ライフサイエンスコーパス: beta-receptor

1 in animals deficient in the interferon alpha/beta receptor.

2 ctivated via a pathway that bypasses the TGF-beta receptor.

3 glycan, is the most abundantly expressed TGF-beta receptor.

4 to tolerate different mutations in the PDGF beta receptor.

5 l blockade of the ALK-5 component of the TGF-beta receptor.

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

7 immunocompromised mice lacking the IFN-alpha/beta receptor.

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

9 ther depleting microglia or blocking the TGF-beta receptors.

10 tions in the genes encoding type I or II TGF-beta receptors.

11 receptors but not transforming growth factor beta receptors.

12 rough the TGF-beta3 ligand that binds to TGF-beta receptors.

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

14 eristic of type I IFNs and bound to IFNalpha/beta receptor 1 (IFNAR1) and IFNAR2, but, unusually, it

15 demonstrated an essential role of IFN-alpha/beta receptor 1 (IFNAR1) specifically in neurons to cont

16 ithin the graft drives stenosis and that TGF-beta receptor 1 (TGF-betaR1) inhibition can prevent it,

17 nsforming growth factor beta (TGF-beta), TGF-beta receptor 1 (TGF-betaR1), connective tissue growth f

18 haSMA, PDGFbetaR, transforming growth factor beta receptor 1 (TGFbetaR1), collagen 1alpha1 (Col1alpha

19 ic effects of two transforming growth factor beta receptor 1 (TGFBR1) kinase inhibitors designed to t

20 1), TGFB2, TGFB3, transforming growth factor beta receptor 1 (TGFBR1), and TGFBR2 are associated with

21 acts closely with PDGF receptor beta and TGF-beta receptor 1 at the cell membrane, suggesting that it

22 TGF-beta receptor 1 inhibition prevents stenosis of tissue-e

23 C2C12 myotubes treated with TGF-beta, a TGF-beta receptor 1 pharmacological inhibitor, adenovirus ex

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

25 LEI, the PS1-protease, TGF-beta, and the TGF-beta receptor 1.

26 n of SMAD2/3 signaling via targeting the TGF-beta receptor 1.

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

28 roximal complex consisting of IFN-alpha and -beta receptors 1 and 2 (IFNAR1, IFNAR2, respectively), t

29 imed at highlighting the role of IFN (alpha, beta) receptor 1 (IFNAR1) in progression to CM.

30 ild-type (WT), TLR7-deficient, and IFN-alpha/beta receptor-1 (IFNAR1)-deficient mice and TLR7-mediate

31 1/12 of Transforming Growth Factor beta (TGF-beta) Receptor-1.

32 lowing stochastic transforming growth factor beta receptor 2 (TgfbetaR2) mutation to show cell autono

33 able to increased transforming growth factor beta receptor 2 (TGFbetaR2) signaling resulting from def

34 that depletion of transforming growth factor-beta receptor 2 (TGFBR2) in CD4(+) T cells, but not CD8(

35 ble form of mouse transforming growth factor-beta receptor 2 [sTGFbetaR2]) delivered using adeno-asso

36 f BEC in severe asthma through targeting TGF-beta receptor 2 mRNA.

37 increased SMAD3 phosphorylation through TGF-beta receptor 2 signaling and abrogated BEC proliferatio

38 uses upregulation of Fzd2, Ifi27l2a, and TGF-beta receptor 2.

39 r TGF-beta signaling in hepatocytes, via TGF-beta receptor-2 (Tgfbr2), promotes HCC and liver fibrosi

40 CpG-induced CD86 levels when anti-IFN-alpha/beta receptor Ab is added.

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

42 M16, a selective inhibitor of the type 1 TGF-beta receptor activin receptor-like kinase 5, orally act

43 3-kinases (PI3K), transforming growth factor beta receptor/activin receptor-like kinase beta, estroge

44 Suppression of TGF-beta receptor activity or ablation of SMAD3 or SMAD4, bu

45 r expression and signaling, and blocking TGF-beta receptor activity potentiates the antiproliferative

46 n of PNAd in mutant PPs requires lymphotoxin beta receptor activity, and its upregulation needs the p

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

48 , tumor necrosis factor (TNF) or lymphotoxin-beta receptor agonist can rescue expression of Erap1, Ta

49 s, we now show that activation of PKA by the beta-receptor agonist isoproterenol or dibutyryl (Db) cA

50 aled a statistically significant increase in beta-receptor agonist-stimulated intracellular cAMP cons

51 tion, we generated zebrafish lacking the TGF-beta receptor Alk5 and found a strikingly specific dilat

52 lt neurogenesis, genetic deletion of the TGF-beta receptor ALK5 reduced the number, migration and den

53 complete deficiency of the Interferon alpha/beta receptor alpha chain (IFNAR1) in a child with fatal

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

55 s from mouse PDA were also responsive to TGF-beta receptor and PI3K/AKT inhibition with regard to sup

56 which in turn signals through the IFN-alpha/beta receptor and STAT1/2 to induce IL-27.

57 tected mice from colitis via the lymphotoxin beta receptor and was expressed mainly by myeloid cells

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

59 apid anti-inflammatory activity of the 2 TGF-beta receptors and of TGF-beta1.

60 Activation of TGF-beta receptors and p38 MAPK increased glycogen synthase

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

62 n among transforming growth factor-beta (TGF-beta) receptors and its modulation by coreceptors repres

63 domain of the platelet-derived growth factor beta-receptor and specifically activate the receptor to

64 e expression and activity of KCa3.1 and PDGF beta-receptors and inhibiting the rise in [Ca(2+)]i.

65 Gene and protein expression of beta-receptors and pathways involved in their intracellu

66 displayed increased phosphorylation of PDGF-beta receptor, and an enhanced mitogenic response, after

67 ondin 1, a latent transforming growth factor-beta receptor, and transcription factors Smad3 and Ets1.

68 ression of several integrin subunits and TGF-beta receptors, and nuclear translocation of p-SMAD2 in

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

70 as an agonistic cytokine but also as a gp130 beta-receptor antagonist, leading to inhibition of IL-6

71 e chain-Fv fragments of the anti-lymphotoxin-beta receptor antibody, statistically significant respon

72 (TNFRSF14, also called HVEM) and lymphotoxin beta receptor are receptors for LIGHT that were expresse

73 MB gamma neurons upstream of the type-I TGF-beta receptor Baboon.

74 OD DCs is likely downstream of the IFN-alpha/beta receptor because DCs from NOD and B6 mice show simi

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

76 Beta-receptor blockade does not alter the tachycardia ph

77 f the sympathetic drive to the heart through beta-receptor blockade has become a standard component o

78 ants received a placebo or the noradrenergic beta-receptor blocker propranolol (40 mg).

79 The beta-receptor blocker propranolol or PKA inhibitor Rp-cA

80 Treatment with an IFN-beta receptor blocking antibody or knockdown of IFN-beta

81 th the platelet-derived growth factor (PDGF) beta receptor, causing receptor activation and cell tran

82 1, p28/IL-6R specifically recruits two gp130 beta-receptor chains for signal transduction.

83 hough IL-27 signals via a heterodimer of the beta-receptor chains gp130 and Wsx-1, p28/IL-6R specific

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

85 TSC1 interacts with the TGF-beta receptor complex and Smad2/3 and is required for th

86 ecule that mediates IL-37 binding to the TGF-beta receptor complex.

87 Furthermore, p52ShcA sequestered TGF-beta receptor complexes to caveolin-associated membrane

88 brane domains of the E5 protein and the PDGF beta receptor contact one another directly.

89 sulted in decreased Smad3 binding to the TGF-beta receptor, decreased Smad3 activation, and increased

90 ignaling mechanism is dependent on IFN-alpha/beta receptors deep within the brain, leading to the act

91 ) and partially restored in interferon alpha/beta receptor-deficient (IFNAR(-/-)) BMMs.

92 apitulate in great part the phenotype of TGF-beta receptor-deficient CD4 T cells, while SMAD4 was nec

93 ne staining (ICS) in ZIKV-infected IFN-alpha/beta receptor-deficient HLA transgenic mice.

94 In IFN-alpha/beta receptor-deficient mice, IFN-gamma treatment during

95 ng both wild-type C57BL/6 mice and IFN-alpha/beta receptor-deficient mice, we show that NS1-CDN immun

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

97 e development and homeostasis defects of TGF-beta-receptor-deficient T cells.

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

99 agated by hepatocytes in an interferon-alpha/beta receptor-dependent manner.

100 bility of flaviviruses to suppress IFN-alpha/beta receptor-dependent signaling, resulting in the orch

101 translocation of p-Smad2 and p-Smad3 in TGF-beta receptor-dependent, but SphK1-independent, manner.

102 ecific deletion of the gene encoding the TGF-beta receptor during chronic lymphocytic choriomeningiti

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

104 T cell receptors, and the abrogation of TGF-beta receptor expression led to failed maintenance of pe

105 most notably the transforming growth factor-beta receptor family.

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

107 remained low, suggesting impaired sinus node beta-receptor function may not fully account for low exe

108 eterozygous missense mutations in either TGF-beta receptor gene (TGFBR1 or TGFBR2), which are predict

109 of the ubiquitously expressed membrane-bound beta-receptor glycoprotein 130 (gp130).

110 r complex composed of the signal-transducing beta-receptor gp130 and the non-signaling membrane-bound

111 r demonstrated that VEPH1 interacts with TGF-beta receptor I (TbetaRI) and inhibits nuclear accumulat

112 this receptor as transforming growth factor beta receptor I (TGF-betaRI) (activin receptor-like kina

113 3, allowing Smad2/3 association with the TGF-beta receptor I and Smad anchor for receptor activation

114 nse to TGF-beta, RASSF1A is recruited to TGF-beta receptor I and targeted for degradation by the co-r

115 ctivin receptor-like kinase 5 pathway of TGF-beta receptor I in astrocytes.

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

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

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

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

120 sion and ESM/EMF contraction depended on TGF-beta receptor I signals.

121 Inhibition of TGF-beta receptor I using SB431542 ablated TGF-beta-induced

122 ing alpha3beta1 integrins, beta-catenin, TGF-beta receptor I, E-cadherin, and phosphorylated Smad2/3.

123 rozygous kinase-inactivating mutation in TGF-beta receptor I, we found that the effects of this mutat

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

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

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

127 icient for the type 1 interferon (IFN) alpha/beta receptor (IFNalpha/betaR-/-).

128 ulatory factor 3 (IRF3), or Interferon-alpha/beta receptor (IFNAR) by in vivo immortalization.

129 and IFN-beta, activate the interferon-alpha/beta receptor (IFNAR) complex.

130 of a neutralizing antibody to the IFN-alpha/beta receptor (IFNAR) for 3 d, beginning 30 min post-inj

131 -alpha/beta) signaling through the IFN-alpha/beta receptor (IFNAR) is essential to limit virus dissem

132 row chimeras between wild-type and IFN-alpha/beta receptor (IFNAR) knockout (KO) mice, and heterozygo

133 ild-type (WT) mice were crossed to IFN-alpha/beta receptor (IFNAR) knockout mice to evaluate the type

134 ce lacking the type I IFN receptor IFN-alpha/beta receptor (IFNAR) or the downstream transcription fa

135 ing a monoclonal antibody to block IFN-alpha/beta receptor (IFNAR) signaling in humanized mice (hu-mi

136 s infection and signal through the IFN-alpha/beta receptor (IFNAR) to induce proteins important for l

137 response through the type I interferon alpha/beta receptor (IFNAR).

138 through the alpha/beta interferon (IFN-alpha/beta) receptor (IFNAR) to induce genes that encode prote

139 ed by direct signaling through the IFN-alpha/beta-receptor (IFNAR), as Ab-mediated blocking of IFNAR1

140 ognate type I IFN receptor (type I IFN alpha/beta receptor [IFNAR]) to interrupt IFN signaling would

141 amma receptor (IFN-gammaR) and the IFN-alpha/beta receptor IFNAR1.

142 Mice deficient in the type I IFN-alpha/beta receptor (Ifnar1(-/-)) and administration of exogen

143 liver that depended on the interferon alpha/beta receptor (IFNAR1).

144 By binding to IFN-alpha and IFN-beta receptors (IFNARs) on neoplastic cells, type I IFNs

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

146 diabetes, here we show that ablation of TGF-beta receptor II (TbetaRII) in T cells, but not Foxp3 de

147 tified an interaction between moesin and TGF-beta receptor II (TbetaRII) that allows moesin to contro

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

149 effect of EGF on transforming growth factor-beta receptor II (TGF-betaRII) in a corneal wound-healin

150 TGF-beta receptor II (TGF-betaRII), critically implicated in

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

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

153 0,11), inducible genetic deletion of the TGF-beta receptor II (TGFBR2) in CD4(+) T cells suppressed t

154 ional deletion of transforming growth factor beta receptor II (Tgfbr2) in keratin 14-positive stratif

155 First, the Tgf-beta receptor II (Tgfbr2) was specifically removed from

156 the gene encoding transforming growth factor beta receptor II (TGFBR2).

157 TGF-beta receptor II appears to be a receptor important for

158 ng hepatocytes (TICs) were isolated from TGF-beta receptor II floxed mice (Tgfbr2(fl/fl) ) and transp

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

160 mor-reactive TCR and a dominant-negative TGF-beta receptor II induces complete and sustained tumor re

161 Transforming growth factor beta receptor II interacting protein 1 (TRIP-1), a predo

162 rs, Rae-1 expression was notably low and TGF-beta receptor II was high in tx-MDSCs when compared to t

163 ated in transforming growth factor beta (TGF-beta) receptor II knockout mice indicating a role for TG

164 aling between beta1 integrin and gp130 (IL-6 beta receptor, IL-6 signal transducer) was mediated by F

165 and conditional deletion of the type II TGF-beta receptor in mammary epithelium, an increased level

166 dipocytes increased the abundance of the TGF-beta receptor in melanoma cells, thereby enhancing cellu

167 LIGHT signals through the lymphotoxin beta receptor in the colon to regulate the innate immune

168 (+) TFH cells through an IL-6- and IFN-alpha/beta receptor-independent mechanism, but B cells were re

169 ir cognate ligands to type I and type II TGF-beta receptors, indicating that Cripto-1 and Cryptic con

170 tact-induced expression of TGF-beta1 and TGF-beta receptor inhibitor SB431542 inhibited contact-induc

171 tion of erlotinib and SB505124, a type I TGF-beta receptor inhibitor.

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

173 A TGF-beta-receptor inhibitor SB431542 (0.5-5muM) decreased th

174 inally, we cloned the tomato ortholog of TGF-beta Receptor Interacting Protein (TRIP1), which was pre

175 e important role of caveolin-1 (CAV1) in TGF-beta receptor internalization and TGF-beta signaling, th

176 a3 were necessary for caveolae-dependent TGF-beta receptor internalization.

177 erial transplantation, we show that this TGF-beta receptor is critical to maintain the HSC pool.

178 The transmembrane domain of the PDGF beta receptor is required for complex formation, but it

179 nstrate that signaling through the IFN-alpha/beta receptor is required for inflammation-induced alloi

180 ype I and type II (TbetaRI and TbetaRII) TGF-beta receptors is well characterized and is essential fo

181 esponse, in the absence or presence of a TGF-beta receptor kinase inhibitor, revealed substantial pos

182 ression of TGF-beta signaling, either by TGF-beta receptor kinase inhibitors or by silencing Smads 2

183 In addition to TGF-beta receptor kinase inhibitors, myofibroblast activatio

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

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

186 ogression in CCHFV-infected interferon alpha/beta receptor knockout (IFNAR(-/-)) mice and age-matched

187 erated endothelium-specific heterozygous TGF-beta receptor knockout (TbetaRII(endo+/-)) mice to explo

188 tion and spread in infected interferon alpha/beta receptor knockout mice via bioluminescence imaging.

189 Finally, systemic blockade of noradrenergic beta receptors led to reduced maternal regulation of inf

190 eceptor family members including lymphotoxin-beta receptor (LTbetaR) and CD40.

191 hanism, including membrane-bound lymphotoxin-beta receptor (LTbetaR) and CXC chemokine receptor 2 (CX

192 cells of the LN anlagen express lymphotoxin beta receptor (LTbetaR) and vascular cell adhesion molec

193 nd after bone marrow transplant, lymphotoxin beta receptor (LTbetaR) controls entry of T cell progeni

194 ene-deficient mice, we find that lymphotoxin beta receptor (LTbetaR) directly controls thymic ECs to

195 we show that signals through the lymphotoxin-beta receptor (LTbetaR) in DC are also required for the

196 canonical NF-kappaB pathway and lymphotoxin-beta receptor (LTbetaR) induced non-canonical NF-kappaB

197 show that signaling through the lymphotoxin-beta receptor (LTbetaR) is critical for kidney organogen

198 DC-derived lymphotoxin beta receptor (LTbetaR) ligands were critical mediators,

199 Lymphotoxin beta receptor (LTbetaR) signaling is crucial for lymphoi

200 icroenvironments is dependent on lymphotoxin-beta receptor (LTbetaR) signaling.

201 of the thymus medulla regulator lymphotoxin beta receptor (LTbetaR), we show that thymic tolerance m

202 te lymphoid cells, which promote lymphotoxin-beta receptor (LTbetaR)-dependent maintenance of DCs.

203 Lymphotoxin beta receptor (LTbetaR)-driven induction of chemokines a

204 flammation via activation of the lymphotoxin beta receptor (LTbetaR).

205 Lymphotoxin beta-receptor (LTbetaR) signalling promotes lymphoid neo

206 harmacological inhibition of the lymphotoxin-beta receptor markedly delays tumor development in mice

207 of apically targeted type I and type II TGF-beta receptors mediated Smad3 signaling from the apical

208 d isoproterenol infusion to quantify cardiac beta-receptor-mediated HR responses.

209 5 mutants displayed lower activity with PDGF beta receptor mutants containing other transmembrane sub

210 Transforming growth factor-beta (TGF-beta) receptor oligomerization has important roles in si

211 ol negatively regulates the stability of TGF-beta receptors on the cell membrane.

212 and ex vivo Pharmacologic inhibition of TGF-beta receptor or SMAD3 abrogates the TGF-beta-stimulated

213 activate the platelet-derived growth factor beta receptor or the erythropoietin receptor in cultured

214 s, HDAC4 (S265/266A)-GFP, did not respond to beta-receptor or PKA activation.

215 echanism of action of sGARP involves the TGF-beta receptor pathway, mice additionally received anti-T

216 e of EGFR and platelet-derived growth factor beta receptor (PDGFbetaR) as well as the oncogenic deriv

217 (TMD) of the platelet-derived growth factor beta receptor (PDGFbetaR), causing dimerization and acti

218 alphaSMA) and platelet-derived growth factor beta receptor (PDGFbetaR).

219 ate that, after ligand stimulation, the PDGF beta receptor (PDGFRbeta) becomes ubiquitinated in a man

220 that Fer associates with the activated PDGF beta-receptor (PDGFRbeta) through multiple autophosphory

221 h TGFbeta type I receptor (TbetaRI) and PDGF beta-receptor (PDGFRbeta), and it was prevented by inhib

222 TGF-beta receptors phosphorylate SMAD2 and SMAD3 transcripti

223 TrxR inhibitor auranofin also increased PDGF-beta receptor phosphorylation.

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

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

226 d mammary carcinomas lacking the type II TGF-beta receptor (PyMT(mgko)) are highly metastatic compare

227 ete TGF-beta1, which in turn activates a TGF-beta receptor/RAC1/SMAD-dependent signaling pathway in t

228 Here we show that the highly homologous TGF-beta receptor-regulated Smads (R-Smads): Smad2 and Smad3

229 We investigated the integrity of cardiac beta-receptor responsiveness, an important mechanism inv

230 Furthermore, inhibition of the TGF-beta receptor restored the adipogenic and antimicrobial

231 dominant-negative transforming growth factor beta receptor restricted to T cells (dnTGFbetaRII mice)

232 ons that restored binding to the mutant PDGF beta receptor, resulting in receptor activation and grow

233 tients with HFpEF displayed impaired cardiac beta-receptor sensitivity compared with senior controls.

234 Seven of 13 HFpEF subjects had beta-receptor sensitivity similar to senior controls but

235 Cardiac beta-receptor sensitivity was lower in HFpEF compared to

236 13 patients with HFpEF with age-appropriate beta-receptor sensitivity, peak HR remained low, suggest

237 FN responses because inhibition of IFN-alpha/beta receptor signaling abrogated DENV-induced DC matura

238 translationally controlled assembly of a TGF-beta receptor signaling complex containing alpha3beta1 i

239 a LRP1 signaling subsequently initiating TGF-beta receptor signaling for intracellular CRT (iCRT)-dep

240 nd ILF-resident CCR6(+) ILC3 via lymphotoxin-beta receptor signaling in cDCs.

241 types, suggesting a possible activation TGF-beta receptor signaling in tumor cells in response to TG

242 While IFNalpha/beta receptor signaling offers minimal protection in the

243 sis, which do not depend on either IFN-alpha/beta receptor signaling or mixed lineage kinase domain-l

244 cells are sensitive biomarkers for IFN-alpha/beta receptor signaling, as NK cell cytotoxicity and IFN

245 Here, we show that TGF-beta-receptor signaling is required during gastrulation

246 perfamily member LIGHT activates lymphotoxin beta-receptor signaling, leading to the production of ch

247 y and oxidative stress-induced alteration of beta-receptor signaling.

248 pression appeared to be mediated via the RAR-beta receptor subtype, as ATRA remarkably induced RAR-be

249 ype I interferon receptor (IFN-alpha and IFN-beta receptor subunit 1 [IFNAR1]), T cells, and B cells

250 hi) T cells from wild-type (WT) or IFN-alpha/beta receptor subunit 1 knockout (IFNAR1(-/-)) mice into

251 a with its receptor IFNAR1 (interferon alpha/beta receptor subunit 1) is vital for host-protective an

252 g antibodies against IFN-gamma and IFN-alpha/beta receptor subunit 1, and their cellular sources were

253 ed loss of PHF6 and the interferon alpha and beta receptor subunit 1.

254 In contrast, mice lacking the IFN-alpha/beta receptor succumbed to the infection, with VSV sprea

255 component of the transforming growth factor-beta receptor superfamily.

256 lly, fibulin-3 interacts with the type I TGF-beta receptor (TbetaRI) to block TGF-beta induced comple

257 l mobility and endocytosis of the type I TGF-beta receptor (TbetaRI) with TGF-beta phosphoprotein sig

258 and II transforming growth factor beta (TGF-beta) receptors (TbetaRI and TbetaRII, respectively) loc

259 ex formation of TbetaRI with the type II TGF-beta receptor (TbetaRII) and subsequent downstream TGF-b

260 en the cytoplasmic domain of the type II TGF-beta receptor (TbetaRII) and the FN receptor (alpha5beta

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

262 n of the serine/threonine kinase type II TGF-beta receptor (TbetaRII), which in turn promotes a Tbeta

263 lasma membrane expression of the type II TGF-beta receptor (TbetaRII).

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

265 ype III transforming growth factor beta (TGF-beta) receptor (TbetaRIII) is a marker that distinguishe

266 ype III transforming growth factor beta (TGF-beta) receptor (TbetaRIII), also known as betaglycan, is

267 Transforming growth factor-beta (TGF-beta) receptors (TbetaRs) are essential components for T

268 expression of dominant-negative type II TGF-beta receptor (TGF-beta-RII-DN) in the posterior left at

269 ty resulting from transforming growth factor-beta receptor (TGF-betaR) deletion and compromised T-cel

270 e receptor (TLR) family, tumor growth factor-beta receptors (TGFbetaR), and T-cell receptor (TCR).

271 d an inhibitor of transforming growth factor beta receptor (TGFBR).

272 use lines with selective deletion of the TGF-beta receptors Tgfbr1/2, Smad2, or Smad3.

273 ove expression of the accessory type III TGF-beta receptor Tgfbr3, also called betaglycan.

274 Type III TGF-beta receptor (TGFBR3) and its shed extracellular domain

275 revealed that expression of the type III TGF-beta receptor (TGFBR3) decreases with advancing stage of

276 of the transforming growth factor-beta (TGF-beta) receptors (TGFBRs) is carefully regulated through

277 o the ubiquitous expression of the IFN-alpha/beta receptor, the IFN-lambda receptor is restricted to

278 utive signaling through the lymphotoxin (LT) beta receptor to be maintained in a fully mature, differ

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

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

281 lacking the alpha/beta interferon (IFN-alpha/beta) receptor to study responses to heterologous DENV i

282 plex with the platelet-derived growth factor beta receptor transmembrane domain and causing ligand-in

283 it to tolerate the same mutation in the PDGF beta receptor transmembrane domain and that a mutation i

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

285 s in complex with transforming growth factor beta receptor type 1 kinase domain were determined by X-

286 F-beta1 signaling pathway, including the TGF-beta receptor type 1.

287 exhibited reduced transforming growth factor-beta receptor type I (TGF-beta RI) expression that did n

288 the pan anti-TGF-beta antibody (1D11) or TGF-beta receptor type I inhibitor (SB431542), kidney pericy

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

290 dominant negative transforming growth factor beta receptor type II (dnTGFbetaRII).

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

292 n of ZEB1, Twist, transforming growth factor-beta receptor type II, and vimentin, and aberrant E-cadh

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

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

295 Strikingly, we found that IFN-alpha/beta receptor (type-I IFN receptor) was expressed by pri

296 ile, vascular smooth muscle cell lymphotoxin beta receptors (VSMC-LTbetaRs) protected against atheros

297 IPS-1, and antibody blockade of the IFNalpha/beta receptor, we further demonstrate that type I IFN si

298 rate and contractility through activation of beta receptors, whereas parasympathetic ACh slows the he

299 d reflects the polarized distribution of TGF-beta receptors, which thus affects SMAD activation irres

300 iated patching/immobilization of a given TGF-beta receptor with fluorescence recovery after photoblea