ライフサイエンスコーパス: activin

1 low upregulation of FoxA2 in the presence of Activin.

2 premature differentiation after exposure to Activin.

3 expression of atrophic factors like Mstn and activin.

4 negatively regulated by myostatin (MSTN) and activins.

5 e previously demonstrated involvement of the activin 2a receptor in drug taking, the role of its liga

6 tigations showed that manipulating levels of activin A (INHBA) could rescue or compromise the RUNX2-m

7 ght weeks after AAV injection, inhibition of activin A and activin B signaling produced moderate ( ap

8 Varying doses of activin A and BMP4 to mimic cytokine gradient polarizati

9 on protocol uses different concentrations of activin A and bone morphogenetic protein 4 (BMP4) to pol

10 definition of novel invention targets (e.g., activin A and CD36) to prevent breast cancer.

11 Here we have studied the activation of activin A and determined crystal structures of the unpro

12 mary human senescent fat progenitors secrete activin A and directly inhibit adipogenesis in non-senes

13 x metalloproteinase-9, and up to 3-fold more activin A and endostatin.

14 ne morphogenetic protein-4 and inhibitors of activin A and fibroblast growth factor-2 signaling (BAP

15 XCL3, CXCL5, and CXCL11; the cytokines IL-6, activin A and GM-CSF; and metalloproteinases matrix meta

16 d liver) identified interactions between the activin A and IL6 signaling pathways.

17 We show activin A and other high affinity ligands directly inhib

18 was found to be mediated by the secretion of activin A and the low levels of IL-10 produced by M16.

19 uscle histopathological features showed that activin A antibody-treated mice displayed an increase in

20 for this differential expression identified activin A as a critical factor controlling the expressio

21 screen of a human protein library identified activin A as a potent regulator of TFH cell differentiat

22 Altogether, we identify activin A as a second negative regulator of muscle mass,

23 mor cells stimulated their growth through an activin A autocrine signaling pathway, a hypothesis conf

24 cocultivation induced marked accumulation of activin A but not transforming growth factor-beta1 in co

25 In NK-DC cocultures, inhibition of activin A by follistatin, a natural inhibitory protein,

26 The NUCC-555 also specifically binds to activin A compared with other TGFbeta superfamily member

27 s, such as injury and wound healing, and how activin A could elicit disease phenotypes such as cancer

28 cts of activin A in skeletal muscle, whereas activin A curbed the IL6-induced acute-phase response in

29 in basic fibroblast growth factor (bFGF) and activin A develop as epiblast-like cells (EpiLCs) and ga

30 orming growth factor-beta was able to induce activin A expression in ASC, in cocultures this inductio

31 Strikingly, both telomere malfunction and activin A expression in epithelial cells can repress CD3

32 inflammatory profile by virtue of their high activin A expression unless additional anti-inflammatory

33 We demonstrate activin A functions as a competitive inhibitor that bloc

34 of smooth muscle cell antigens in ASC, only activin A IgG blocked the effect of EC-ASC conditioned m

35 In EC-ASC cocultures, activin A IgG or ALK4/5/7 receptor inhibitors blocked ex

36 culating levels of the tumorkines IL6 and/or activin A in animals in the absence of tumors as a tacti

37 , IL6 exacerbated the detrimental effects of activin A in skeletal muscle, whereas activin A curbed t

38 posure significantly increased the levels of activin A in the NAc of animals that had self-administer

39 ion of the CCL2/CCR2 pair in macrophages, as activin A increased CCR2 expression but inhibited the ac

40 oncentrations of the closely related protein activin A increased in parallel with hepcidin in serum f

41 Mouse fat tissue activin A increased with aging.

42 Here we report that activin A induces lateral ganglionic eminence (LGE) char

43 (ACVR2B/Fc) to test the effects of myostatin/activin A inhibition in the R6/2 mouse model of HD.

44 Ultimately, activin A inhibition resulted in rapid recovery of muscl

45 The introduction of activin A into normal muscle increased the expression of

46 Activin A is a member of the TGF-beta superfamily and wa

47 Here we show that activin A is the long-sought second negative muscle regu

48 Activin A levels in the NAc were assessed via ELISA and

49 weeks, whereas mice with elevated levels of activin A lost 11% of their body weight.

50 These functions could help explain how activin A modulates physiological signaling during extra

51 Activin A orchestrated the expression of multiple genes

52 Blocking activin A partially restored lipid accumulation and expr

53 Analysis of body composition revealed that activin A primarily triggered loss of lean mass, whereas

54 JAK inhibitor suppressed senescent cell activin A production and blunted senescent cell-mediated

55 ter cardiotoxin-induced muscle damage, local activin A protein expression increased by threefold to n

56 In fact, activin A receptor blockade during the M-CSF-driven diff

57 eral disease-related microRNAs targeting the activin A receptor type 1C (ACVR1C), a component of the

58 dorsomorphin homolog 1 (DMH1) or CRISPR/Cas9 activin A receptor type I (ACVR1) knockout in OPCs.

59 ocarcinomas contain somatic mutations in the activin A receptor type IB (ACVR1B) gene, indicating tha

60 t common FOP mutation [c.617G>A, p.R206H] of Activin A Receptor, type 1 (ACVR1) and that affects the

61 the bone morphogenic protein receptor kinase activin A receptor, type I (ACVR1), and the subsequent r

62 P(+) astrocytes that were immunopositive for activin A remained unaltered.

63 mage signaling, shorter telomeres, increased activin A secretion and an altered DNA damage response c

64 signaling pathway, a hypothesis confirmed by activin A secretion in cultured GCT cells, which prolife

65 Our high-resolution structures of pro-activin A share features seen in the pro-TGF-beta1 and p

66 Inhibition of myostatin/activin A signaling activated transcriptional profiles t

67 Activin A specific inhibition, on top of GDF8 inhibition

68 partial signaling blockade upon myostatin or activin A stimulation, and this leads to only a small in

69 with DeltamiR-UL148D are more responsive to activin A stimulation, as demonstrated by their increase

70 n rate was positively correlated with a high activin A to inhibin A ratio.

71 ombination of T3SS-mediated GMT delivery and Activin A treatment showed an additive effect, resulting

72 TFH cell programming by activin A was antagonized by the cytokine IL-2.

73 s, among a set of 84 cytokines investigated, activin A was the second highest induced gene, with CXCL

74 Although transforming growth factor-beta and activin A were individually sufficient to initiate expre

75 In summary, selective inhibition of activin A with a monoclonal antibody in muscle injury le

76 Neutralization of activin A with a specific monoclonal antibody in this mu

77 Activin A's ability to drive TFH cell differentiation in

78 Activin A, a member of the transforming growth factor-be

79 ally-aged INK-ATTAC mice reduced circulating activin A, blunted fat loss, and enhanced adipogenic tra

80 ptor in drug taking, the role of its ligand, activin A, in cocaine relapse is unknown.

81 ese data suggest that increased secretion of activin A, particularly from microglia, in the NAc repre

82 proved JAK1/2 inhibitor, reduced circulating activin A, preserved fat mass, reduced lipotoxicity, and

83 In conclusion, our study reports that activin A, produced during NK-DC interactions, represent

84 yonic stem cells to study the role of BRA in activin A-induced endoderm and BMP4-induced mesoderm pro

85 tivin antagonists were then shown to inhibit activin A-mediated cell proliferation in ex vivo ovary c

86 glia in the NAc that were immunopositive for activin A.

87 reted levels of the inhibin betaA homodimer, activin A.

88 ed in the presence of high concentrations of activin A.

89 a indicate a sensitive response of muscle to activin A.

90 sive to the noncanonical inflammatory ligand Activin A.

91 tiated following treatment with the chimeric Activin A/BMP2 ligand AB235.

92 55 to the activin A:ActRII that disrupts the activin A:ActRII complex's binding with ALK4-ECD-Fc in a

93 confirmed target binding of NUCC-555 to the activin A:ActRII that disrupts the activin A:ActRII comp

94 Activin, a member of the transforming growth factor-beta

95 paB activity is required to upregulate INHBA/Activin, a morphogen in the TGFbeta superfamily.

96 NA expression in MM cells is up-regulated by activin, a predominant cytokine among those increased in

97 Here, we show that the cytokine activin-A instructs the generation of CD4(+) T cells tha

98 Moreover, mechanistic studies reveal that activin-A signaling induces the activation of the transc

99 atory T (Treg) cells induced by the cytokine activin-A suppress TH2-mediated allergic responses and l

100 ion to the inhibitory effects of TGFbeta1 or activin-A, autocrine BMP signaling was supportive to NK

101 In fact, IRF4 silencing abrogates activin-A-driven IL10 and ICOS up-regulation and impairs

102 Overall, our findings uncover an activin-A-induced IRF4-aryl hydrocarbon receptor (AhR)-d

103 Still, the effects of activin-A-induced regulatory T (Act-A-iTreg) cells on th

104 Finally, activin-A-induced TFH programming was dependent on signa

105 d impairs the suppressive functions of human activin-A-induced Tr1-like (act-A-iTr1) cells.

106 -binding EGF-like growth factor (HB-EGF) and activin AB in LTBI samples.

107 However, antibody-mediated neutralization of activin activity during murine malaria infection did not

108 y is perturbed in malaria infection but that activins, although raised in malaria infection, may not

109 d in muscle atrophy, such as angiotensin-II, activin and Acvr2b, in SIRT6 depleted cells.

110 esoderm in human pluripotent stem cells with ACTIVIN and BMP or with GSK3-beta inhibition.

111 ACTIVIN and BMP-induced mesoderm patterned into cardiac

112 Previous studies show that both activin and Bmp4 act as crucial mesenchymal odontogenic

113 Signaling driven by TGFbeta ligand Activin and constitutively active receptors Alk4 and Alk

114 Targeting activin and its related signaling pathways holds promise

115 Remarkably, codelivery of activin and myostatin inhibitors induced a synergistic r

116 In conclusion, activin and TGF-beta are strongly connected signaling pa

117 most prominent TGF-beta superfamily members activin and TGF-beta in advanced colorectal cancer.

118 e-based assay that combined serum and tissue activin and TGF-beta ligand levels predicts outcome in C

119 mRNA expression of activin and TGF-beta pathway members were queried in sil

120 tor expression is common in solid tumors for activin and TGF-beta pathway members.

121 Assessing activin and TGF-beta signaling as a unit yields importan

122 and cancer cachexia, combined inhibition of activins and myostatin increased mass or prevented muscl

123 These potential activin antagonists were then shown to inhibit activin A

124 ased strategy for identifying small-molecule activin antagonists.

125 Myostatin and the activins are capable of binding to both ActRIIA and ActR

126 Activins are growth factors with multiple roles in the d

127 Activins are members of the TGF-beta superfamily and dri

128 GF-beta family ligands myostatin, GDF11, and activins are negative regulators of skeletal muscle mass

129 Like all TGF-beta family of growth factors, activins are synthesized as large precursors from which

130 toxicity were tested in two well-established activin assays: FSHbeta transcription and HepG2 cell apo

131 Here, we report that Tgfbeta ligands and activin B (ActB) act in concert in the mammalian spinal

132 In the absence of uterine FST, activin B expression and signaling are up-regulated, and

133 expression of BMP2 in human hepatocytes and activin B in mouse liver.

134 r AAV injection, inhibition of activin A and activin B signaling produced moderate ( approximately 20

135 Overexpression of Inhbb or addition of activin B stimulates rat islet cell and beta-cell prolif

136 of Plasmodium berghei-infected mice; hepatic activin B was also upregulated at peak parasitemia durin

137 nd and inhibited the TGF-beta family ligands Activin B, BMP-6, and BMP-7, but not the frog Cerberus l

138 In contrast, activin B, which can signal through the BMP/SMAD pathway

139 r Nodal, whereas Cryptic interacts only with Activin B.

140 Activin belongs to the TGFbeta superfamily, which is ass

141 Activin-beta has a key role in this regulation, which is

142 Here we report that Activin-beta, a TGF-beta family ligand, is expressed by

143 identified in the interface between the two activin betaA subunits and was used for a virtual high-t

144 Remarkably, mice lacking activin-betaA ( Inhba(-/-)) and mice with neural crest-s

145 competitive manner at the critical myostatin/activin binding site, hence preventing signal transducti

146 first-in-class small-molecule antagonist of activin binding to ALK4, which opens a completely new ap

147 ceptor type IIB (ActRIIB) modified to reduce activin binding.

148 Thus, activin/BMP gradients specify distinct mesodermal subpop

149 Tgfbeta ligands and Activins comprise the other arm and signal via Smads 2/3

150 Furthermore, in mice, inhibition of activin conveys survival benefits in pancreatitis.

151 Consequently, YAP-null hESCs exposed to Activin differentiate precisely into beating cardiomyocy

152 ein (ActRIIB.Fc), a ligand trap for TGF-beta/activin family members including myostatin, can prevent

153 st-type pluripotency that is maintained with ACTIVIN/FGF2 signaling.

154 (ALK) receptors 4/5/7 recognizing TGF-beta, activin, growth and differentiation factor, and nodal li

155 3 phosphorylation via activin receptors, but activins have not been studied in the context of PKD.

156 igh activin/low BMP) and posterior-like (low activin/high BMP) mesodermal populations.

157 and prevents the gene from being induced by Activin in proliferating hESCs.

158 of Inhba, which encodes the betaA subunit of Activin, in the UGS mesenchyme.

159 a induced cellular migration is dependent on activin, indicating pathway cross-regulation and functio

160 report that PI3K signalling antagonizes the Activin-induced definitive endoderm (DE) differentiation

161 Activin-induced neurons also exhibit appropriate striata

162 ize beta-catenin, which then synergizes with Activin-induced SMADs to activate a subset of ME genes t

163 Interestingly, exposure of YAP(-/-) hESCs to Activin induces cardiac mesoderm markers (BAF60c and HAN

164 Activin is a critical modulator of inflammatory response

165 Taken together, activin is a novel candidate as a clinical marker to ide

166 Here, we demonstrate that serum activin is elevated and strongly correlates with disease

167 cal cohort of pancreatitis patients and high activin levels in patients at admission are predictive o

168 In addition, serum activin levels were measured from a retrospective clinic

169 ceive non-redundant signaling from the three Activin ligands, activating the transcription factor dSm

170 n, which acts as a soluble trap to sequester activin ligands, effectively inhibited cyst formation in

171 Mice with PKD had increased expression of activin ligands, even at early stages of disease.

172 s of phosphorylated Smad2/3 upon exposure to activin ligands.

173 n part on the ability of broad inhibition of activin-like kinase (ALK) receptors 4/5/7 recognizing TG

174 le inhibitor of the TGF-beta type I receptor activin-like kinase (ALK5) (SB431542), demonstrating tha

175 Here we show that the activin-like kinase 1 (ALK1) mediates LDL uptake into en

176 s simulations and free energy calculation of Activin-Like Kinase 2 (ALK2), we found that GS domain ph

177 this study, we discovered that signaling via activin-like kinase 3 (ALK3/BMPR1A), a BMP type 1 recept

178 f EPDCs to the AV junction, the Bmp receptor activin-like kinase 3 (Alk3; or Bmpr1a) was conditionall

179 In this study we show that the Activin-like ligand Dawdle (Daw) is a major regulator of

180 preclinical trials to identify inhibitors of activin-like receptor kinase (ALK) 1 as effective agents

181 g and specified distinct anterior-like (high activin/low BMP) and posterior-like (low activin/high BM

182 would benefit from aggressive treatment and activin may be a therapeutic target in severe acute panc

183 goal of a compound that may be effective in activin-mediated diseases.

184 th gonadotropin-releasing hormone (GnRH) and activins, members of the transforming growth factor beta

185 Bone morphogenetic protein and activin membrane-bound inhibitor (BAMBI) is a transmembr

186 on of the bone morphogenic protein (BMP) and activin membrane-bound inhibitor (BAMBI), which enhances

187 phroblastoma overexpressed gene, and BMP and activin membrane-bound inhibitor (BAMBI).

188 g the TGF-beta pseudoreceptor BAMBI (BMP and activin membrane-bound inhibitor), which leads to an inc

189 to the colony edge and induced a gradient of Activin-Nodal signaling that patterned mesendodermal fat

190 Activin/Nodal growth factors control a broad range of bi

191 of extravillous trophoblast, whereas loss of activin/nodal inhibition leads to the formation of syncy

192 ignaling, we unexpectedly identified the BMP/Activin/Nodal inhibitor Coco as an enhancer of TGFbeta1

193 Inhibition of activin/nodal signaling leads to formation of extravillo

194 We show that activin/nodal signaling switches the terminal fate of th

195 e morphogenetic protein and/or inhibitors of activin/nodal signaling to obtain cells that express tro

196 ion with the pluripotency factor Oct4 and on Activin/Nodal signaling.

197 t currently remain unanswered on the role of Activin/Nodal signalling in stem cell self-renewal, diff

198 e an overview of the mechanisms by which the Activin/Nodal signalling pathway governs stem cell funct

199 We describe recent findings that associate Activin/Nodal signalling to pathological conditions, foc

200 d by interactions between morphogens such as activin/nodal, BMPs and Wnt/beta-catenin that define ant

201 independent of loss of cell-cell contact and Activin/Nodal-dependent pluripotency and a peptide is de

202 gene transcript alterations and a switch to Activin/Nodal-dependent pluripotency.

203 and that the differential effects of loss of activin or Bmp4 signaling on maxillary and mandibular mo

204 ranscription in vivo, they also suggest that activins, or related ligands, could play more important

205 ng recapitulates SOX9-dependent defects, and Activin partially rescues them.

206 unction of ALK4, a key receptor for the MSTN/activin pathway in skeletal muscle.

207 g IGSF1 as an important regulator of TGFbeta/Activin pathways in the pituitary.

208 eveloping therapies that interfere with MSTN/activin pathways.

209 acellular factors, most notably enhancers of Activin/pSMAD2 signaling.

210 low molecular weight complex that stimulated Activin receptor (Acvr) signaling far more potently than

211 generated mice with conditional deletion of activin receptor (ACVR) type 2A, ACVR2B, or both, in ost

212 ACVR2B/Fc, an inhibitor of the Activin Receptor 2B signaling, has been shown to preserv

213 We find that the Activin receptor Baboon is required in R8 to receive non

214 recurrent activating mutation affecting the activin receptor gene ACVR1 in 20% of DIPGs.

215 We report that RAP-011, an activin receptor IIA (ActRIIA) ligand trap, improved ine

216 Our data led us to propose activin receptor IIB as a novel DYNLT1 ligand and sugges

217 In addition, treatment with a soluble activin receptor IIB fusion (sActRIIB-Fc) protein, which

218 ns in the ACVR1 gene, which encodes a type I activin receptor serine/threonine kinase, in 21% of DIPG

219 steoblasts, to determine the contribution of activin receptor signaling in regulating bone mass.

220 Activin receptor signaling, including the transcription

221 Taken together, these results indicate that activin receptor signaling, predominantly through ACVR2A

222 and its murine ortholog RAP-011) acts as an activin receptor type IIA ligand trap, increasing hemogl

223 containing the extracellular domain of human activin receptor type IIB (ActRIIB) modified to reduce a

224 We recently reported that an activin receptor type IIB inhibitor produced hypertrophy

225 The ability of the muscles to respond to activin receptor type IIB inhibitor treatment correlated

226 g diseases, with a decrease of myostatin and activin receptor, and an increase of the myostatin antag

227 etween pro- and anti-angiogenic signaling by activin receptor-like kinase (ALK) 1, 5, and TGF-beta ty

228 BMP-binding TGF-beta superfamily receptors, activin receptor-like kinase (ALK)3/6, and the Smad2/3 p

229 ns were used to determine the involvement of activin receptor-like kinase 1 (ALK1) and ALK5 downstrea

230 dent on the endoglin signaling pathway using activin receptor-like kinase 1 (ALK1) Fc blocking peptid

231 Signaling through high-affinity activin receptor-like kinase 1 (ALK1) in endothelial cel

232 Activin receptor-like kinase 1 (ALK1) is an endothelial

233 -of-function mutations in the genes encoding activin receptor-like kinase 1 (ALK1), endoglin, Smad4,

234 pro-domain-complexed BMP9 to type I receptor activin receptor-like kinase 1 (ALK1), type II receptors

235 g was reduced in TbetaRII(+/-) ECs; however, activin receptor-like kinase 1 (ALK1)-mediated Smad1/5 p

236 e arterial-specific TGFbeta type I receptor, activin receptor-like kinase 1 (ALK1; ACVRL1), causes he

237 Small interfering RNA knockdown of activin receptor-like kinase 1 inhibited the BMP9-induce

238 Activin receptor-like kinase 5 (ALK5) is the major type

239 to the TGF-beta type I receptor (also termed activin receptor-like kinase 5 (ALK5)), in a similar fas

240 growth factor beta receptor I (TGF-betaRI) (activin receptor-like kinase 5 [ALK-5]) and TGF-beta rec

241 at, conversely, the type I TGF-beta receptor activin receptor-like kinase 5 is dispensable for trypsi

242 min preferentially induces activation of the activin receptor-like kinase 5 pathway of TGF-beta recep

243 n a small increase in TGF-beta signaling via activin receptor-like kinase 5 to maintain early integri

244 ed the TGF-beta type 1 receptor (also termed activin receptor-like kinase 5) in renal epithelial cell

245 ve inhibitor of the type 1 TGF-beta receptor activin receptor-like kinase 5, orally active) to inhibi

246 K), transforming growth factor beta receptor/activin receptor-like kinase beta, estrogen receptor, an

247 treatment of SB-431542, an inhibitor of the activin receptor-like kinase receptors, to enhance myoge

248 et cell and beta-cell proliferation, and the activin receptors RIIA and RIIB are required for the ful

249 family and drive SMAD2/3 phosphorylation via activin receptors, but activins have not been studied in

250 eases in TA mass, indicating that endogenous activins repress muscle growth.

251 tivin, TGF-beta treatment leads to increased activin secretion in colon cancer cells and TGF-beta ind

252 R7- and R8-derived Activin selectively restricts the dendritic fields of th

253 ogenetic protein 4 (BMP4) plus inhibitors of ACTIVIN signaling (A83-01) and FGF2 (PD173074), followed

254 dition to ActRIIB in mediating myostatin and activin signaling and highlight the need for blocking bo

255 These data point to activin signaling as a key pathway in PKD and a promisin

256 These findings establish Activin signaling as a major metabolic regulator and unc

257 dings support a model in which repression of activin signaling by FST enables uterine receptivity by

258 Primary osteoblasts expressed activin signaling components, including ACVR2A, ACVR2B,

259 Tm20 neurons lacking Activin signaling expanded their dendritic fields and ab

260 Inhibition of Activin signaling in CAST/Ei mice diminishes their CNS r

261 To investigate activin signaling in osteoblasts in vivo, we analyzed th

262 d culture studies we show that inhibition of Activin signaling in the female UGS leads to a similar p

263 NODAL/Activin signaling induces dramatic chromatin landscape c

264 NODAL/Activin signaling orchestrates key processes during embr

265 The activin signaling pathway is an attractive candidate to

266 arly stages of pancreatic tumorigenesis; the activin signaling pathway therefore might be a therapeut

267 esenchyme, these data indicate that Bmp4 and activin signaling pathways converge on activation of the

268 Canonical Activin signaling promotes dendritic termination without

269 Moreover, compromising Activin signaling recapitulates SOX9-dependent defects,

270 A balance of Nodal/Activin signaling regulates the anterior boundary of the

271 However, the mechanism by which nodal/activin signaling regulates XY PGC fate is unknown.

272 n and increased expression of the downstream activin signaling targets ID1 and ID2.

273 show that simultaneous modulation of WNT and ACTIVIN signaling yields CD34(+) hematopoietic cells wit

274 ssion of genes involved in tumor metabolism, activin signaling, and apoptosis.

275 PK, the putative downstream factors of nodal/activin signaling, in PGC sexual fate decision.

276 GF signaling, together with downstream nodal/activin signaling, promotes male differentiation in XY g

277 riptional responses requires continued NODAL/Activin signaling.

278 targets the cellular receptor ACVR1B of the activin signalling axis.

279 Moreover, ASPN perturbed the Wnt, BMP and Activin signalling pathways, suggesting that ASPN thereb

280 pathways that can inhibit both TGF-beta and activin signals while enhancing bone morphogenetic prote

281 contrast, IGSF1 strongly down-regulates the activin-Smad pathway, leading to reduced expression of F

282 Activin/SMAD signaling in human embryonic stem cells (hE

283 In the presence of Wnt ligand, the Activin/SMAD transcription network switches to cooperate

284 mbryonic stem cells (hESCs) to show that the Activin-SMAD2/3 signaling pathway cooperates with the co

285 Thus, the Wnt3a/beta-catenin and Activin/SMAD2,3 pathways act in concert to counteract YA

286 The Wnt3a/beta-catenin and Activin/SMAD2,3 signaling pathways synergize to induce e

287 However, subsequent Activin/SMAD2,3 signaling selectively increases transcri

288 Thus, Activin/Smad3 signaling is induced following withdrawal

289 alysis identified inhibin beta-B (Inhbb), an activin subunit and member of the transforming growth fa

290 GF-beta growth suppression is independent of activin, TGF-beta treatment leads to increased activin s

291 by preventing WNT3 expression in response to Activin, thereby blocking a direct route to embryonic ca

292 cid mutation of the BMP receptor responds to activin, thereby turning soft tissues into bone.

293 CRISPR/CAS9 knockout of YAP in hESCs enables Activin to induce Wnt3 expression and stabilize beta-cat

294 wo whole-genome expression screens yield the Activin transcript Inhba as most correlated with this ab

295 I bone morphogenetic protein receptor ACVR1 (Activin type 1 receptor).

296 cription factor activities through alternate Activin type 2 receptors.

297 New function of the myostatin/activin type I receptor (ALK4) as a mediator of muscle a

298 We have used i.p. injection of activin type IIB receptor (ActRIIB)-mFc (an inhibitor of

299 ic administration of the soluble form of the activin type IIB receptor (ACVR2B/Fc).

300 he expansion of EYFP+ cells, while Wnt3a and Activin were marginally effective.