ライフサイエンスコーパス: TGF-beta3

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

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

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

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

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

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

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

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

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

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

11 ate pathophysiological processes mediated by TGF-beta3.

12 rway remodeling by directly interacting with TGF-beta3.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

33 = 0.05) miR-29a-3p was predicted to regulate TGF-beta3 and Clec7a, genes involved in innate responses

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

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

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

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

38 1(TG)) mice had elevated levels of TGF-beta1-TGF-beta3 and subsequent hypertension.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

61 10% fetal calf serum, TGF-gamma1, TGF-beta2, TGF-beta3, basic fibroblast growth factor (bFGF), or TGF

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

173 92 increased and restored the expression of TGF-beta3, Smad3, and SMC markers in HPASMC of normal su

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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