the cell membrane.

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

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

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

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

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

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

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

206 TGF-beta receptors phosphorylate SMAD2 and SMAD3 transcr

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

208 se (HMGCR) and ATP-citrate lyase (ACLY) in a TGF-beta receptor/PI3K/protein kinase B-dependent manner

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

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

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

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

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

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

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

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

217 Furthermore, inhibition of the TGF-beta receptor restored the adipogenic and antimicrob

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

219 s via LRP1 signaling subsequently initiating TGF-beta receptor signaling for intracellular CRT (iCRT)

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

249 The type III TGF-beta receptor (TbetaRIII) is a TGF-beta co-receptor

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 tion of the transforming growth factor-beta (TGF-beta) receptors (TGFBRs) is carefully regulated thro

268 receptor that presents ligand to the type II TGF-beta receptor to initiate signaling.

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

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

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

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

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

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

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

276 264.7, by overexpressing a dominant negative TGF-beta receptor type II (TbetaRIIDN) construct.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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