ライフサイエンスコーパス: TGF

1 TGF-beta depends on RAS and mitogen-activated protein ki

2 TGF-beta is extensively implicated in the pathogenesis o

3 TGF-beta is used routinely for expansion of conventional

4 TGF-beta regulates iTreg cell outcomes through 2 distinc

5 TGF-beta treatment increased glycolysis in PASMCs, but d

6 TGF-beta-driven fibrosis is mediated through Smad-depend

7 TGF-beta1 (transforming growth factor beta1), downstream

8 TGF-beta1 induces microglia to metabolically tune from a

9 TGF-beta1 signalling also reversed the AnxA8 loss-induce

10 TGF-beta1 similarly attenuates PPM1A and PTEN expression

11 TGF-beta1 was increased in moderate-severe OSA patients

12 TGFs detected by the GBM with sources at farther horizon

13 ession of transforming growth factor beta 1 (TGF-beta1) because of interleukin-4 (IL-4)- and signal t

14 -CSF) and transforming growth factor-beta 1 (TGF-beta1) in the presence or absence of PRF.

15 uction of transforming growth factor beta 1 (TGF-beta1), a cytokine known to inhibit CD56(+) cell dev

16 y against transforming growth factor-beta 1 (TGF-beta1), the most common growth factor used in chondr

17 Immunoreactivity and mRNA levels of IGF-1, TGF-beta1, and beta3-adrenoceptor were increased at days

18 gingiva (IL-6, IL-17A, IL-17F, RANKL, IL-10, TGF-beta and GITR; P < 0.05), and the proliferation of b

19 s and stimulated the cells to produce IL-10, TGF-beta, or both at the immunization site, which might

20 This TIC-driven, IL-33-TGF-beta feedforward loop could potentially be exploited

21 Activin A, a TGF-beta family member, is a strong pro-metastatic cytok

22 Gdf15 encodes a TGF-beta superfamily member that is rapidly activated in

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

24 is, we examined the proteomic profiling of a TGF-beta1-induced in vitro model of fibrosis in NRK-49F

25 d myofibroblast induction occurred through a TGF-beta independent mechanism.

26 mote itching during skin would healing via a TGF-beta-IL-31 axis with implications for treatment of w

27 Aberrant TGF-beta signalling and EMT are implicated in the pathog

28 ich was reduced in the presence of activated TGF-beta1.

29 duces H19 expression which in turn activates TGF-beta signaling and EndMT via a TET1-dependent epigen

30 apnea (OSA) increases serum levels of active TGF-beta1 in patients with cutaneous melanoma (CM), asse

31 In addition, TGF-beta upregulates the expression of the IL-33 recepto

32 e absence and overexpression of SMAD7 affect TGF-beta signaling and modulates beta-cell proliferation

33 After TGF-beta, Smad3 and TGF-beta-activated kinase 1 (TAK1) k

34 rmation, and tumor development in mice after TGF-beta treatment.

35 < 0.05), decreasing apoptosis (p < 0.05) and TGF-beta-positive signal (p < 0.05) in surrounding tissu

36 showed that SCI bladders released IGF-1 and TGF-beta1 to stimulate elastin and collagen for bladder

37 positive regulatory T cells and IL-10(+) and TGF-beta1(+) skin-resident macrophages.

38 se of human MCF-7 cells to retinoic acid and TGF-beta, applied individually and in combination.

39 er deposition of collagen in the airways and TGF-beta in lung fluid.

40 ession of furin and downstream TGF-beta1 and TGF-beta2.

41 ll with elevated expression of TGF-beta2 and TGF-beta3, and activation of their downstream signaling

42 We hypothesized that the EGFR and TGF-beta signaling pathways cooperate during chlamydial

43 elial cells and stimulated both the EGFR and TGF-beta signaling pathways.

44 er, the combined inhibition of both EGFR and TGF-betaR1 signaling reduced inclusions by over 90% and

45 ued P2RX7-deficient Trm cell generation, and TGF-beta sensitivity was dictated by P2RX7 agonists and

46 ation in vitro, focusing on the integrin and TGF-beta/SMAD pathways.

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

48 In addition to overexpression of p53 and TGF-beta pathway genes, we identified high levels of MYC

49 timulation occurred in a proinflammatory and TGF-beta-low cytokine microenvironment.

50 After TGF-beta, Smad3 and TGF-beta-activated kinase 1 (TAK1) kinase levels were mo

51 nings of alphavbeta8 binding specificity and TGF-beta activation.

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

53 is partially redundant with that of another TGF-beta family member, activin A.

54 d by NS8593 treatment in UUO kidneys, as are TGF-beta1/Smad signaling events.

55 ive function and that inactivation of ARID1A/TGF-beta axis promotes migration and invasion of PTEN-de

56 collagens in cardiac fibroblasts as well as TGF-beta (transforming growth factor-beta)-activated myo

57 integrin alphaVbeta6 association as well as TGF-beta-mediated permeability across alveolar epithelia

58 M induction, we propose that eCRT attenuates TGF-beta-mediated fibrosis/scarring to achieve tissue re

59 with neural cell markers and expressed BDNF, TGF-beta1, GFAP, and IL-6.

60 ration, and transforming growth factor beta (TGF-beta and BMP signaling through SMAD members has dist

61 pression of transforming growth factor beta (TGF-beta) and widespread fibrosis.

62 upregulates transforming growth factor beta (TGF-beta) expression, whose signaling pathway synergizes

63 ted a novel transforming growth factor beta (TGF-beta) R2-41BB chimeric receptor that improved solid

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

65 nd abnormal transforming growth factor beta (TGF-beta) signaling in smooth muscle.

66 [IIS]) and transforming growth factor beta (TGF-beta) signaling repress odr-10 expression.

67 )-6, IL-10, transforming growth factor beta (TGF-beta), and interferon gamma (IFN-gamma).

68 ctor (FGF), transforming growth factor beta (TGF-beta), and WNT pathways, we derived PSCs from mice,

69 ase (iNOS), transforming growth factor beta (TGF-beta), NADPH oxidase isoform 4 (Nox4), caspase-3 and

70 Transforming growth factor beta (TGF-beta), which induces the expression of CD103 on tiss

71 ry cytokine transforming growth factor beta (TGF-beta).

72 apart from Transforming Growth Factor beta (TGF-beta1)-mediated induction.

73 Transforming growth factor-beta (TGF-beta) is well-known to induce breast cancer migratio

74 f enhancing transforming growth factor-beta (TGF-beta) mediated tenogenesis in human adipose-derived

75 Transforming growth factor-beta (TGF-beta) promotes tumor invasion and metastasis by indu

76 found that transforming growth factor-beta (TGF-beta) superfamily member activin A is increased in t

77 actors (eg, transforming growth factor-beta [TGF-beta1], epidermal growth factor [EGF], platelet-deri

78 h enhanced transforming growth factor-beta1 (TGF-beta1) biliary secretion.

79 Transforming growth factor-beta1 (TGF-beta1) plays a premier role in fibrosis.

80 Active transforming growth factor-beta1 (TGF-beta1), a cytokine partially regulated by hypoxia an

81 surface of transforming growth factor-beta1 (TGF-beta1)-activated human myofibroblasts underwent mult

82 nstream of transforming growth factor-beta1 (TGF-beta1).

83 cytokine (transforming growth factor beta1 [TGF-beta1]) were suppressed in E. faecalis-induced DCs,

84 ng, suggesting reciprocal regulation between TGF-beta and EGFR signaling during chlamydial infection.

85 spatially restricted generation of bioactive TGF-beta from latent stores requires the cooperation of

86 ing in muscle and that the inhibitor blocked TGF-beta1-mediated Smad2 phosphorylation.

87 ation and function were enhanced by blocking TGF-beta signalling, promoting bone morphogenic protein

88 cules and peptide modulators to inhibit BMP, TGF-beta (SMAD), and canonical Wnt pathways that reduced

89 perturbing DNA binding by various STFs (BMP/TGF-beta-directed SMADs or WNT-induced TCFs) and affecti

90 um supplemented with TGF-beta1, KGN, or both TGF-beta1 + KGN.

91 We found that ERK1/2 was activated by TGF-beta and required to regulate expression of Scleraxi

92 cellular and molecular pathways activated by TGF-beta, which determine the suppressor or enhancing ac

93 and PDGFR abrogated the induction of GLS1 by TGF-beta.

94 EMT and stemness characteristics induced by TGF-beta might be associated with epigenetic regulation

95 for GLS1 expression, which are inhibited by TGF-beta.

96 pha5 and beta1 integrins was not mediated by TGF-beta signaling nor inhibited by RAP.

97 and utilization, partially recapitulated by TGF-beta treatment.

98 and 27 molecular functions were regulated by TGF-beta1.

99 Regulation of Scleraxis by TGF-beta did not require new protein synthesis; however,

100 ing how integrins interact with signaling by TGF-beta and/or other growth factors (GFs) within the te

101 and soft agar colony formation stimulated by TGF-beta required GLS1 activity.

102 ed including cell cycle, pathways in cancer, TGF-beta signaling, FoxO signaling, fatty acid biosynthe

103 ) signaling cascade, distinct from canonical TGF-beta signaling.

104 hans cells; analysis of BMP versus canonical TGF-beta signaling in DCs and Treg cells; and modeling o

105 t associations pointing to wnt/beta-catenin, TGF-beta and sonic hedgehog pathways.

106 essive CD4 antibody(12,13), and named it CD4 TGF-beta Trap (4T-Trap).

107 rap, 4T-Trap selectively inhibited T(H) cell TGF-beta signalling in tumour-draining lymph nodes, caus

108 In the same cell, TGF-beta induced coexpression of Smad3 and TAK1 proteins

109 In carcinoma cells, TGF-beta-SMAD and RREB1 directly drive expression of SNA

110 In conclusion, TGF-beta1 levels are associated with melanoma aggressive

111 n that ubiquitin E3 ligases potently control TGF-beta signaling through targeted degradation of key r

112 te that monocytes in the presence of GM-CSF, TGF-beta1, and the Notch ligand DLL4 differentiate withi

113 effect of calcitriol on homeostatic (M-CSF, TGF-beta-treated) and proinflammatory (GM-CSF-treated) h

114 in neurons, supporting a role for the CX3CL1-TGF-beta2/3-Smad2 pathway in the control of adult neurog

115 loss in response to the profibrotic cytokine TGF-beta.

116 Anti-inflammatory TAMs secreted the cytokine TGF-beta that, upon engagement of its receptors in breas

117 induced mouse and human cardiomyocyte death, TGF-beta-induced cardiac fibroblast Smad2/3 activation,

118 ced fibrotic tissue production and decreased TGF-beta-mediated SMAD activation.

119 VDeltamiR-US5-2 mutant resulted in decreased TGF-beta expression and restoration of myelopoiesis.

120 ts of these microRNAs implicated derepressed TGF-beta signaling as a shared seizure-modifying mechani

121 dy, we demonstrate that myeloid cell-derived TGF-beta1 signaling is increased in a profibrotic ischem

122 y reduces expression of furin and downstream TGF-beta1 and TGF-beta2.

123 ngs reveal a new requirement for endothelial TGF-beta signaling in OFT morphogenesis and suggest an i

124 IL-15 enhanced TGF-beta-mediated conversion through Ras:RAC1 signaling

125 PPP2R5e knockdown exacerbated TGF-beta-mediated profibrotic signaling, indicating a ro

126 eg restimulation in the absence of exogenous TGF-beta1.

127 In vitro assays revealed exogenous TGF-beta1 increased OASIS expression coincident with fib

128 nism, augmenting transforming growth factor (TGF) beta signaling.

129 rotein (BMP) and transforming growth factor (TGF) beta signaling.

130 sts treated with transforming growth factor (TGF) beta-1 or generated directly from cultured BM treat

131 rotic effects of transforming growth factor (TGF)-beta as a potential mechanism for inconsistent clin

132 was evaluated in transforming growth factor (TGF-beta)-incubated LX-2 cells and culture-activated pri

133 ammatory (TNF-alpha, IL-6) and pro-fibrotic (TGF-beta1) cytokines were significantly increased in pla

134 Finally, TGF-betaR signaling inhibition suppressed the expression

135 Terrestrial gamma ray flashes (TGFs) are a class of enigmatic electrical discharges in

136 ealed that H19X was an obligatory factor for TGF-beta-induced ECM synthesis as well as differentiatio

137 d Scleraxis was a potential intermediate for TGF-beta-regulated expression of Fibromodulin and Adamts

138 nonical effector Smad3 was not necessary for TGF-beta-mediated regulation of Scleraxis.

139 o TGFbeta stimulation, is a prerequisite for TGF signaling, we investigated the role of protein diaph

140 We demonstrated that MKP5 was required for TGF-beta1 signaling in muscle and that the inhibitor blo

141 factors, including IDO-1, arginase-1, Foxp3, TGF-beta, IL-10, and decreased levels of proinflammatory

142 TGF-beta while protecting infected HPCs from TGF-beta-mediated effects on viral latency and reactivat

143 ining immunosuppressive gene products (e.g., TGF-beta).

144 te repolarized the tumor-promoting CD206(hi) TGF-beta1(+) MPhi via inhibition of FROUNT and thus remo

145 CM patients, OSA was associated with higher TGF-beta1 levels and greater melanoma aggressiveness onl

146 Additionally, the present study highlights TGF-beta1 as an attractive target for manipulation in th

147 Here we investigated how TGF-beta regulates expression of fibrous markers: Sclera

148 However, TGF-beta can lead to adipocyte state loss when it is pre

149 es the acetylation status of tubulin, HSP90, TGF-beta, and peroxiredoxins.

150 hich are frequently associated with impaired TGF-beta signaling.

151 igase Kelch-like protein 42 (KLHL42) impairs TGF-beta-dependent profibrotic signaling.

152 In TGF-beta-treated PASMCs, glucose, glutamine and fatty ac

153 UVEC) with SHIP-1 knockdown were analyzed in TGF-beta1 or BLM, respectively, induced fibrotic respons

154 ogenitor cells (HPCs) through an increase in TGF-beta production.

155 tem, manifested by a significant increase in TGF-beta, which weakened the therapeutic effect of micel

156 ch as Calponin (CNN1), and genes involved in TGF-beta signaling, such as AKT Serine/Threonine Kinase

157 dence indicates a role for miR-31 (MIR31) in TGF-beta1-induced liver fibrosis.

158 pathway blockade can result in reduction in TGF-beta expression, thus, a PLGA microsphere encapsulat

159 al rats and test if a polymeric diet rich in TGF-beta2 could reduce TNBS-induced intestinal inflammat

160 3 is induced by extracellular cues including TGF-beta2 and lysophosphatidic acid.

161 sults confirmed numerous pathways, including TGF-beta signaling, affected by dexamethasone.

162 educed goblet cell hyperplasia and increased TGF-beta production.

163 ion, mucus hyperconcentration, and increased TGF-beta1.

164 fection, and specifically miR-US5-2, induces TGF-beta secretion, which inhibits myelopoiesis in uninf

165 M-driven TGFBR2 expression, while inhibiting TGF-beta signaling decreased tECM-mediated expression of

166 We find that the intracellular TGF-beta signaling in adipocytes is inhibited by the tra

167 This binding is essential for activating L-TGF-beta presented by a variety of cell types.

168 to latent transforming growth factor-beta (L-TGF-beta).

169 ectodomain and its intact natural ligand, L-TGF-beta, as well as two different inhibitory antibody f

170 strategies to inhibit alphavbeta8-mediated L-TGF-beta activation.

171 re TGF-beta signals within the confines of L-TGF-beta and the release and diffusion of TGF-beta are n

172 teins with impaired ability to anchor latent TGF-beta1 on the cell surface.

173 addition to collagens, such as Ltbp2 (latent TGF-beta-binding protein 2) and Sulf1 (sulfatase 1), whi

174 ease-associated mutants in presenting latent TGF-beta1 to the cell surface.

175 echanism of TGF-beta activation where mature TGF-beta signals within the confines of L-TGF-beta and t

176 Mechanistically, TGF-beta signaling is required for the generation and ma

177 ent stiffness leads to stromal cell-mediated TGF-beta family signaling relying on the induction and u

178 GVHD increased microglia TGF-beta-activated kinase-1 (TAK1) activation and NF-kap

179 may be a potential candidate for modulating TGF-beta signaling to reduce multiorgan fibrosis during

180 A study from Kiepas et al. revealed a new TGF-beta-dependent role for Src homology/collagen adapto

181 We aimed to define the role of the SP/NK1R/TGF-beta1/miR-31 axis in regulating biliary proliferatio

182 Next, the role of several noncanonical TGF-beta pathways were tested.

183 to act directly downstream of SOX9, but not TGF-beta3.

184 SMC-specific ablation of TGF-beta signaling in Apoe(-/-) mice on a hypercholester

185 ng stiffness in the presence (or absence) of TGF-beta1.

186 its executionary molecules, accentuation of TGF-beta signaling, Smads and XBP1 nuclear translocation

187 work we show that the profibrotic actions of TGF-beta are mediated, at least in part, through a metab

188 s the link between endothelial activation of TGF-beta signaling, induction of endothelial-to-mesenchy

189 SMAD3 phosphorylation and the activation of TGF-beta1-induced fibrotic genes.

190 These data reveal antagonism of TGF-beta/SMAD3 activation by BMP signaling in SMAD3 muta

191 me in PGE(2) metabolism under the control of TGF-beta and microRNA 218.

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

193 L-TGF-beta and the release and diffusion of TGF-beta are not required.

194 Synergistic pro-fibrotic effects of TGF-beta were observed across GCs and appeared to be med

195 nactivation also decreased the expression of TGF-beta1 (transforming growth factor-beta-1) and CTGF (

196 correlates well with elevated expression of TGF-beta2 and TGF-beta3, and activation of their downstr

197 These findings identify a function of TGF-beta in the development of ILC2s from their progenit

198 Correspondingly, inhibition of TGF-beta signaling occluded the antiseizure effects of t

199 rotein 1 (RREB1) as a critical integrator of TGF-beta and Ras signals during both developmental and c

200 er hydroxyproline content and mRNA levels of TGF- beta and collagen in the liver.

201 Moreover, the high levels of TGF-beta might be related to the increased drug-resistan

202 trate that ARID1A-deficiency lead to loss of TGF-beta tumor suppressive function and that inactivatio

203 Our studies reveal a mechanism of TGF-beta activation where mature TGF-beta signals within

204 beta in fibrosis, highlighting mechanisms of TGF-beta activation and signaling, the cellular targets

205 ptional effector(20,21), as a key partner of TGF-beta-activated SMAD transcription factors in EMT.

206 ompared the in vitro chondrogenic potency of TGF-beta1 and KGN using a high resolution micropellet mo

207 were then differentiated in the presence of TGF-beta, whereas IL-17-producing effector T cells were

208 ulated TGFBR1, and TGFBR2 in the presence of TGF-beta1 and increased active NR4A1.

209 ce that this H19/TET1-mediated regulation of TGF-beta signaling and EndMT occurs in mouse pulmonary m

210 cture with a critical role as a regulator of TGF-beta secretion.

211 g RNA (lncRNA) H19X as a master regulator of TGF-beta-driven tissue fibrosis.

212 ion leads to SMAD7 activation, repression of TGF-beta1, resulting in CD56(+) cell development.

213 This review discusses the role of TGF-beta in fibrosis, highlighting mechanisms of TGF-bet

214 To better understand the role of TGF-beta signaling in OFT formation, we generated zebraf

215 lung cells for high-throughput screening of TGF-beta signaling via high-content imaging of nuclear t

216 em cell homeostasis by inducing secretion of TGF-beta while protecting infected HPCs from TGF-beta-me

217 ration by enhancing CD8(+) T cell sensing of TGF-beta, which was necessary for tissue residency.

218 can secrete TGF-beta, whether all sources of TGF-beta are functionally equivalent is unknown.

219 ation and signaling, the cellular targets of TGF-beta actions, and the challenges of therapeutic tran

220 king groups, CI-iPSCs showed upregulation of TGF-beta and Wnt signaling-related genes, which are know

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

222 e we show the existence of two categories of TGFs - those that were accompanied by quasi-simultaneous

223 ucing T cells, however, are not dependent on TGF-beta signaling.

224 underlying these effects with an emphasis on TGF-beta and nuclear receptor subfamily 4 group A member

225 reg cell development but is not expressed on TGF-beta-induced Treg cells.

226 pe was independent of the effect of IL-15 or TGF-beta on mTOR, as the culture of NK cells in the pres

227 els of IL-6 and TNF-alpha, but not IL-1RA or TGF-beta, were significantly associated with increased r

228 Long-term neutralization of IL-6 or TGF-beta protected TNF(-/-) mice from an otherwise letha

229 Inhibition of either the EGFR or TGF-betaR1 signaling substantially reduced inclusion dev

230 ermine whether high extracellular glucose or TGF-beta levels increase phosphorylation of ACTN4.

231 at exposure to high extracellular glucose or TGF-beta stimulates phosphorylation of ACTN4 at S159 in

232 g, focal adhesion kinase (FAK) signaling, or TGF-beta signaling independently led to compromised pro-

233 In OSA patients, TGF-beta1 levels correlated with mitotic index, Breslow

234 Overexpression of SULF1 promotes TGF-beta-induced myofibroblast activation and partially

235 for efficient re-expression of the receptor TGF-betaRII through calcineurin signaling.

236 MAPK-activated RREB1 recruits TGF-beta-activated SMAD factors to SNAIL.

237 Silencing of JMJD2B reduced TGF-beta2-induced expression of mesenchymal genes, preve

238 Although many immune cells can secrete TGF-beta, whether all sources of TGF-beta are functional

239 of IRI on the heart, it was noted that serum TGF-beta1 levels decreased in conditioned groups, wherea

240 ignaling, p53 signaling, Jak-STAT signaling, TGF-beta and notch signaling), rap1-signaling, axon-guid

241 de, inflammation, complement, WNT signaling, TGF-beta and BMP signaling, lipid metabolism, iron homeo

242 mesenchymal transition, expression of Slug, TGF-beta3, phospho-AKT and phospho-PRAS40, but increased

243 ction of signaling pathways including Smads, TGF-beta, and vitamin D.

244 ; however, the roles of these ligases in SSc-TGF-beta signaling remain unclear.

245 Compared with a non-targeted TGF-beta-Trap, 4T-Trap selectively inhibited T(H) cell T

246 s from PH versus control specimens, and that TGF-beta treatment would phenocopy these metabolic chang

247 We conclude that TGF-beta1-induced fibrogenesis in renal fibroblasts is a

248 Transcriptome profiling displayed that TGF-beta pathway activation and ossification-related pro

249 We further provided evidence that TGF-beta disrupts the lineage commitment and promotes th

250 Additionally, we find that TGF-beta signalling via Smad3/Smad4 is sufficient for th

251 Taken together, these results highlight that TGF-beta influences the trajectory of early T-cell activ

252 Here we show that TGF-beta signaling programs the development of ILC2s fro

253 We show that TGF-beta, via AhR induction, and PI3K signaling promotes

254 We showed that TGF-beta stimulated expression of Scleraxis mRNA by 2 h

255 These results suggest that TGF-beta induced EMT and cancer stemness acquisition cou

256 Our results suggest that TGF-beta1 may be broadly beneficial for patients with co

257 The TGF-beta ligand DAF-7 likely acts upstream of IIS and li

258 The TGF-beta superfamily comprises two distinct branches: th

259 istance between the Fermi spacecraft and the TGF source.

260 a bispecific receptor decoy by attaching the TGF-beta-neutralizing TGFBR2 extracellular domain to iba

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

262 ction on tyrosine residues required both the TGF-beta1-dependent production of hydrogen peroxide and

263 Signaling by the TGF-beta superfamily is important in the regulation of h

264 We mechanistically dissected the TGF-beta family-driven regulation of Sca-1, one of the m

265 blockade of IL-6R signaling exacerbated the TGF-beta-induced dysregulation of tight junction protein

266 RT6 binding to the promoters of genes in the TGF-beta signaling pathway decreased significantly with

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

268 d, for the first time, the dependence of the TGF-associated EMP-peak-amplitude on the horizontal offs

269 hogenetic proteins (BMPs) are members of the TGF-beta family that signal via the BMP receptor (BMPR)

270 ome epigenetically reprograms members of the TGF-beta family, including neuronal regeneration-related

271 strate that the Activin/Nodal pathway of the TGF-beta superfamily, but not the BMP pathway, is the pr

272 Although highly selective for ALK2 over the TGF-betaR1 receptor ALK5, M4K2009 is also moderately act

273 inhibit CD56(+) lineage development through TGF-beta1 production and PRL stimulation leads to SMAD7

274 broblast transition and OASIS contributed to TGF-beta1-mediated myofibroblast migration and increased

275 we show that infected HPCs are refractory to TGF-beta signaling as another HCMV miRNA, miR-UL22A, dow

276 ssiveness and analyze the factors related to TGF-beta1 levels in obese and non-obese OSA patients.

277 that HCMV-infected cells become resistant to TGF-beta signaling through targeting of SMAD3 by miR-UL2

278 id cell (ILC1)-like phenotype in response to TGF-beta exposure.

279 s that converted most readily in response to TGF-beta.

280 to activate SHH target genes in response to TGF-beta.

281 marker to identify cells that have undergone TGF-beta signaling, we compared the HIV RNA/DNA contents

282 understand the molecular events underpinning TGF-beta1-induced fibrogenesis, we examined the proteomi

283 e conventional CD4(+) T cells that underwent TGF-beta-mediated conversion in the periphery (called pe

284 iated host invasion by chlamydia upregulated TGF-beta expression and signaling, which cooperated with

285 results revealed that Chlamydia upregulated TGF-beta expression as early as 6 h postinfection of epi

286 BMP7-LCs versus TGF-beta1-LCs were phenotypically characterized and thei

287 ) and neonatal fibroblasts (HFFs) mainly via TGF-beta canonical signaling and Smad2/3 activation; RAP

288 hat are directly or indirectly regulated via TGF-beta.

289 ion and invasion, but the mechanism by which TGF-beta signaling converts into cell motility is not co

290 seen in the human condition associated with TGF-beta1 deficiency.

291 h zymosan or LPS during differentiation with TGF-beta and 1,25diOHvitD3, full-length Dicer became abu

292 t sufficient to super-induce expression with TGF-beta treatment.

293 ound that activation of PKM2 interfered with TGF-beta1 signaling, which is necessary for the developm

294 ion of target genes in PAECs stimulated with TGF-beta, VEGF or serotonin.

295 ed for 7-14 days in medium supplemented with TGF-beta1, KGN, or both TGF-beta1 + KGN.

296 rated directly from cultured BM treated with TGF beta-1 was pursued for insights into possible functi

297 our lung cancer cell lines were treated with TGF-beta.

298 neration in corneal keratocytes treated with TGF-beta1.

299 Treatment with TGF-beta1 elicited distinct phenotypes on substrata of d

300 Treatment with TGF-beta1 protected vision, as measured by 2 behavioral