ライフサイエンスコーパス: TGF-beta1

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

2 TGF-beta1 also increased levels of inflammatory cytokine

3 TGF-beta1 and granzyme B expression were also enriched w

4 TGF-beta1 induces microglia to metabolically tune from a

5 TGF-beta1 inhibited IL-33-mediated Akt and ERK phosphory

6 TGF-beta1 is involved in many pathological conditions, i

7 TGF-beta1 orchestrates the multifaceted program of renal

8 TGF-beta1 pathway antagonism has been proposed for the t

9 TGF-beta1 promotes the differentiation of Th17 cells, wh

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

11 TGF-beta1 similarly attenuates PPM1A and PTEN expression

12 TGF-beta1 was identified as a regulator of NPY in hepato

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

14 TGF-beta1-dependent cardiomyocyte depolarization resulte

15 TGF-beta1-induced renal epithelial cytostasis was also c

16 TGF-beta1-p53 cooperativity regulates a profibrotic geno

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

18 ation and transforming growth factor-beta 1 (TGF-beta1) expression/secretion were evaluated.

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

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

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

22 hways by which transforming growth factor-1 (TGF-beta1) activates pro-fibrogenic mechanisms have been

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

24 aRII mice, there was increased microRNA-125b/TGF-beta1/TGF-beta receptor 1/VEGF-A signaling.

25 NA expression of liver IL-6, IL-17A, IL-17F, TGF-beta1, alpha-SMA, TGR5, NTCP, OATP1a1, and ileum ASB

26 uman kidney tubular epithelial cells (HK-2), TGF-beta1 treatment induced fibrotic changes, including

27 domain protein LIM domain only 7 (LMO7) is a TGF-beta1 target gene in hepatoma cells, but its role in

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

29 xpression, in the presence of Gln, abrogated TGF-beta1-induced expression of profibrotic markers.

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

31 OSS activated TGF-beta1 levels significantly more than SS at all shear

32 OSS-generated active TGF-beta1 stimulated higher pSmad2 signaling and endothe

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

34 imulated, human B lymphocytes produce active TGF-beta1 from surface GARP/latent TGF-beta1 complexes w

35 In addition, TGF-beta1 induces 2-3-fold higher level of ECM proteins

36 and changes in EndoMT markers in MLEC after TGF-beta1 stimulation confirmed the in vivo findings.

37 tions being present in Cu/Zn-SOD, TNF-alpha, TGF-beta1, FASN and IGF-I.

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

39 ing, as well as reduced thrombospondin-1 and TGF-beta1.

40 Also, cytokines such as IL-10 and TGF-beta1 significantly reduce cytokine secretion by ILC

41 flammatory mediators IL (interleukin)-10 and TGF-beta1, and the angiogenic growth factor VEGF (vascul

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

43 a significant correlation between IL-34 and TGF-beta1 expressions.

44 Levels of both IL-34 and TGF-beta1 were thus correlated with the total leukocyte

45 mmunosuppressive cytokines IL-10, IL-35, and TGF-beta1, EBV latency III-transformed B cells were able

46 of growth factors VEGF (45%), EGF (57%) and TGF-beta1 (42%) on ELISA.

47 Px-4), inflammatory cytokines (TNF-alpha and TGF-beta1), lipid metabolism (FASN and CYP7A1), and orga

48 increased presence of IL-17+IL-22+ cells and TGF-beta1 in colorectal cancer compared to normal adjace

49 , connective tissue growth factor (CTGF) and TGF-beta1, in UUO kidney.

50 K) and ERK1/2(MAPK)) were then examined, and TGF-beta1 and EGF were found to have differential effect

51 ndings suggest that targeting the FGFBP1 and TGF-beta1 signaling axis holds promise for slowing age-

52 proliferation, HSC activation/fibrosis, and TGF-beta1 expression/secretion were decreased.

53 ites for hypoxia-inducible factors (HIF) and TGF-beta1-activated SMAD proteins on the human PLOD2 gen

54 ed with attenuation of the hyperglycemia and TGF-beta1-induced enhanced ROS production, increased exp

55 lecular determinants underlying hypoxia- and TGF-beta1-induced PLOD2 expression and its impact on col

56 and SMAD signaling pathways for hypoxia- and TGF-beta1-mediated regulation of PLOD2 expression, a key

57 d protein expressions of both Collagen I and TGF-beta1.

58 riments in PDAC cells revealed that PAR2 and TGF-beta1 synergy may involve TGF-beta1 induction of enz

59 retion levels of cytokines VEGF-A, PGE2, and TGF-beta1 in hybrid spheroid system.

60 tic conditions including stiff substrata and TGF-beta1, and analyzed in terms of morphology, stiffnes

61 yte phenotypes, including albumin uptake and TGF-beta1 triggered cell death.

62 itionally, MA-35 concurrently showed an anti-TGF-beta1 effect by inhibiting Smad3 phosphorylation, re

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

64 hese effects were functionally important, as TGF-beta1 injection suppressed IL-33-induced systemic cy

65 Kaempferol significantly attenuated TGF-beta1-mediated profibrotic pathways in vitro and in

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

67 miR-200b-3p mimic transfection before TGF-beta1 stimulation maintained epithelial marker expre

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

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

70 Increased transforming growth factor beta1 (TGF-beta1) in mammary adipose tissue in obese mice activ

71 tection of transforming growth factor beta1 (TGF-beta1) protein in clinical samples.

72 ctors like transforming growth factor beta1 (TGF-beta1), myofibroblastic MSC differentiation is assoc

73 lood-based transforming growth factor beta1 (TGF-beta1).

74 rs such as transforming growth factor-beta1 (TGF-beta1) and mechanical influences such as local tissu

75 gnaling of transforming growth factor-beta1 (TGF-beta1) and tumor necrosis factor-alpha (TNF-alpha) p

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

77 Transforming growth factor-beta1 (TGF-beta1) expression suppresses MICA expression in hepa

78 agen I and transforming growth factor-beta1 (TGF-beta1) following the administration of DMNA containi

79 ion of the transforming growth factor-beta1 (TGF-beta1) in skeletal muscles and at their NMJs.

80 Transforming growth factor-beta1 (TGF-beta1) is elevated in the peritoneal fluid from wome

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

82 -dependent transforming growth factor-beta1 (TGF-beta1) signaling to activate activator protein-1 (AP

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

84 aorta) of transforming growth factor-beta1 (TGF-beta1), connective tissue growth factor, matrix meta

85 ypoxia and transforming growth factor-beta1 (TGF-beta1), well-known stimuli for the formation of a fi

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

87 restrains transforming growth factor-beta1 (TGF-beta1).

88 ate latent transforming growth factor-beta1 (TGF-beta1).

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

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

91 previously unknown pathological link between TGF-beta1 repressors, contributing to CKD.

92 Elevated levels of bioactive TGF-beta1 are associated with asymmetric fate choice in

93 ecific chemical inhibitor, EHT 1864, blocked TGF-beta1-induced fibrotic reprogramming in kidney epith

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

95 Thus, PPARgamma ligands, by blocking TGF-beta1-induced p38 MAPK phosphorylation, prevent incr

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

97 P-4 mediates upregulation of angiogenesis by TGF-beta1.

98 ockdown abrogated free radical generation by TGF-beta1 in HK-2 cells, consistent with the role of Rac

99 to be the only TSPAN family gene induced by TGF-beta1 and MYOCD, and reduced by SRF deficiency in VS

100 xo-miRs (miR-125a, miR-351) was regulated by TGF-beta1 and was able to differentiate the sham and IRI

101 Cell-lysate proteins regulated by TGF-beta1 were characterised by increased ribosomal prot

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

103 and 7 molecular functions were regulated by TGF-beta1.

104 demonstrates that infiltrating myeloid cell TGF-beta1 is responsible for the development of traumati

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

106 ocyte-cardiomyocyte gap junctional coupling, TGF-beta1 depolarized cardiomyocytes coupled to myofibro

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

108 Addition of the cytokine TGF-beta1, which promotes wound healing, to dermal DCs i

109 showed that the major profibrotic cytokine, TGF-beta1 promoted rapid Rac1-GTP loading in human kidne

110 Consistently, EDP-305 decreased TGF-beta1-induced YAP nuclear localization in human kidn

111 ntify a privileged role of Treg cell-derived TGF-beta1 in regulating allergy and autoimmunity at dist

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

113 ed immunosensor was validated by determining TGF-beta1 in real saliva samples.

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

115 the KRAS-variant had significantly elevated TGF-beta1 plasma levels (median, 23 376.49 vs 18 476.52

116 epletion in HK-2 cells, moreover, eliminated TGF-beta1-mediated non-SMAD pathway activation [e.g., Sr

117 ore, miR-200b-3p mimics reversed established TGF-beta1-induced EMT in BEAS-2B cells.

118 Finally, exogenous TGF-beta1 to -beta3, each restituted the normal scar phe

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

120 covered by NF-kappaB inhibition or exogenous TGF-beta1 treatment.

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

122 cells induces accumulation of extracellular TGF-beta1, forming what appears to be a sialidase - TGF-

123 the induction of key pro-fibrogenic factors, TGF-beta1, TGF-beta2, periostin and endothelin-1, by hum

124 l transgenic goat model of cardiac fibrosis (TGF-beta1 overexpression) to demonstrate that endurance

125 Rac-GTPase promotes fibrotic TGF-beta1 signaling and chronic kidney disease via EGFR,

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

127 immobilization of the specific antibody for TGF-beta1 using Mix&Go polymer.

128 Rac1-directed redox response is critical for TGF-beta1-driven epithelial dysfunction orchestrated, in

129 changes were confirmed at protein level for TGF-beta1 and ENG.

130 rcinoma (PDAC) PAR2 protein is necessary for TGF-beta1-dependent cell motility.

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

132 ntact HIF sites were absolutely required for TGF-beta1 to exert its effect on SMAD-binding sites.

133 diated sEphrin-B2 generation is required for TGF-beta1-induced myofibroblast activation.

134 rs for VSMC differentiation, we screened for TGF-beta1 and MYOCD/serum response factor (SRF)-regulate

135 treated with three commonly-employed GCs+ /-TGF-beta1.

136 tokine has limited the development of global TGF-beta1 signaling inhibitors as therapeutic agents.

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

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

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

140 study with our current understanding of how TGF-beta1 regulates microglia polarization, we highlight

141 Recombinant human TGF-beta1 (rhTGF-beta1) prevented denervation-induced re

142 This work identifies TGF-beta1 and BMP-2 as potent inhibitors of IL-34 expres

143 Here we identify TGF-beta1 as a principle repressor of PPM1A, as conditio

144 MRTF-A knockdown by siRNA or shRNA impaired TGF-beta1 and TCM induction of alpha-SMA and calponin 1,

145 study investigated the role of miRNA-200b in TGF-beta1-induced EMT in human bronchial epithelial cell

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

147 d inhibits the formation of stress fibers in TGF-beta1 treated HSCs.

148 entration of glutamate was also increased in TGF-beta1-differentiated myofibroblasts compared with co

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

150 icators of hypertrophy were not mitigated in TGF-beta1 + KGN cultures, suggesting that KGN does not o

151 marate, malate, and citrate were observed in TGF-beta1-differentiated myofibroblasts.

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

153 mice (intratracheal bleomycin and inducible TGF-beta1).

154 r DOT1L small interfering RNA also inhibited TGF-beta1 and serum-induced activation of renal intersti

155 integrin aVbeta6 in the kidney and inhibited TGF-beta1-induced responses in cultured renal epithelial

156 n of CAFs and tumor cells with either intact TGF-beta1 expression or devoid of TGF-beta1 in vivo show

157 Of interest, TGF-beta1 treatment enhanced TRPV4 activation in a PI3K-

158 that PAR2 and TGF-beta1 synergy may involve TGF-beta1 induction of enzymes that cause autocrine clea

159 2 loss on hepatic fibrogenesis that involves TGF-beta1 activation.

160 ll types use surface GARP to activate latent TGF-beta1 was not known.

161 mutant NRROS proteins fail to anchor latent TGF-beta1 at the cell surface in comparison to wild-type

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

163 ce active TGF-beta1 from surface GARP/latent TGF-beta1 complexes with isotype switching to IgA produc

164 een the integrin alphaVbeta8 and GARP/latent TGF-beta1 complexes.

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

166 utant NRROS proteins co-localize with latent TGF-beta1 intracellularly.

167 dulation of important cellular pathways like TGF-beta1 and STAT1 can explain the sensitivity of tissu

168 basis for this codependency is unclear, many TGF-beta1-responsive genes possess p53 binding motifs.

169 able polymer microspheres (TRI microspheres; TGF-beta1, Rapamycin (Rapa), and IL-2).

170 linearity extending between 15 and 3000pg/mL TGF-beta1 which is adequate for the determination of the

171 The expression of regulatory molecules, TGF-beta1/2, phospho-Akt (Ser473), PPARalpha, sterol reg

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

173 Notably, TGF-beta1 reduced hippocampal dendritic spine loss and m

174 ntly, keratocytes cultured in the absence of TGF-beta1 showed no stiffness-dependent differences in a

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

176 this anchoring is required for activation of TGF-beta1 in macrophages and microglia.

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

178 RNA sequencing analysis of TGF-beta1-activated LX-2 cells showed that ML290 treatme

179 nal fibroblasts stimulated by application of TGF-beta1, the major profibrotic cytokine, thereby suppr

180 ow conduction and ectopic activity, block of TGF-beta1 signaling completely abolished both arrhythmog

181 gression of renal fibrosis, dual blockade of TGF-beta1 and TNF-alpha is desired as its therapeutic ap

182 roxyphenolic compounds as potent blockers of TGF-beta1 responses (IC50 50 nM), Snail1 expression, and

183 AAV-mediated delivery of TGF-beta1 rescued degenerating cones in 3 mouse models o

184 her intact TGF-beta1 expression or devoid of TGF-beta1 in vivo showed a significant increase in tumor

185 rylation, resulting in the downregulation of TGF-beta1-induced fibrotic gene expression.

186 fails to repress the inflammatory effect of TGF-beta1 which is suppressed upon TAK1 inhibition.

187 (5/18, 28%) reported a protective effect of TGF-beta1, while 3 (3/10, 30%) suggested increased risk

188 tent with our previously reported effects of TGF-beta1 on IgE-mediated activation, demonstrate that T

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

190 nalling pathway activation and expression of TGF-beta1 and BMP-2 between healthy and diseased tendon

191 Enhanced expression of TGF-beta1 mRNA and cytokine was evidenced in the livers

192 ro model showed that IH-induced increases of TGF-beta1 expression in melanoma cells is attenuated in

193 racellular CRT (iCRT)-dependent induction of TGF-beta1 and ECM proteins.

194 ditional renal tubular-specific induction of TGF-beta1 in mice dramatically downregulates kidney PPM1

195 Inhibition of TGF-beta1 receptor kinase in HF MyoFb promotes dediffere

196 t, genetic and pharmacological inhibition of TGF-beta1/Smad3 signals suppressed endogenous glucose pr

197 Injections of an inhibitor of TGF-beta1 signaling SB-431542 also decreased the weights

198 ick Correlation, Entropy and interactions of TGF-beta1 in Saliva and Headaches, VE-cadherin in Serum

199 Knockdown of TGF-beta1 expression in the tumor cells negatively affec

200 ear stress, which activates higher levels of TGF-beta1 to drive vascular remodeling.

201 ouse bone and found decreased mRNA levels of TGF-beta1, TGF-beta2 and TGF-beta3.

202 -associated virus-mediated overexpression of TGF-beta1 promoted cone survival and function in 3 disti

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

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

205 00b-3p mimics inhibit EMT in the presence of TGF-beta1 in PBECs derived from lung allograft.

206 and PTEN expression, even in the presence of TGF-beta1, along with decreased fibrogenesis.

207 ompounds and screen siRNAs for regulators of TGF-beta1-induced type I collagen expression.

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

209 es 90 days after ICH, confirming the role of TGF-beta1 in functional recovery from ICH.

210 d a significant increase in the secretion of TGF-beta1 ligand along with enhanced protein expression

211 monstrate the repressive function of FHL2 on TGF-beta1 expression and contribute to the understanding

212 R2-APs, PAR2 mutation and PAR2 inhibitors on TGF-beta1-induced migration, reporter gene activity, and

213 acquired a robust myofibroblast phenotype on TGF-beta1 stimulation.

214 , micropellets exposed to TGF-beta1 alone or TGF-beta1 + KGN in combination were larger and produced

215 Moreover, in non-obese patients with OSA, TGF-beta1 levels correlate with OSA severity and leptin

216 The cooperative p53-TGF-beta1 genomic cluster includes genes involved in cel

217 In BAVnon-dil patients, TGF-beta1 and MMP-2 gene expression increased significan

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

219 that patients with early increases in plasma TGF-beta1 concentrations had better outcomes 90 days aft

220 miR-200b-3p was downregulated post-TGF-beta1 treatment compared with control in BEAS-2B.

221 e we show how integrin alphaVbeta6 binds pro-TGF-beta1 in an orientation biologically relevant for fo

222 We have determined a structure of pro-TGF-beta1 with the proprotein convertase cleavage site m

223 nsforming growth factor-beta1 precursor (pro-TGF-beta1), integrins bind to the prodomain, apply force

224 mine alphaVbeta8 for atypical binding to pro-TGF-beta1.

225 hancing the effect of EtOH on IL-15, RANTES, TGF-beta1, and TNF-alpha cytokines while restoring MCP-2

226 Recombinant TGF-beta1 or tumour cell conditioned medium (TCM) elevat

227 olated and treated in vitro with recombinant TGF-beta1 (rTGF-beta1) to induce alpha-SMA expression.

228 ort and mucus hyperconcentration and reduced TGF-beta1.Conclusions: Losartan effectively reversed CF-

229 ion or knockdown of ROCK1 expectedly reduced TGF-beta1 induced fibrotic responses.

230 ing macrophage (M2) polarization by reducing TGF-beta1 expression by SSCs, which was recovered by NF-

231 vitro analysis revealed that MSLN regulates TGF-beta1-inducible activation of WT PFs by disrupting t

232 fibrosis development, the factors regulating TGF-beta1 signaling are poorly understood.

233 icles were engineered to sustainably release TGF-beta1, IL-2, and rapamycin, to induce Treg different

234 A) microparticles were engineered to release TGF-beta1, Rapamycin, and IL-2, to locally sustain a mic

235 tive disorders), persistently elevated renal TGF-beta1 levels result in the relentless progression of

236 Transcriptome analysis revealed TGF-beta1-dependent changes in 29 of 63 ion channel/pump

237 hypoxia-inducible factor-1alpha and reversed TGF-beta1-induced metabolic reprogramming.

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

239 and a transcriptional coregulator of several TGF-beta1 profibrotic response genes by complexing with

240 a1, forming what appears to be a sialidase - TGF-beta1 - sialidase positive feedback loop.

241 Further, SMAD/TGF-beta1 signaling was down-regulated in CSF plasmablas

242 rmal fibroblasts showed that P311 stimulated TGF-beta1 to -beta3 translation, a process that involved

243 miR-200b-3p mimics suppress TGF-beta1-induced EMT via inhibition of ZNF532 and ZEB2.

244 (PMCs) showed that CTGF blockade suppressed TGF-beta1-induced fibroblast proliferation and myofibrob

245 ted by oxygen-glucose deprivation suppressed TGF-beta1-induced hyperpolarization and VSMC differentia

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

247 on IgE-mediated activation, demonstrate that TGF-beta1 can provide broad inhibitory signals to activa

248 Given that TGF-beta1 and myocardin (MYOCD) are potent activators fo

249 rat ventricular myofibroblasts revealed that TGF-beta1, applied for 24 to 48 hours at clinically rele

250 These results show that TGF-beta1 activation on the surface of human Tregs impli

251 Taken together, our data show that TGF-beta1 modulates microglia-mediated neuroinflammation

252 In this report, we show that TGF-beta1 promotes HIV latency by upregulating a transcr

253 a) in the markers between groups showed that TGF-beta1 and TIMP-1 levels were significantly decreased

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

255 All in all, our results suggest that TGF-beta1 stimulation increases active beta-catenin conc

256 romotes functional recovery, suggesting that TGF-beta1 may be a therapeutic target for acute brain in

257 scriptional coactivators TAZ and YAP and the TGF-beta1 (TGFbeta) effector Smad3 regulate a common set

258 high levels of profibrotic cytokines and the TGF-beta1 pathway is activated.

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

260 nd chemokines (induced Ccl2 and Ccl7) in the TGF-beta1 group.

261 findings implicate p53 as a cofactor in the TGF-beta1-induced signaling pathway and a transcriptiona

262 pha target gene, which directly inhibits the TGF-beta1 mediated activation of cardiac fibroblasts thr

263 Expression changes of the TGF-beta1 active dimer and ENG were analyzed also by Wes

264 e site mutated to mimic the structure of the TGF-beta1 proprotein.

265 es were similar or slightly greater than the TGF-beta1-only cultures, depending on the BMSC donor.

266 Here we demonstrate that the TGF-beta1/Smad3 signaling pathway promotes hepatic gluco

267 ns as a transcriptional regulator within the TGF-beta1 cluster with an emphasis on the potent fibrosi

268 Third, TGF-beta1 inhibited ETV1-induced invasion by benign RWPE

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

270 HCC, to the level of MICA expression through TGF-beta1-dependent mechanisms.

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

272 4 days of induction, micropellets exposed to TGF-beta1 alone or TGF-beta1 + KGN in combination were l

273 e protein-to-creatinine ratio >/=800 mg/g to TGF-beta1 mAb (2-, 10-, or 50-mg monthly subcutaneous do

274 with endometriosis, and exposure of HPMCs to TGF-beta1 exacerbates this abnormal phenotype.

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

276 c potency in human BMSC cultures relative to TGF-beta1, does not obstruct hypertrophy, and may not be

277 ry revealed that Tgfbr1(iko) SMCs respond to TGF-beta1 stimulation via robust up-regulation of cyclop

278 activity than wild-type VSMCs in response to TGF-beta1 stimulation.

279 elated transcription factor 3 in response to TGF-beta1, thereby allowing LC differentiation marked by

280 tes induction of angiogenesis in response to TGF-beta1.

281 eta3 in microtubules enhances sensitivity to TGF-beta1 stimulation in human microvascular endothelial

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

283 Overall, our data suggest variable TGF-beta1 activation and signaling occurs with competing

284 The serum levels of 25-hydroxy VD, TGF-beta1, TIMP-1, MMP2 and MMP9 were measured at baseli

285 ete anti-inflammatory cytokines (i.e., VEGF, TGF-beta1, and PGE2) when stimulated with amyloid beta42

286 was used to profile miRNA in control versus TGF-beta1 (1, 4, and 24 h) stimulated BEAS-2B cells.

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

288 In vitro, TGF-beta1, TGF-beta2, and TGF-beta3 stimulated a Smad3-d

289 When TGF-beta1 + KGN was used, GAG quantities were similar or

290 the bone marrow of Jak2(V617F) mice, whereas TGF-beta1 or Cxcl12 stimulation induces collagen deposit

291 the phosphorylation of p38 and ERK1/2, with TGF-beta1 upregulating p-p38 but not pERK1/2 and EGF upr

292 Following activation with TGF-beta1 and IL-1beta, we demonstrated an increased fib

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

294 ngiogenesis markers in animals injected with TGF-beta1, and these effects did not occur in Thbs4(-/-)

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

296 In cardiac fibroblasts stimulated with TGF-beta1, phenotypic switches of cardiac fibroblasts to

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

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