ライフサイエンスコーパス: Smad protein

1 ties for phosphorylated and unphosphorylated Smad protein.

2 a co-factor, rather than an antagonist, of a Smad protein.

3 re, Expansion does not function as a typical Smad protein.

4 ng called daf-14 and found that it encodes a Smad protein.

5 rs capable of activating specific downstream Smad proteins.

6 ne/threonine kinase receptors that signal to Smad proteins.

7 by activating downstream targets such as the Smad proteins.

8 lly rescued by TGFbeta1 or overexpression of Smad proteins.

9 surface receptors and signaling by means of Smad proteins.

10 1 and -5 and to mediate degradation of these Smad proteins.

11 acterized as the transcriptional partner for Smad proteins.

12 rimary mediator of TGFbeta responses are the Smad proteins.

13 curs through the activation of intracellular Smad proteins.

14 these molecules act to alter the activity of Smad proteins.

15 F-beta type I receptor via TGF-beta-specific Smad proteins.

16 th factor-beta (TGF-beta) is mediated by the Smad proteins.

17 aling by Bmp receptors is mediated mainly by Smad proteins.

18 omo- and heteromeric complex formation among Smad proteins.

19 a-induced transactivation through binding to Smad proteins.

20 tor inhibitor type I depended upon all three SMAD proteins.

21 kinases and cytoplasmic effectors, including Smad proteins.

22 -M cells leads to nuclear translocation of R-Smad proteins.

23 transduce the signal to the nucleus through Smad proteins.

24 nd prevents stress-imposed downregulation of Smad proteins.

25 beta signaling through interactions with the Smad proteins.

26 own to be regulated by TGFbeta through the R-Smad proteins.

27 some cells resistant to TGF-beta via binding Smad proteins.

28 beta signaling and can be regulated by other Smad proteins.

29 naling by inhibition of phosphorylation of R-Smad proteins.

30 synthesis, including synthesis of inhibitory Smad proteins.

31 tates its transfer to the receptor-activated Smad proteins.

32 fies a symmetric interface between these two Smad proteins.

33 s of TGF-beta family ligands are mediated by Smad proteins.

34 and their dedicated signal transducers, the Smad proteins.

35 eins has recently been discovered to involve Smad proteins.

36 2 oligonucleotide contained both Sp1/Sp3 and Smad proteins.

37 then regulates gene expression by activating Smad proteins.

38 tial functional redundancy between these two Smad proteins.

39 d1, Smad5 and Smad8 and in overall levels of Smad proteins.

40 s were performed to assess the activation of Smad proteins.

41 of these signaling responses are mediated by Smad proteins.

42 to proteasome-mediated turnover of activated Smad proteins.

43 y to bind to and repress the activity of the Smad proteins.

44 These effects are largely mediated by Smad proteins.

45 ular mediators of TGF-beta signaling are the Smad proteins.

46 renal fibrosis, is mediated, in part, by the Smad proteins.

47 he BMPRI kinase, which in turn activates the Smad proteins.

48 y an important role in the regulation of the Smad proteins.

49 actor-beta pathway, particularly through the Smad proteins.

50 threonine kinase receptors and intracellular Smad proteins.

51 to interact with and repress the activity of Smad proteins.

52 ance, possibly through a mechanism involving SMAD proteins.

53 n between HOX proteins and the MH2 domain of Smad proteins.

54 hosphorylation of receptor-regulated Smad (R-Smad) protein.

55 scription of the TGF-beta2 gene and involves Smad proteins, a class of intracellular signaling protei

56 ectin gene and is dependent on the action of Smad proteins, a class of intracellular signaling protei

57 Smad proteins activated by TGF-beta form a complex with

58 from a novel competitive interaction between Smad proteins activated by TGF-beta(1) and nuclear facto

59 malian isoforms of Suv39h proteins, and that Smad proteins activated by the TGF-beta signaling pathwa

60 f target gene expression, and the control of Smad protein activity and degradation.

61 Our working model suggests that Smad protein activity is delicately balanced by Ski and

62 The family of Smad proteins acts as intracellular signal transducers o

63 Smad proteins also competed with the Satb1-NuRD complex

64 Here we show that Smad proteins also regulate gene expression by using a p

65 of Mothers Against Decapentaplegic homolog (SMAD) proteins, although alternate pathways are modulate

66 he preferential binding of SARA to monomeric Smad protein and Trx-SARA-mediated disruption of active

67 We show here that both Smad proteins and AP-1 complex are involved in TGF-beta1

68 These results suggest that Smad proteins and AP-1 complex synergize to mediate TGF-

69 Whether the opposing activities mediated by Smad proteins and CD2AP involve molecular cross-talk is

70 The oncogenic protein Ski associates with Smad proteins and counteracts their activation of gene e

71 of Trb3 coincides with reduced expression of Smad proteins and decrease in BMP and TGFbeta signalling

72 oked nuclear translocation of phosphorylated SMAD proteins and enhanced both glial differentiation an

73 iptional responses through interactions with Smad proteins and HDAC.

74 may be due to increased competition between Smad proteins and IL-1beta signaling pathways for limiti

75 of interaction between TGF-beta(1)-regulated Smad proteins and NFkappaB proteins regulated by inflamm

76 the BMP signaling pathway, cooperating with Smad proteins and other transcriptional activators.

77 m of TGF-beta1 that are mediated by distinct Smad proteins and promotes myofibroblast phenotype.

78 These mutations lead to loss of signaling to SMAD proteins and reduced hepcidin production.

79 rtoire of transcription factors that include Smad proteins and Sp1.

80 hat MSG1 interacts with both the DNA-binding Smad proteins and the p300/CBP coactivators through its

81 that there is formation of a complex between Smad proteins and the regulatory subunit of PKA, with re

82 MH1 and linker domains of receptor-mediated Smad proteins, and associate with the endogenous TGFbeta

83 ed receptor, nuclear complex formation among Smad proteins, and inactivation of ligand-activated Smad

84 EID-2 interacts constitutively with Smad proteins, and most strongly with Smad3.

85 harboring mutations in TGF-beta receptors or Smad proteins, and this may represent a significant even

86 ranscriptional mechanism that implicates the Smad proteins, and we have mapped a putative enhancer el

87 Smad6 and Smad7, a subgroup of Smad proteins, antagonize the signals elicited by transf

88 F-beta signal transduction pathway involving Smad proteins appears to regulate the cellular expressio

89 Smad proteins are a class of tumor suppressors that play

90 Smad proteins are central mediators in the canonical tra

91 a potent mediator in renal fibrosis and that Smad proteins are critical intracellular mediators in TG

92 Smad proteins are critical intracellular mediators of th

93 Smad proteins are critical intracellular signaling media

94 Smad proteins are essential intracellular signal transdu

95 Smad proteins are eukarytic transcription regulators in

96 Although Smad proteins are identified as key signal transducers i

97 The Smad proteins are important intracellular mediators of t

98 Smad proteins are intracellular mediators of signalling

99 Smad proteins are intracellular mediators of transformin

100 Smad proteins are intracellular mediators of transformin

101 Smad proteins are intracellular signaling effectors of t

102 Smad proteins are key intracellular signaling effectors

103 SMAD proteins are known to oligomerize and hetero-associ

104 SMAD proteins are major intracellular effectors shared b

105 y which the activities and expression of the Smad proteins are modulated.

106 We show that Smad proteins are necessary, but not sufficient, for TGF

107 In the nucleus, the Smad proteins are negatively regulated by two closely re

108 e that although highly similar structurally, Smad proteins are not functionally homologous.

109 Smad proteins are receptor-activated transcription facto

110 SMAD proteins are shown to be involved in a number of po

111 Smad proteins are signaling transducers downstream from

112 Smad proteins are substrates of the TGF-beta type I rece

113 Smad proteins are the most well-characterized intracellu

114 Because Smad proteins are tumor suppressors, we hypothesized tha

115 Small mothers against decapentaplegic (SMAD) proteins are a family of signal transduction molec

116 The receptor-regulated Smad (R-Smad) proteins are regulated by ubiquitin-mediated degra

117 llular effectors of TGF-beta signalling, the Smad proteins, are activated by receptors and translocat

118 f Dpp signaling led to the identification of Smad proteins as central mediators of signal transductio

119 The identification of Sp and Smad proteins as essential, independent activators of th

120 The study supports a common mechanism of Smad protein assembly in TGF-beta superfamily signaling.

121 Activated Smad proteins associate with different DNA-binding cofac

122 stimulation, TGFbeta receptors phosphorylate Smad proteins at carboxy-terminal SS(V/M)S consensus mot

123 Upon cell stimulation with TGF-beta, SMAD proteins become engaged in a multitude of complexes

124 Trafficking of Smad proteins between the cytoplasm and nucleus is a cri

125 Phosphorylated R-Smad proteins bind to Smad4, and the complexes formed mo

126 The kinetics of bHLHZIP and Smad protein binding at the PE2.1 element were examined

127 o heterologous bHLH domains, associated with Smad proteins both in the absence of DNA and at the PE2.

128 on (BiFC) to study complex formation between Smad proteins both in vivo and in response to exogenous

129 not only through TGF-beta receptor-regulated Smad proteins but also through an independent pathway in

130 c activation of promoters by combinations of Smad proteins but failed to repress in the absence of Sm

131 esponses induced by TGF-beta are mediated by Smad proteins, but certain evidence has suggested that T

132 tors did not prevent nuclear localization of Smad proteins, but they inhibited Smad-mediated transcri

133 nds on the phosphorylation and activation of Smad proteins by heteromeric complexes of ligand-specifi

134 s transmitted through the phosphorylation of Smad proteins by TGF-beta receptor serine/threonine kina

135 rough phosphorylation of receptor-associated Smad proteins by the type I receptor.

136 Our studies provide strong evidence that SMAD proteins can bind to a natural TGF-beta responsive

137 SMAD proteins can mediate transforming growth factor bet

138 Whereas Smad proteins collaborate with Sp1 in activating several

139 Smad proteins contain a conserved basic motif in their N

140 Smad proteins convey canonical intracellular signals for

141 nal activation suggests a mechanism by which SMAD proteins coordinate with chromatin at critical prom

142 viously been characterized as unable to bind Smad proteins directly.

143 We find that two Smad proteins, effectors of the Drosophila Dpp/TGF-beta

144 signal (NLS)-like motif, conserved among all Smad proteins, eliminated its ligand-induced nuclear tra

145 eated with or without Ski siRNA, and Ski and Smad protein expression, transcriptional reporter activa

146 , and Western analysis was used to determine SMAD protein expression.

147 tant Ski or SnoN defective in binding to the Smad proteins failed to induce oncogenic transformation.

148 The members of the Smad protein family are intracellular mediators of trans

149 To study the protein interactome of the SMAD protein family we generated a quantitative proteomi

150 g the cytosolic signaling transducers of the Smad protein family.

151 tly transducing TGF-beta signals through the Smad protein family.

152 llows for inducible expression of GFP-tagged SMAD proteins followed by affinity purification and quan

153 es that selectively target the receptors and Smad proteins for degradation.

154 rial binding sites for Tin and Dpp-activated Smad proteins for its activity.

155 d linker phosphorylation marks the activated Smad proteins for proteasome-mediated destruction.

156 Thus, Sp1 and Smad proteins form complexes and their synergy plays an

157 The phosphorylated Smad proteins form heteromeric complexes with Smad4 and

158 Smad proteins generally function as intermediate compone

159 pathway of gene activation by TGF-beta1 via Smad proteins has recently been elucidated, suppression

160 Although Smad proteins have been identified as intracellular medi

161 ect target for transcriptional activation by Smad proteins; however, the independence of this Nkx2-5

162 Smad4 encodes the only common Smad protein in mammals, which is a critical nuclear med

163 Smad4 encodes the only common Smad protein in mammals, which is a critical nuclear med

164 idue, the phosphorylation site of its parent Smad protein in vivo.

165 eaks (DSBs) markers, we studied the roles of Smad proteins in DDR and the crosstalk between TGFbeta a

166 On the other hand, presence of SMAD proteins in iron or TGF-beta-treated cells, includi

167 vement and possible interaction of Cbfa1 and Smad proteins in mediating the effects of TGF-beta on OP

168 g growth factor-beta (TGF-beta) signaling by Smad proteins in mice.

169 The ability of Ski to engage Smad proteins in nonproductive complexes provides new in

170 bited cell proliferation, phosphorylation of SMAD proteins in response to TGF-beta, and TGF-beta-indu

171 stigate the relative importance of these two Smad proteins in TGF-beta1 signal transduction, we have

172 ast formation, suppressed phosphorylation of Smad proteins in TGFbeta pathway and inhibited key respo

173 TFE3 cooperates with Smad proteins in the activation of the LAMC1 promoter in

174 hes a novel role for Ecsit as a cofactor for Smad proteins in the Bmp signaling pathway.

175 nizes TGF-beta signaling by sequestering the Smad proteins in the cytoplasm.

176 tracellular compartmentalization of cellular SMAD proteins in the presence and absence of TGFbeta was

177 The role of non-Smad proteins in the regulation of transforming growth f

178 ed by TGF-beta, we investigated the roles of Smad proteins in the up-regulation of beta(5) gene activ

179 t dentate gyrus and expression of downstream Smad proteins in this neurogenic zone.

180 naling pathways and specific roles played by Smad proteins in this process have not been defined.

181 H cells and in human ONH tissues (N = 4) and Smad proteins in total cell lysate of ONH cells and tiss

182 In order to identify novel partners of Smad proteins in transcriptional regulation, we performe

183 ditionally, the TGF-beta1 receptor-regulated Smad proteins, in particular Smad3, are rate-limiting fo

184 to other BMP and TGF-beta/Activin-regulated Smad proteins including Smad1 and Smad2, but not Smad4.

185 a receptor-mediated activation of downstream SMAD proteins, including SMAD1.

186 A subclass of Smad proteins, including Smad6 and Smad7, has been shown

187 Once in the nucleus Smad proteins interact with other DNA binding proteins t

188 ptor II (TGFbetaRII) on the cell surface and SMAD proteins intracellularly.

189 n the N-terminal region of Smad 3, the major Smad protein involved in TGF-beta signal transduction.

190 n the N-terminal region of Smad 3, the major Smad protein involved in TGF-beta signaling.

191 The altered phosphorylation of Smad proteins involves phospholipase C-mediated signalin

192 Nuclear translocation of Smad proteins is a critical step in signal transduction

193 ough ligand-induced nuclear translocation of Smad proteins is clearly established, the pathway mediat

194 ation of miRNA biogenesis by ligand-specific SMAD proteins is critical for control of the vascular sm

195 epress the growth inhibitory function of the Smad proteins is required for their transforming activit

196 regulate TGF-beta action independent of the Smad proteins is the c-Abl nonreceptor tyrosine kinase.

197 hibitory pathway of TGF-beta mediated by the Smad proteins is well studied, the signaling pathway lea

198 or beta1 (TGF beta1), through its downstream Smad proteins, is involved in keeping AEC II quiescent i

199 )), conserved among all the pathway-specific Smad proteins, is required for Smad 3 nuclear import in

200 ing the N-terminal domain found in all other Smad proteins known to date.

201 t this time, how the absence of a functional SMAD protein leads to a tumor is unknown.

202 Second, silencing of SMAD protein levels using short interfering RNAs reveale

203 tores A359 expression in cells that lack the Smad protein MAD; ectopic expression of BUNCHED suppress

204 been shown that a complex of the Drosophila Smad proteins, Mad and Medea, binds with high affinity t

205 Smad proteins may displace EZH2 directly from the Il9 lo

206 in, indicating that nuclear translocation of Smad proteins may occur through direct binding to import

207 growth factor beta-independent role for any Smad protein, may be widely utilized for regulating mito

208 Here we show that Hiw binds to the Smad protein Medea (Med).

209 Smad proteins mediate transforming growth factor beta (T

210 Smad proteins mediate transforming growth factor beta si

211 Smad proteins mediate transforming growth factor-beta (T

212 The Smad proteins mediate transforming growth factor-beta (T

213 The family of Smad proteins mediates transforming growth factor-beta (

214 ays), suggesting that persistently activated Smad proteins might participate in returning the liver t

215 observations, all validated with endogenous SMAD proteins, modify previous models regarding the asse

216 We identified cDNAs encoding the Xenopus Smad proteins most closely related to mammalian Smad8, a

217 PIAS3 interacts with Smad proteins, most strongly with Smad3.

218 y, Lis1 binds directly to and stabilizes the SMAD protein Mothers against decapentaplegic (Mad), faci

219 equence that overlaps a binding site for the Smad protein, Mothers Against Dpp (Mad).

220 The activity of Smad proteins must be tightly regulated to exert the bio

221 The in situ localization of Runx and Smad proteins must impact the mechanisms by which these

222 s(44)), conserved among all pathway-specific Smad proteins, not only is responsible for constitutive

223 growth factor beta (TGF-beta) signaling via Smad proteins occurs in various cell types.

224 The two major Smad proteins of the BMP pathway, Smad1 and Smad5, inter

225 KIgamma2 does not affect the basal levels of Smad proteins or activity of the receptors.

226 utants defective for binding to WW domain or SMAD proteins or the nuclear matrix retain this growth r

227 hancer activity was increased by TGFbeta1 or Smad protein overexpression.

228 e primary mediators of this activity are the SMAD proteins, particularly SMAD3.

229 Here we show that a Dpp-activated Smad protein, phosphorylated Mad, is colocalized in eve-

230 Smad proteins play a critical role in this process by bi

231 Smad proteins play a key role in the intracellular signa

232 Smad proteins play key roles in intracellular signaling

233 Smad proteins play pivotal roles in mediating the transf

234 levels of phosphorylated receptor-associated Smad proteins (pR-Smad2 and pR-Smad3), whereas Smad4-pos

235 Thillainadesan et al. provide evidence that Smad proteins promote locus-specific active DNA demethyl

236 and point mutants was used to examine RUNX2-SMAD protein-protein interaction and the biological cons

237 To determine if disruption of specific Smad protein-protein interactions would selectively inhi

238 ctly with a homotrimer of receptor-regulated Smad protein (R-Smad), e.g. Smad2 or Smad3, to form a he

239 through phosphorylation and activation of R-Smad proteins, receptor-regulated Smads, by heteromeric

240 Smad proteins regulate transcription in response to tran

241 ignaling pathway, the function of individual Smad proteins remains poorly understood.

242 nd phosphorylation in the TGF-beta-activated Smad protein signal transduction process.

243 and molecular modeling indicate that p53 and Smad proteins simultaneously occupy overlapping p53 and

244 its receptor induces phosphorylation of the Smad proteins Smad2 and Smad3, which then form heteromer

245 Here, we show that the receptor regulated Smad proteins (Smad2 and Smad3) and common mediator Smad

246 nt, whereas overexpression of the inhibitory SMAD proteins, SMAD6/7, reversed the antihypertrophic ef

247 ce of Smad4 expression or when an inhibitory Smad protein, Smad7, is overexpressed.

248 at activation of all of the pathway-specific Smad proteins (Smads 1, 2, 3, 5, 8, and 9) exposes the c

249 Actr-Ib, Actr-II and Actr-IIb, Alk-1, and Smad proteins (Smads 1-5 and Smad8) in the septal region

250 -beta2 and induces its downstream effectors, Smad proteins (Smads), to associate with DNA.

251 pplicable to human tumours with abnormal p53/Smad protein status.

252 this appears to function independent of the Smad proteins, suggesting that other TGF-beta-regulated

253 ceptors, which signal via a different set of SMAD proteins than BMPs.

254 e role of KLF14, as a TGFbeta-inducible, non-Smad protein that silences the TGFbeta receptor II (TGFb

255 The type I receptor and Smad proteins that are required in vivo for Mullerian du

256 wn effects on pRb, might directly target the Smad proteins that mediate TGF-beta signaling.

257 investigate the subcellular distributions of Smad proteins, the intracellular mediators of transformi

258 itted into the nucleus through intracellular Smad proteins, the model provides quantitative insight i

259 to activate intracellular mediators, such as Smad proteins, the p38 mitogen-activated protein kinase

260 on depends on Tgfbeta receptor activation of Smad proteins; the induction correlates with Smad2 phosp

261 Smad proteins therefore mediate transcriptional activati

262 inc atom using four invariant residues among Smad proteins, three cysteines and one histidine.

263 rs through ligand binding, the activation of Smad proteins through phosphorylation, the transcription

264 (Fos/Jun) protein complexes to -327/-322 and SMAD proteins to -329/-328.

265 ds, but while ZEB-1/deltaEF1 synergizes with Smad proteins to activate transcription, promote osteobl

266 th effects of activin via phosphorylation of SMAD proteins to affect gene transcription.

267 s account reviews available evidence linking SMAD proteins to CAC and explores the potential areas fo

268 beta (TGFbeta) signals primarily through the Smad proteins to regulate cell growth, differentiation,

269 expressed cytokine that signals through the Smad proteins to regulate many diverse cellular processe

270 to their receptors leads to translocation of Smad proteins to the nucleus where they activate transcr

271 ecreased Satb1 expression through binding of Smad proteins to the Satb1 promoter.

272 lated by post-translational modifications of Smad proteins to translate quantitative difference in li

273 Smad proteins transduce bone morphogenetic protein (BMP)

274 Smad proteins transduce signals carried by the transform

275 Smad proteins transduce signals from transforming growth

276 Smad proteins transduce signals from transforming growth

277 Smad proteins transduce transforming growth factor-beta

278 Upon BMP binding to the receptor complex, Smad proteins translocate to the nucleus and modulate ge

279 tion by activated type I TGF-beta receptors, Smad proteins translocate to the nucleus, where they ser

280 Smad proteins undergo rapid nuclear translocation upon s

281 eins, including Bix2 and Bix3, interact with Smad proteins via a motif that is also present in the re

282 e mediated by transcription via BMP-specific Smad proteins, we investigated the involvement of PI 3-k

283 mplexes between SnoN, Ski, and the activated Smad proteins were detected from 2 to 120 h during the m

284 Interactions between mZnf8 and Smad proteins were further analyzed with various in vitr

285 We found that Smad proteins were slightly activated in quiescent liver

286 TFE3 exhibited cooperative DNA binding with Smad proteins, whereas no cooperativity was observed bet

287 TGFbeta signaling involves activation of Smad proteins which directly regulate target gene expres

288 t on a mesoderm-specific enhancer that binds Smad proteins, which activate transcription in response

289 the activation and nuclear translocation of Smad proteins, which activate transcription of specific

290 It is concluded that Smad proteins, which can regulate endothelial responses

291 at transforming growth factor beta activates Smad proteins, which induce expression of the embryonic

292 tor activation results in phosphorylation of Smad proteins, which subsequently translocate to the nuc

293 to ligand stimulates nuclear localization of Smad proteins, which then regulate target gene expressio

294 The Smad proteins, which translocate into the nucleus after

295 quire its ability to bind to and repress the Smad proteins, while the antitumorigenic activity can be

296 ave demonstrated the physical association of Smad proteins with AML1 and AML1/ETO by immunoprecipitat

297 Interaction of Smad proteins with cellular partners in the cytoplasm an

298 orylation, including heterodimerization of R-Smad proteins with Smad4 and nuclear translocation of th

299 se data suggest a model where association of Smad proteins with Suv39h methyltransferases can repress

300 o the nucleus form the basis for a model how Smad proteins work to transmit TGF-beta signals.