ライフサイエンスコーパス: TGF-beta3

1 ammalian isoforms, TGF-beta1, TGF-beta2, and TGF-beta3.

2 E has been shown to be directly regulated by TGF-beta3.

3 le to restore all the functional outcomes of TGF-beta3.

4 ium was associated with a transient surge in TGF-beta3.

5 ased mRNA levels of TGF-beta1, TGF-beta2 and TGF-beta3.

6 hway is dominant in palatal fusion driven by Tgf-beta3.

7 ent to induce fusion of shelves deficient in Tgf-beta3.

8 was overcome by the addition of recombinant TGF-beta3.

9 E7 did not alter expression of TGF-beta1 and TGF-beta3.

10 egulate the use of alternative promoters for TGF-beta3.

11 mechanisms of chronicity than TGF-beta2 and TGF-beta3.

12 ate pathophysiological processes mediated by TGF-beta3.

13 in vitro and in vivo by exogenous TGF-beta1-TGF-beta3.

14 rway remodeling by directly interacting with TGF-beta3.

15 ammals as follows: TGF-beta1, TGF-beta2, and TGF-beta3.

16 nsitive to the negative regulation of HGF by TGF-beta3.

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

18 ell-cell interface to cell cytosol caused by TGF-beta3.

19 ditions including the potential niche signal TGF-beta3.

20 nant human transforming growth factor-beta3 (TGF-beta3; 100 ng) and/or recombinant human stromal deri

21 In this study, local administration of TGF-beta3 (200 ng/testis) to the testis was shown to rev

22 Both TGF-beta3 (3 ng/ml) and TNFalpha (10 ng/ml) were shown t

23 s unexpectedly high fibroblast expression of TGF-beta3, a molecule with reported antifibrotic and ant

24 Moreover, exogenously added TGF-beta3 accelerated epithelial wound closure in type 2

25 this cell line correlated with the EC50 for TGF-beta3 activation of ERK2.

26 functional transforming growth factor-beta3 (TGF-beta3) active-site motif (RXXD), inhibits 125I-label

27 orm was activated by 6-fold within 10 min of TGF-beta3 addition to the TGF-beta-sensitive BCC line Hs

28 In addition, our data demonstrate that TGF-beta3 affected a sustained activation of the stress-

29 In 6 wk, TGF-beta3 alone recruited substantial numbers of ASCs (5

30 cumulation, treatment of wild-type MEFs with TGF-beta3 also resulted in down-regulation of both Cdc2

31 Transforming growth factor-beta3 (TGF-beta3), an established mediator of avian atrioventri

32 a on the -/- MEE but to a lesser extent than TGF-beta3 and additionally induced lamellipodia on their

33 y phosphorylated in vivo in response to both TGF-beta3 and BMP2 as determined using an antibody again

34 In addition, both TGF-beta3 and BMP2 increased Smad1-Smad4 hetero-oligomer

35 = 0.05) miR-29a-3p was predicted to regulate TGF-beta3 and Clec7a, genes involved in innate responses

36 s suggest that although the dual delivery of TGF-beta3 and IGF-1 may not synergistically enhance the

37 In contrast, TGF-beta2 and TGF-beta3 and PDGF-A are present in both macrophages and

38 TGF-beta3 and SDF-1beta codelivery induced significantly

39 ) and MSCs (302+/-52), whereas codelivery of TGF-beta3 and SDF-1beta was particularly chemotactic to

40 1(TG)) mice had elevated levels of TGF-beta1-TGF-beta3 and subsequent hypertension.

41 ied by an increase in the immunostaining for TGF-beta3 and TGF-beta-receptor RII and a decrease in im

42 d the effects of intracoronary expression of TGF-beta3 and TGF-beta1 on luminal loss after angioplast

43 irst time that BTB dynamics are regulated by TGF-beta3 and TNFalpha via an enhancement of protein end

44 ation, associated with increased activity of TGF-beta3 and Wnt/beta-catenin signaling pathways.

45 lecules and signaling pathways, specifically TGF-beta3 and Wnt4/beta-catenin, in the latter.

46 ted into the acellular collagen sponge cube, TGF-beta3 and/or SDF-1beta recruited significantly more

47 ested that transforming growth factor-beta3 (TGF-beta3) and tumor necrosis factor alpha (TNFalpha) se

48 F-1alpha), transforming growth factor-beta3 (TGF-beta3), and tissue inhibitor of metalloproteinases-2

49 alone, (iii) GMP-loaded IGF-1 and gel-loaded TGF-beta3, and (iv) GMP-loaded IGF-1 and GMP-loaded TGF-

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

51 ed expression of Th2-related factors, IL-10, TGF-beta3, and CCR3.

52 xpression of TGF-beta1, but not TGF-beta2 or TGF-beta3, and elevated C-C chemokines macrophage chemoa

53 igh levels of mRNA for TGF-beta1, TGF-beta2, TGF-beta3, and lower levels of TGF-beta receptor II (TGF

54 ese data illustrate that local production of TGF-beta3, and perhaps other TGF-betas and cytokines, by

55 kDa complexes with TGF-beta1, TGF-beta2, and TGF-beta3, and reverses the inhibitory activity of TGF-b

56 els of COMT and higher levels of HIF-1alpha, TGF-beta3, and TIMP-2 when compared with those from norm

57 demonstrate an up-regulation of HIF-1alpha, TGF-beta3, and TIMP-2 when compared with wild-type mice;

58 the intrinsic activity of ERK, illustrating TGF-beta3 apparently regulates Sertoli-germ cell ES func

59 TGF-beta1, TGF-beta2, and TGF-beta3 are abundant in seminal plasma, and Affymetrix

60 filopodia, illustrating that the effects of TGF-beta3 are transduced by cell surface receptors which

61 Cytokines (e.g., TGF-beta3) are known to regulate BTB dynamics by enhanci

62 owth factors beta (TGF-betal, TGF-beta2, and TGF-beta3) are secreted as latent complexes and activate

63 More importantly, we have pinpointed TGF-beta3 as the major upstream molecular that triggers

64 tocols involving medium supplementation with TGF-beta3, as assessed by gene expression, biochemical,

65 We show that TGF-beta1 and TGF-beta3, as well as a third unknown ligand present in

66 en T(reg) cells and HFSCs mediated by the GR-TGF-beta3 axis, highlighting a possible means of manipul

67 10% fetal calf serum, TGF-gamma1, TGF-beta2, TGF-beta3, basic fibroblast growth factor (bFGF), or TGF

68 ta are not consistent with overexpression of TGF-beta3 being responsible for failed trophoblast invas

69 Although TGF-beta1 and TGF-beta3 bind and assemble their ternary complexes in a

70 In most cells, TGF-beta1 and TGF-beta3 bind to TbetaRII with much higher affinity tha

71 close proximity, in a mode that differs from TGF-beta3 binding to type II receptors.

72 up-regulated in TCDD-CD4(+) cells including TGF-beta3, Blimp-1, and granzyme B, as well as genes ass

73 genic (BMP2) or chondrogenic (combination of TGF-beta3, BMP2 and SOX9) genes within networks of 3D pr

74 showed significant binding to TGF-beta2 and TGF-beta3 but not TGF-beta1, and the binding to all thre

75 TGFBRII-Fc is an inhibitor of TGF-beta1 and TGF-beta3, but not TGF-beta2, signaling.

76 taRI and TbetaRII dimers upon treatment with TGF-beta3, but not with TGF-beta3 WD.

77 etaRI with affinities indistinguishable from TGF-beta3, but with one-half the stoichiometry.

78 Here we found that the production of TGF-beta3 by developing T(H)17 cells was dependent on IL

79 combined induction of aqueous TGF-beta1 and TGF-beta3 by PI in glaucoma surgery may impact surgery s

80 res showed absence of the active fragment of TGF-beta3 by Western blot analysis and a approximately 5

81 Exogenous recombinant TGF-beta3 can rescue fusion in -/- palatal shelves by in

82 heparin/heparan sulfate, and those involving TGF-beta3 cannot be affected.

83 mRNA expression of miR-29c targets (COL3A1, TGF-beta3, CDK2, SPARC) and miR-200c targets (CDK2, FN1,

84 cantly higher for ASCs and SSCs by SDF-1 and TGF-beta3 codelivery.

85 progression, and expression of TGF-beta2 and TGF-beta3 commences at critical junctures during progres

86 structure is similar to previously reported TGF-beta3 complex except with a 10 degrees rotation in T

87 Functional analysis indicated that TGF-beta3 contributed to wound healing in NL corneas.

88 In all cell lines, the core of the TGF-beta3 CpG island was predominantly unmethylated, irr

89 ifferentiate, phenocopying the defect of the TGF-beta3-deficient mice.

90 udy, we investigated the mechanisms by which TGF-beta3 deletions caused cleft palate in 129 x CF-1 mi

91 th inhibition and gene induction mediated by TGF-beta3 demonstrate that recombinant TGF-beta1 LAP is

92 - and TGF-beta2-induced EMT were found to be TGF-beta3 dependent, establishing essential roles for mu

93 e the three factors TGF-beta1, TGF-beta2 and TGF-beta3 did not block myogenic signals from the neural

94 TGF-beta2 and TGF-beta3 did not exhibit consistent long-term changes.

95 In contrast, TGF-beta3 did not increase SAPK/JNK activity in the TGF-

96 However, TGF-beta3 did not stimulate endothelial proliferation ab

97 GF)-beta isoforms (TGF-beta1, TGF-beta2, and TGF-beta3) differ in their putative roles in radiation-i

98 ells, the increased stromal POSTN induced by TGF-beta3 directly accelerated the growth, migration and

99 the immunomodulatory molecules TGF-beta2 and TGF-beta3 displayed significant decreases that may have

100 plasmin activity regulates release of active TGF-beta3 during chick AV canal EMT.

101 ontrols, illustrating the specificity of the TGF-beta3 effects on protein endocytosis.

102 By contrast, exogenous addition of TGF-beta3 either had no effect or increased adhesion for

103 sma, and Affymetrix microarray revealed that TGF-beta3 elicits changes in Ect1 cell expression of sev

104 ent responses to chondrogenic agonists, with TGF-beta3 enhancing cartilage-specific extracellular mat

105 y-six weeks after irradiation, TGF-beta2 and TGF-beta3 expression had returned to normal.

106 ssion and, to a lesser degree, TGF-beta2 and TGF-beta3 expression.

107 at eCRT induces the synthesis and release of TGF-beta3 first via LRP1 or other receptor signaling and

108 Consistent with elevated fibroblastic TGF-beta3, fmod(-/-) fibroblasts were significantly less

109 as and suggests the therapeutic potential of TGF-beta3 for treating corneal and skin wounds in diabet

110 F-beta3 latency/activation mechanism and why TGF-beta3 functions distinctly from TGF-beta1, suggestin

111 rafted skin of mice with a disruption of the TGF-beta3 gene developed similarly to grafts of wild typ

112 d hair follicle formation, while lack of the TGF-beta3 gene did not have any effects.

113 Mice with a knockout mutation of the TGF-beta3 gene die a few hours after birth.

114 ation of MCF-7 cells in vitro, (3) stimulate TGF-beta3 gene expression in cell culture, (4) inhibit t

115 n complexes that bind to the promoter of the TGF-beta3 gene to increase its transcription.

116 ion of the transforming growth factor-beta3 (TGF-beta3) gene caused cleft palate in homozygous null (

117 The human transforming growth factor-beta3 (TGF-beta3) gene has a typical CpG island, the core of wh

118 In contrast, TGF-beta3 had little effect on either DNA synthesis or E

119 In vitro, TGF-beta2, but not TGF-beta1 and TGF-beta3, had a biphasic dose response on the prolifera

120 The related cytokines, TGF-beta2 and TGF-beta3, had similar effects.

121 n 14-synthesizing MEE cells following mating Tgf-beta3 heterozygous mice with Keratin 14 promoter dir

122 palatal transcriptomes of wild type (WT) and Tgf-beta3 -/- homozygous (HM) mouse embryos at the cruci

123 th observation times, whereas, TGF-beta2 and TGF-beta3 immunoreactivity exhibited minimal postradiati

124 Here we report the crystal structure of TGF-beta3 in complex with the extracellular domains of b

125 er expression levels of active TGF-beta1 and TGF-beta3 in normal tongue and esophageal submucosa comp

126 a3, and (iv) GMP-loaded IGF-1 and GMP-loaded TGF-beta3 in OPF composite hydrogels.

127 s, MMP-13 expression was strongly induced by TGF-beta3 in palatal fibroblasts.

128 To test whether the effect of TGF-beta3 in palatogenesis is isoform-specific in vivo,

129 the expression of TGF-beta1, TGF-beta2, and TGF-beta3 in placenta and placental bed of pregnancies c

130 Here we report that overexpression of TGF-beta3 in primary Sertoli cells cultured in vitro ind

131 lts demonstrate an isoform-specific role for TGF-beta3 in the palatal epithelium during palate format

132 umor suppression and implicates TGF-beta2 or TGF-beta3 in the prevention of metastasis.

133 the IC50 for inhibition of DNA synthesis by TGF-beta3 in this cell line correlated with the EC50 for

134 arter to one-half the signalling activity of TGF-beta3 in three established assays for TGF-beta funct

135 hen compared to a dual delivery of IGF-1 and TGF-beta3, independent of the TGF-beta3 release kinetics

136 rs completely failed to fuse, treatment with TGF-beta3 induced complete palatal fusion, TGF-beta1 or

137 rtoli cell epithelium was shown to block the TGF-beta3-induced acceleration in protein endocytosis.

138 to be a crucial regulator that mediated the TGF-beta3-induced BTB disruption.

139 When TbetaR1 was knocked down, the TGF-beta3-induced increase in the kinetics of JAM-A and

140 ediated endocytosis was shown to inhibit the TGF-beta3-induced protein internalization.

141 Moreover, TGF-beta3-induced T(H)17 cells were functionally and mol

142 Expression of TGF-beta3 inhibits constrictive remodeling after PTCA an

143 TGF-beta3 is normally expressed in the medial edge epith

144 shown that transforming growth factor beta3 (Tgf-beta3) is an absolute requirement for successful pal

145 , these findings revealed that Lyn regulates TGF-beta3 isoform and modulates the development of airwa

146 ivate the SAPK/JNK type of MAPK and that the TGF-beta3 isoform can regulate MAPK activity.

147 Here we demonstrate the ability of the TGF-beta3 isoform to activate the signaling component ER

148 -beta1 and TGF-beta2, and to a lesser extent TGF-beta3 isoforms block the ability of normal but not p

149 The rescued palatal fusion in Tgf-beta3-/-/K14-Smad2 mice, however, never proceeded to

150 In marked contrast, TPA treatment of TGF-beta3 knockout grafts induced widespread areas of ke

151 Dynamic allostery explains the TGF-beta3 latency/activation mechanism and why TGF-beta3

152 more susceptible to migration inhibition by TGF-beta3, leading to profound delays in dermal cell mig

153 nate over its antifibrotic effects when high TGF-beta3 levels disrupt early fibroblastic wound ingres

154 ammation, demonstrating that knock-in of the TGF-beta3 ligand can prevent the vasculogenesis defects

155 but cell signaling is triggered through the TGF-beta3 ligand that binds to TGF-beta receptors.

156 These results suggest that TGF-beta3 may regulate palatal fusion by inducing filopo

157 c42 is a crucial regulatory component in the TGF-beta3-mediated cascade of events that leads to the d

158 This inhibition of TGF-beta3-mediated protein endocytosis was further valid

159 present study, the cleft palate phenotype in Tgf-beta3-/- mice was rescued by overexpression of a Sma

160 etching for 36 hours increased TGF-beta1 and TGF-beta3 mRNA levels approximately twofold, without alt

161 responsible for translational inhibition of TGF-beta3 mRNA, is only evident in breast cancer cells.

162 Furthermore, TGF-beta3 neutralizing Abs not only inhibited the expres

163 in regulating murine palate development, and Tgf-beta3 null mutants develop cleft palate with 100% pe

164 urface of the MEE cells using SEM to compare TGF-beta3-null embryos (E 12.5-E 16.5) with +/+ and +/-

165 o phospho-SMAD2 was identified in the MEE in Tgf-beta3-null mutant mice (Tgf-beta3-/-), which was cor

166 f TGF (transforming growth factor)-beta1 and TGF-beta3, occurred with increased TGFBR2/TGFBR1/SMAD2 s

167 The specific effect of TGF-beta3 on protein internalization was further confirm

168 The protective function of TGF-beta3 on TPA-induced cell death was not because of g

169 plained by specific counteracting effects of TGF-beta3 on TPA-induced disruption of keratinocyte foca

170 Activation of Alk-5 in the Tgf-beta3 (-/-) palatal epithelium is able to rescue pal

171 ibodies to TGF-beta1 and -beta2 or exogenous TGF-beta3 peptide by local application and intraperitone

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

173 ividual TGF-beta isoforms, and in particular TGF-beta3, play in control of epidermal homeostasis.

174 Tgf-beta3 plays a critical role in regulating murine pal

175 ith purified TGF-beta isoforms revealed that TGF-beta3 plays a direct and specific function in protec

176 Transforming growth factor-beta3 (TGF-beta3) plays a critical role in palatal epithelial c

177 Strikingly, a significant increase in TGF-beta3 rather than TGF-beta1 was observed in Lyn(-/-)

178 ation of TGF-beta1 and -beta2 or addition of TGF-beta3 reduces scar formation.

179 TGF-beta3 reduces TGF-beta1-induced ECM deposition in cu

180 an in vitro release study demonstrated that TGF-beta3 release kinetics could be modulated by the GF

181 y of IGF-1 and TGF-beta3, independent of the TGF-beta3 release kinetics.

182 the ratio of 4:800:1 for TGF-beta1:TGF-beta2:TGF-beta3 respectively.

183 o acid residues of TGF-beta1, TGF-beta2, and TGF-beta3, respectively, inhibit the binding of 125I-lab

184 an (rh) TGF-beta1, porcine (p) TGF-beta2, rh TGF-beta3, rh activin, or p inhibin was added to the med

185 ed scarring in fmod(-/-) mice indicates that TGF-beta3's antimotility effects predominate over its an

186 Latent, but not active, TGF-beta3 secretion also increased whereas the levels of

187 However, TGF-beta3 selectively disrupts Sertoli-germ cell adhesio

188 The combination of Wnt3a and TGF-beta3 showed synergistic effects, promoting chondrog

189 rning in the palatal shelves with respect to TGF-beta3 signaling and the mechanism of secondary palat

190 very little is known about the mechanisms of Tgf-beta3 signaling during this process.

191 ndent pathways work redundantly to transduce TGF-beta3 signaling in palatal epithelial cells.

192 genes that are CP-related and/or involved in Tgf-beta3 signaling.

193 In addition, both recombinant and adenoviral TGF-beta3 significantly promoted epithelial-to-mesenchym

194 92 increased and restored the expression of TGF-beta3, Smad3, and SMC markers in HPASMC of normal su

195 proximately 92 inhibits PDLIM5 to induce the TGF-beta3/SMAD3 pathway, contributing to the pathogenesi

196 um, treatment with a pan-specific (but not a TGF-beta3 specific) TGF-beta-neutralizing antibody and w

197 In vitro, TGF-beta1, TGF-beta2, and TGF-beta3 stimulated a Smad3-dependent matrix-preserving

198 TGF-beta3 supports ASC survival while having a limited e

199 Vitamin C (VitC) and TGF-beta3 (T3) were used for 4 weeks to stimulate self-a

200 hways is dependent on the association of the TGF-beta3-TbetaR1 complex with adaptors TAB1 and CD2AP b

201 y arteries received an adenovirus expressing TGF-beta3, TGF-beta1, or lacZ (beta-galactosidase), or P

202 d active levels of TGF-beta1, TGF-beta2, and TGF-beta3 that arise as a specific consequence of decrea

203 re cultured as high density micromass' using TGF-beta3 to induce chondrogenesis.

204 Additionally, local administration of TGF-beta3 to testes in vivo was shown to reversibly pert

205 Interestingly, addition of TGF-beta3 to the culture medium which caused fusion betw

206 ells expressing the TGF-beta1, TGF-beta2, or TGF-beta3 transcripts were identified by in situ hybridi

207 curred to a similar if not greater extent in TGF-beta3-treated versus control keratinocytes.

208 rease in the external elastic lamina area in TGF-beta3-treated vessels (+0.73+/-0.32 mm2) contrasted

209 n content increased at the site of injury in TGF-beta3-treated vessels (26.1+/-14.2%) but decreased i

210 Instead, TGF-beta3 treatment led to a significant reduction in TP

211 sal values and were attained at 30 min after TGF-beta3 treatment.

212 mature TGF-beta1 ligand with a sequence from TGF-beta3 using targeted recombination to create chimeri

213 elivery of transforming growth factor beta3 (TGF-beta3), using a 3D woven poly(epsilon-caprolactone)

214 ngioplasty confirmed reduced luminal loss in TGF-beta3 vessels (-0.65+/-0.10 mm2) compared with lacZ

215 TGF-beta3 was shown to activate Cdc42 to its active GTP-

216 ed primary and metastatic melanomas, whereas TGF-beta3 was uniformly and highly expressed in these le

217 TGF-beta3 WD was further shown to retain one-quarter to

218 The substituted dimer, TGF-beta3 WD, bound the TbetaRII extracellular domain an

219 upon treatment with TGF-beta3, but not with TGF-beta3 WD.

220 beta1, -beta2, and, to a much lesser extent, TGF-beta3 were present within the placental bed but only

221 r procedure at any time point, TGF-beta1 and TGF-beta3 were significantly induced above baseline leve

222 to induce transforming growth factor beta3 (TGF-beta3), which activates Smad2/3 in HFSCs and facilit

223 ed in the MEE in Tgf-beta3-null mutant mice (Tgf-beta3-/-), which was correlated with the persistence

224 eceptor (sTbetaRII-B.Fc) bound TGF-beta1 and TGF-beta3 with high affinity (K(d) values = 31.7 +/- 22.

225 ately indicating that in vivo replacement of TGF-beta3 with TGF-beta1 can only partially correct the

226 effect of transforming growth factor-beta3 (TGF-beta3) with varying release kinetics and/or insulin-

227 lomas, as well as staining for TGF-beta1 and TGF-beta3 within adjacent hepatocytes.

228 m of the rat testis, we sought to examine if TGF-beta3 would also regulate anchoring junction dynamic