ライフサイエンスコーパス: TGF-beta2

1 nregulates transforming growth factor beta2 (TGF-beta2).

2 iinflammatory myeloid cells via secretion of TGF-beta2.

3 to SPARC, does not appear to be regulated by TGF-beta2.

4 required for regulation of FLT3 signaling by TGF-beta2.

5 , through the Akt-mediated downregulation of TGF-beta2.

6 ated with thrombin TNF-alpha, monocytes, and TGF-beta2.

7 tion in SP cells of ABCG2, Sca-1, Wnt-1, and TGF-beta2.

8 ctors-vascular endothelial growth factor and TGF-beta2.

9 f hematopoietic stem and progenitor cells to TGF-beta2.

10 ge in either gene or protein expression with TGF-beta2.

11 wn targets, transcription factors ZEB1/2 and TGF-beta2.

12 tly tested the ability of TbetaRII-B to bind TGF-beta2.

13 ed more robust changes than those induced by TGF-beta2.

14 uced by platelet-derived growth factor-BB or TGF-beta2.

15 while upregulation of SPARC had no effect on TGF-beta2.

16 don differentiation is partially mediated by TGF-beta2.

17 fetal lenses were cultured and treated with TGF-beta2 (1 or 10 ng/mL), FGF-2 (20 or 50 ng/mL), HGF (

18 rowth-factor reduced Matrigel also inhibited TGF-beta2; (2) independent matrix components, as the pur

19 We found that KSHV downregulates TGF-beta2, a cytokine related to TGF-beta1 that is known

20 Addition of TGF-beta2 accelerates transdifferentiation and contracti

21 TGF-beta2 activity was increased in cocultures of HLFs w

22 increased in Tgfb2+/- mice, suggesting that TGF-beta2 affects the earliest stages of T-cell developm

23 tively, but had no effect on that induced by TGF-beta2 alone.

24 Thus, pregnancy-associated MaSCs require a TGF-beta2/alphavbeta3/Slug pathway, which may contribute

25 TGF-beta2 also induced sustained release of MMP-2 and -9

26 iates inhibition of proliferation induced by TGF-beta2, although the response to this cytokine was re

27 identified transforming growth factor-beta2 (TGF-beta2), an isoform of the TGF-beta family, as a mole

28 tured in the presence or absence of 10 ng/mL TGF-beta2 and 20 mug/mL recombinant human SPARC (rhSP) f

29 Taken together, our data suggest a role for TGF-beta2 and as yet unknown serum factors in the aging

30 ELISA was used to determine the effects of TGF-beta2 and BMPs on TM fibronectin (FN) secretion.

31 In cultured cells, TGF-beta2 and cell-cell contact had relatively little ef

32 also associated with increased deposition of TGF-beta2 and collagen I at the ONH (P <0.01).

33 the factors that regulate the processing of TGF-beta2 and extracellular matrix (ECM) proteins into t

34 lin by TM cells inhibits BMP-4 antagonism of TGF-beta2 and leads to increased ECM deposition and elev

35 profiling of the 5'-UPR of the genes, Gli1, TGF-beta2 and Msx2, responding to the Shh/Ptc1 signaling

36 ivity of p38alpha and abundant expression of TGF-beta2 and retinaldehyde dehydrogenase.

37 ubjects' fibroblasts showed a lower level of TGF-beta2 and significantly increased the epithelial cel

38 l intersection between pathways activated by TGF-beta2 and SPARC in the formation of PCO.

39 rest cells results in elevated expression of TGF-beta2 and TGF-beta receptor type III (TbetaRIII); ac

40 Although exogenous TGF-beta2 and TGF-beta2 in aqueous humor suppress S-phas

41 TbetaRI showed significant binding to TGF-beta2 and TGF-beta3 but not TGF-beta1, and the bindi

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

43 nd found decreased mRNA levels of TGF-beta1, TGF-beta2 and TGF-beta3.

44 TGF-beta2 and VEGF levels were measured with ELISA.

45 TGF-beta2 and VEGF production was significantly greater

46 tein levels, suggesting interactions between TGF-beta2 and Wnt signaling.

47 F-1 and surfactant proteins and up-regulated TGF-beta2 and ZEB1 expression in type II cells.

48 increased the C3 split products and the C9, TGF-beta2, and basic FGF levels in the retinal pigment e

49 ement component C3 split products, C9, VEGF, TGF-beta2, and basic FGF.

50 Vascular endothelial growth factor, TGF-beta2, and beta-fibroblast growth factor were elevat

51 from three primary components, CSF-1/IL-34, TGF-beta2, and cholesterol.

52 f neurons induced gp130-dependent TGF-beta1, TGF-beta2, and IL-27 production.

53 the impact of IL-13 on epithelial TGF-beta1, TGF-beta2, and MUC5AC were determined in cultured bronch

54 Epithelial TGF-beta1, TGF-beta2, and mucin expression were evaluated in endobr

55 ctive Akt blocked RES inhibition of CREB and TGF-beta2, and rescued RES inhibition of cellular invasi

56 promotes activation of pro-TGF-beta1 and pro-TGF-beta2, and TGF-beta2 in turn increases furin levels.

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

58 reased total and active levels of TGF-beta1, TGF-beta2, and TGF-beta3 that arise as a specific conseq

59 resents three mammalian isoforms, TGF-beta1, TGF-beta2, and TGF-beta3.

60 beta exist in mammals as follows: TGF-beta1, TGF-beta2, and TGF-beta3.

61 c) formed a high affinity complex that bound TGF-beta2, and this complex inhibited TGF-beta2 in a bio

62 cal differences in degree of PCO between the TGF-beta2- and FCS/PBS-treated groups at 3 and 14 days a

63 Nor were there differences between the anti-TGF-beta2- and the null antibody-treated groups, with th

64 S-treated control group), a human monoclonal TGF-beta2 antibody (anti-TGF-beta2-treated group), or a

65 The human monoclonal anti-TGF-beta2 antibody CAT-152 (10 microg/mL) effectively in

66 nsforming growth factor (TGF)-beta2 and anti-TGF-beta2 antibody in a rodent model of posterior capsul

67 No sustained effect of TGF-beta2 or anti-TGF-beta2 antibody on PCO was found in rodents at the do

68 A neutralizing TGF-beta2 antibody partially inhibited IL-13-induced muc

69 TGF-beta2 appears not to induce mitotic arrest in the de

70 Unlike TGF-beta1 and -beta3, TGF-beta2 appears to require the co-receptor betaglycan

71 d transforming growth factor (TGF)-beta1 and TGF-beta2 as critical active soluble factors released by

72 Taken together, these observations identify TGF-beta2 as the crucial mediator of NPC immunomodulatio

73 ally, we found a novel role for dysregulated TGF-beta2, as well as adipocyte dysfunction, as demonstr

74 We have previously shown that TGF-beta2 at low concentrations enhances flt3 ligand-ind

75 effect; or (3) inhibition of a constitutive TGF-beta2 autocrine feedback loop, as addition of exogen

76 On the TGF-beta2 background, the keratocytes were treated with

77 Furthermore, TGF-beta2 beads induced the expression of Scleraxis in t

78 Cultured TM cells were treated with TGF-beta2 because TGF-beta2 is associated with primary o

79 ession of the cytokines TNF-alpha, IL-1beta, TGF-beta2, -beta3, and IL-10 and demonstrated defective

80 2.8 and 74.6 +/- 15.8 pm, respectively), but TGF-beta2 binding was undetectable at corresponding dose

81 xpress BMP1, BMP1 expression is regulated by TGF-beta2, BMP1 is biologically active, and BMP1 regulat

82 new disease framework whereby activation of TGF-beta2, bone morphogenetic protein 4, Wnt/beta-cateni

83 In vitro, TGF-beta2, but not TGF-beta1 and TGF-beta3, had a biphas

84 presence of unknown nonprotein serum factors TGF-beta2, but not TGF-beta1 or -beta3, enhances progeni

85 IL-13 increased the release of TGF-beta2, but not TGF-beta1, from epithelial cells.

86 TGF-beta2, but not TGF-beta1, increased mucin expression

87 Addition of TGF-beta2, but not TGF-beta1, rescued the RES-mediated d

88 TGF-beta2, but not TGF-beta1, was increased in asthmatic

89 retion induced by thrombin and thrombin plus TGF-beta2 by 65% and 20%, respectively, but had no effec

90 ted by inflammation by 75.5% (P < 0.05), and TGF-beta2 by 91.8% (P < 0.01).

91 ta suggest that stress induced production of TGF-beta2 by BEC can modify liver allograft function by

92 These data suggest that TGF-beta2 can act cell autonomously and is important for

93 To investigate expression of active TGF-beta2, capsular bags were incubated in serum-free EM

94 Exposure to RELM-beta increased TGF-beta1, TGF-beta2, collagen I, fibronectin, smooth muscle alpha-

95 TGF-beta1 and TGF-beta2 concentrations in media were measured by using

96 modulates miR-29b expression under basal and TGF-beta2 conditions.

97 ent study was conducted to determine whether TGF-beta2 contributes to mitotic inhibition during endot

98 l endothelial cells, it is not known whether TGF-beta2 contributes to the mitotic inhibition that occ

99 Notably, TGF-beta2 controls furin activity in an ALK-5-dependent

100 of the papillary fibroblast lineage, whereas TGF-beta2 controls proliferation, differentiation and EC

101 In fetal TGF-beta2-deficient HSCs, a defect only appears after se

102 TGF-beta2-deficient mice show hematopoietic defects, dem

103 ls while promoting Th1 cell development in a TGF-beta2-dependent manner.

104 TGF-beta2 did not induce hevin, whereas SPARC expression

105 This RES-mediated TGF-beta2 downregulation led to the inhibition of both T

106 consistent with the strong up-regulation of TGF-beta2 during iPSC differentiation.

107 Moreover, intrathecal delivery of TGF-beta2 during the effector phase of EAE ameliorated d

108 The age-related changes in the TGF-beta2 effect correlated with life span in BXD recomb

109 on of epithelial cells, whereas knockdown of TGF-beta2 enhanced epithelial cell proliferation.

110 l transplantation experiments indicated that TGF-beta2 expressed both in the (micro)environment and i

111 rsening in association with normalization of TGF-beta2 expression and high expression of TGF-beta1.

112 evaluated bronchial epithelial TGF-beta1 and TGF-beta2 expression and their effects on mucin expressi

113 These data show that TGF-beta2 expression by murine melanoma cells is necessa

114 Quercetin down regulated TGF-betaR2 and TGF-beta2 expression in HKCs suggesting a significant li

115 In biopsy tissue, epithelial TGF-beta2 expression levels were higher than TGF-beta1 i

116 TGF-beta2 expression was lower in CDH lungs.

117 B) transcription factor is known to regulate TGF-beta2 expression, and RES treatment decreased phosph

118 In addition to the inhibition of TGF-beta2 expression, RES increased the level of epithel

119 ration of LECs in the presence or absence of TGF-beta2, FGF-2, and HGF.

120 of LECs, either alone or in the presence of TGF-beta2, FGF-2, or HGF.

121 with 2.5 ng/mL activated, recombinant human TGF-beta2 for 24, 48, and 72 hours.

122 sforming growth factor-beta1 (TGF-beta1) and TGF-beta2, forcing these growth factors into a state of

123 ese findings indicate that Matrigel inhibits TGF-beta2 gene expression and point to a mechanism depen

124 present study, we show that hypoxia-induced TGF-beta2 gene expression is dependent on thrombospondin

125 or-1alpha and culminated in up-regulation of TGF-beta2 gene expression.

126 Transfection of the TGF-beta2 gene into B16 cells resulted in the production

127 modulate transforming growth factor beta 2 (TGF-beta2) gene expression.

128 An increased aqueous level of TGF-beta2 has been found in many primary open-angle glau

129 These results show that TGF-beta2 has the potential to signal in the absence of

130 Higher levels of IL-17A, TGF-beta1, TGF-beta2, IL-6, IL-23, and IL-1beta mRNA transcripts an

131 bound TGF-beta2, and this complex inhibited TGF-beta2 in a biological inhibition assay.

132 Although exogenous TGF-beta2 and TGF-beta2 in aqueous humor suppress S-phase entry in cul

133 SHV microRNAs are sufficient to downregulate TGF-beta2 in endothelial cells, they are not required du

134 ere asthmatics' fibroblasts induced enhanced TGF-beta2 in exosomes leading to a reduced proliferation

135 udy confirms the well documented presence of TGF-beta2 in glaucomatous aqueous.

136 ults suggest a new functional requirement of TGF-beta2 in growth arrest and differentiation of murine

137 latory axis that includes PPARs, Prdm16, and TGF-beta2 in hematopoiesis.

138 cin expression, and the role of TGF-beta1 or TGF-beta2 in interleukin (IL)-13-induced mucin expressio

139 cessary and sufficient for downregulation of TGF-beta2 in KSHV-infected cells.

140 u hybridization and immunohistochemistry for TGF-beta2 in postnatal lung sections.

141 GECs produced TGF-beta1 and TGF-beta2 in response to infection.

142 Overexpression of TGF-beta2 in severe asthmatics' fibroblasts induced enha

143 SPARC was upregulated by TGF-beta2 in the human TM cells (3.8 +/- 1.7-fold, n = 6

144 e mechanistic relationship between SPARC and TGF-beta2 in trabecular meshwork (TM) is unknown.

145 tion of pro-TGF-beta1 and pro-TGF-beta2, and TGF-beta2 in turn increases furin levels.

146 of active transforming growth factor-beta2 (TGF-beta2) in the aqueous humor is the main cause of fib

147 ment of mitral valve interstitial cells with TGF-beta2 increased beta-catenin signaling at mRNA and p

148 Exogenous TGF-beta2 increased mRNA expression compared to their co

149 rine feedback loop, as addition of exogenous TGF-beta2 increased p-Smad3 and restored TGF-beta2 mRNA

150 TGF-beta2 increased the production of collagen type I, f

151 TGF-beta1 and TGF-beta2 induced miR-132 expression in keratinocytes, a

152 Although the incubation of TM cells with TGF-beta2 induced miR-29a and suppressed miR-29b levels,

153 Transforming growth factor beta2 (TGF-beta2) induced alphavbeta3 expression, enhancing Slu

154 nd inhibits transforming growth factor-beta2(TGF-beta2)-induced EMT of RPE cells by deacetylating SMA

155 An ELISA showed TGF-beta2-induced BMP1 secretion compared to their contr

156 152 (10 microg/mL) effectively inhibited all TGF-beta2-induced effects.

157 TGF-beta1- and TGF-beta2-induced EMT were found to be TGF-beta3 depende

158 TGF-beta2-induced SPARC expression was suppressed by inh

159 inases mediate both overlapping and distinct TGF-beta2-induced transcriptional responses.

160 y an important permissive role in maximizing TGF-beta2-induced VEGF expression in RPE cells.

161 podocytes, it is demonstrated that autocrine TGF-beta2 induces G0/G1 arrest and differentiation under

162 TGF-beta2 induction of BMP1 may be responsible for incre

163 In contrast, treatment with TGF-beta2 inhibited cell death of retinal ganglion cells

164 TGF-beta2 inhibited the migration and proliferation of b

165 tent infection, as the addition of exogenous TGF-beta2 inhibits the KSHV-induced stability of these s

166 mas, including Stat1, ADAP, IGFBP-6, PDGF-A, TGF-beta2, Int-3, VEGFR2, BAX, BAG-1, c-Jun, FasL, TRAIL

167 sive bleb aqueous and controls in the amount TGF-beta2, interleukins IL-6, IL-10, and chemokine (C-X-

168 We previously showed that TGF-beta2 is a genetically determined positive regulator

169 an in wild-type littermates, indicating that TGF-beta2 is a genetically determined positive regulator

170 Thus, TGF-beta2 is a novel, genetically determined positive re

171 TM cells were treated with TGF-beta2 because TGF-beta2 is associated with primary open-angle glaucoma

172 ously that transforming growth factor-beta2 (TGF-beta2) is a genetically determined positive regulato

173 previously shown that one TGF-beta isoform, TGF-beta2, is, in fact, a positive regulator of murine h

174 TGF-beta2 knockdown in the K-1735 melanoma cells signifi

175 TGF-beta2 levels increased significantly in asthmatic cu

176 ations or deletions in the gene encoding the TGF-beta2 ligand for a phenotype within the LDS spectrum

177 ere compared to those from mice null for the TGF-beta2 ligand.

178 TGF-beta2 lowered the levels of both proteins, but p27ki

179 in the TM and suggest that its modulation by TGF-beta2 may be important in controlling ECM synthesis.

180 Therefore, KSHV downregulation of TGF-beta2 may increase aberrant vascularization in KS tu

181 F, GRO, MIP-1beta, IL-1alpha, TGF-beta1, and TGF-beta2 may play a significant role in regulating inva

182 ound that both Gas6 and Axl are required for TGF-beta2-mediated cell growth suppression.

183 SPARC may be a downstream regulatory node of TGF-beta2-mediated IOP elevation.

184 ubjects had increased circulating TGF-beta1, TGF-beta2, monocyte chemotactic protein-1, C-reactive pr

185 Importantly, miR-21 overexpression increased TGF-beta2 mRNA and secreted protein level, consistent wi

186 ous TGF-beta2 increased p-Smad3 and restored TGF-beta2 mRNA levels.

187 We found that the TGF-beta2 mRNA was highly expressed by the K-1735 cells,

188 When exposed to recombinant TGF-beta1 (or TGF-beta2), nonpermissive culture podocytes switch to G2

189 nificant non-overlapping phenotypes with the TGF-beta2 null mouse, implying the existence of TbetaRII

190 nown about the impact of either TGF-beta1 or TGF-beta2 on asthmatic airway epithelial mucin expressio

191 In these mice, the enhancing effect of TGF-beta2 on flt3 signaling, but not the generic antipro

192 can be attributed to the enhancing effect of TGF-beta2 on HSPC proliferation observed in vitro and ar

193 The action of TGF-beta2 on LEC migration and proliferation is influenc

194 The effects of TGF-beta1 or TGF-beta2 on mucin MUC5AC protein and mRNA expression, a

195 r the evaluation of the effects of SPARC and TGF-beta2 on PCO in vitro.

196 udy we report that the stimulatory effect of TGF-beta2 on the proliferation of LSK cells increases wi

197 The stimulatory effect of TGF-beta2 on the proliferation of LSK cells requires one

198 No sustained effect of TGF-beta2 or anti-TGF-beta2 antibody on PCO was found in

199 aneous mRNA expression of TGF-beta1, but not TGF-beta2 or TGF-beta3, and elevated C-C chemokines macr

200 tivity was measured in TM cells treated with TGF-beta2 or with a combination of TGF-beta2/UK383367.

201 he ligands transforming growth factor-beta2 (TGF-beta2) or bone morphogenetic protein-4 (BMP4) in an

202 otein levels also showed a rapid increase in TGF-beta2 (p < 0.006) following oxidative stress.

203 lated to deposition of laminin (P <0.05) and TGF-beta2 (P <0.05).

204 kers, and increased TGF-beta1 (P=0.0009) and TGF-beta2 (P=0.0001) secretion in dermal fibroblast cell

205 e found elevated plasma TGF-beta1 (P=0.009), TGF-beta2 (P=0.004) and additional inflammatory markers,

206 largely determined by the aged environment, TGF-beta2 plays a major modulatory role that is subject

207 The costimulated VEGF production by TGF-beta2 plus thrombin was an average of three times hi

208 n combination with TNF-alpha, monocytes, and TGF-beta2 potently stimulated VEGF expression in hRPE ce

209 Elevated levels of TGF-beta2 present in AH of POAG patients may elevate int

210 These data suggest that TGF-beta2 production by asthmatic bronchial epithelial c

211 tion of regulatory T cells by downregulating TGF-beta2 production from DCs.

212 TGF-beta2 production was inhibited by Matrigel at the le

213 -beta2 was not explained by its geometry, as TGF-beta2 production was not inhibited by plating cells

214 wn basement membrane in organotypic culture, TGF-beta2 production was reduced.

215 e three consensus sequences and can activate TGF-beta2 promoter in normal and Akt-transformed cell li

216 binding in transforming growth factor beta2 (TGF-beta2) promoter.

217 diac fibroblasts through PI3K/AKT to produce TGF-beta2, promoting fibroblast-to-myofibroblast transfo

218 Cells were treated with recombinant human TGF-beta2 protein at 0 to 10 ng/mL for 0 to 72 hours.

219 Production of TGF-beta2 protein by cultured rabbit corneal epithelial

220 TGF-beta2 protein, mRNA, and gene transcriptional promot

221 etween nasal and bronchial ALI production of TGF-beta2 (r = 0.64, P = .001) and VEGF (r = 0.73, P < .

222 K (-49.1 +/- 24.6%, n = 10, P = 0.0001), and TGF-beta2 receptor (-83.6 +/- 14.4%, n = 6, P = 0.003).

223 inase (p38), Smad3, p42, JNK, RhoA, PI3K, or TGF-beta2 receptor for 2 hours, and then TGF-beta2 was a

224 /6, thrombospondin-1 knockout (TSP-1KO), and TGF-beta2 receptor II double-negative (TGF-beta2 RII DN)

225 which the basement membrane was left intact, TGF-beta2 remained confined to the corneal epithelium, c

226 , and TGF-beta2 receptor II double-negative (TGF-beta2 RII DN) mice, leaving behind a healthy monolay

227 the complex regulatory mechanisms mediating TGF-beta2 signaling and ECM production in the TM.

228 GF-beta- and BMP-reporter mice, we show that TGF-beta2 signaling antagonizes BMP signaling in HFSCs b

229 ynergizes BMP-mediated refractivity, whereas Tgf-beta2 signaling counterbalances it.

230 (TbetaRII-B), has been suggested to mediate TGF-beta2 signaling in the absence of TbetaRIII, we dire

231 tudy was to determine whether BMPs can alter TGF-beta2 signaling in the TM and whether there are defe

232 st that a loop between the Gas6/Axl axis and TGF-beta2 signaling plays a significant role in the indu

233 celerates anagen initiation, whereas loss of Tgf-beta2 signaling significantly delays it, supporting

234 ndogenous molecules in human TM may regulate TGF-beta2 signaling via inhibition of BMP family members

235 ence of TbetaRIII independent mechanisms for TGF-beta2 signaling.

236 nhibitor of TGF-beta1 and TGF-beta3, but not TGF-beta2, signaling.

237 Cultured human TM cells treated with TGF-beta2 significantly increased FN levels, and BMP-4 b

238 Exogenous TGF-beta2 significantly induced FST mRNA and protein exp

239 downregulation led to the inhibition of both TGF-beta2/Smad-dependent and -independent pathways, and

240 nd genetic studies unveil Tmeff1 as a direct TGF-beta2/Smad2/3 target gene, expressed by activated HF

241 Autocrine TGF-beta2/Smad3/Cdkn2b signaling in podocytes specifies

242 Here, we show that TGF-beta2 specifically and predominantly cell autonomous

243 delays in HF regeneration, whereas exogenous TGF-beta2 stimulates HFSCs in vivo and in vitro.

244 TGF-beta1 or TGF-beta2 stimulates this signaling mechanism by up-regu

245 ed to block SMAD3 function in the context of TGF-beta2 stimulation.

246 f corneal fibrosis and opacity studied under TGF-beta2 stimulation.

247 the trabecular meshwork (TM) under basal and TGF-beta2 stimulatory conditions.

248 ssor of various ECM proteins under basal and TGF-beta2 stimulatory conditions.

249 TGF-beta2 suppressed proliferation of HLE B-3 cells, whe

250 Connective tissue growth factor (CTGF) is a TGF-beta2 target gene with high constitutive TM expressi

251 In contrast, TGF-beta2 targeted internalized biotinylated proteins to

252 in the absence of TbetaRIII when sufficient TGF-beta2, TbetaRI, and TbetaRII or TbetaRII-B are prese

253 At the end of the procedure, 10 microL TGF-beta2 (TGF-beta2-treated group), fetal calf serum (F

254 In SZs, IL-1beta, (GRIK2/3), TGF-beta2, TGF-betaR1, histone deacetylase 1 (HDAC1), de

255 nscriptional activation of the gene encoding TGF-beta2 that acted in a paracrine manner on peritoneal

256 CAT-152 inhibited all the effects of TGF-beta2 that were examined and therefore has the poten

257 beta RI, RII, and RIII occurred too late for TGF-beta2 to have a significant role in inhibiting proli

258 y-like tube formation insofar as adding back TGF-beta2 to infected cells blocks KSHV-induced long-ter

259 ransformation; Loxl2 also acts downstream of TGF-beta2 to stimulate myofibroblast migration.

260 The preference of TGF-beta2 to TbetaRI suggests a variation in its recepto

261 Addition of exogenous TGF-beta2 to the cocultures increases mineralization; th

262 s (BMPs), which, coupled with the ability of TGF-beta2 to upregulate FST levels, may indicate a possi

263 However, transfer (i.v.) of TGF-beta2-treated 2,4,6-trinitrobenzene sulfonic acid-pu

264 We postulated that TGF-beta2-treated Ag-pulsed APC (tolerogenic APC (tol-AP

265 ated in vitro by exposure to antigen-pulsed, TGF-beta2-treated APCs expressed genes related to immune

266 D8+ T regs after stimulation with OVA-pulsed TGF-beta2-treated APCs.

267 e end of the procedure, 10 microL TGF-beta2 (TGF-beta2-treated group), fetal calf serum (FCS)/phospha

268 a human monoclonal TGF-beta2 antibody (anti-TGF-beta2-treated group), or a null control IgG4 antibod

269 oculation of in vitro-generated tolerogenic (TGF-beta2-treated, Ag-pulsed) APC (tol-APC).

270 ylation of JNK and c-jun was detected before TGF-beta2 treatment.

271 minutes and 1 hour, respectively, following TGF-beta2 treatment.

272 ated with TGF-beta2 or with a combination of TGF-beta2/UK383367.

273 d mucin expression may occur in part through TGF-beta2 up-regulation.

274 TGF-beta2 upregulates SPARC expression in human TM throu

275 We hypothesized that TGF-beta2 upregulates SPARC expression in TM.

276 lts show that by blocking both TGF-beta1 and TGF-beta2 using neutralizing antibodies, it is possible

277 TGF-beta2, vascular epithelial growth factor (VEGF), a d

278 om asthmatic children differentially express TGF-beta2, VEGF, ADAM33, or periostin compared with cell

279 om asthmatic children differentially express TGF-beta2, VEGF, and periostin compared with cells from

280 or TGF-beta2 receptor for 2 hours, and then TGF-beta2 was added for 24 hours in serum-free media.

281 When T or TGF-beta2 was added to Sertoli cell cultures with establ

282 ary epithelial cells stimulated by IL-17A or TGF-beta2 was also inhibited by 124.1% and 69.9%, respec

283 Proliferation suppression by TGF-beta2 was blocked by adding FGF-2 or HGF.

284 In the intact mouse cornea, TGF-beta2 was confined to the uninjured epithelium, but

285 Active TGF-beta2 was detected in these cultures.

286 TGF-beta2 was determined to be a major substance produce

287 more, exogenous application of TGF-beta1 and TGF-beta2 was found to enhance c-JunSer-63 phosphorylati

288 titative trait locus (QTL) for the effect of TGF-beta2 was identified on chromosome 4 overlapping wit

289 ELISA and MLR assays showed that TGF-beta2 was involved in mediating the suppression in v

290 In addition, Matrigel's ability to reduce TGF-beta2 was not explained by its geometry, as TGF-beta

291 additive, whereas that by co-incubation with TGF-beta2 was synergistic.

292 Transforming growth factor-beta2 (TGF-beta2) was predominantly overexpressed in UV-induced

293 oliferative effect of high concentrations of TGF-beta2, was abrogated, confirming the location of thi

294 bited by hypoxia, whereas the miR-29 target, TGF-beta2, was coordinately decreased.

295 imal amounts of free bioactive TGF-beta1 and TGF-beta2 were detected in conditioned medium, treatment

296 evated levels of mRNA encoding TGF-beta1 and TGF-beta2 were significantly reduced.

297 VEDS dermal fibroblasts secreted more TGF-beta2, whereas downstream canonical/noncanonical TGF

298 over a hitherto unrecognized DP transmitter, TGF-beta2, which activates Smad2/3 transiently in HFSCs

299 ut it may involve transforming growth factor TGF-beta2, which is found in higher amounts in the aqueo

300 edium was supplemented with 0, 1 or 10 ng/mL TGF-beta2 with or without 10 microg/mL CAT-152 (n = 4 in