ライフサイエンスコーパス: PDGF-BB

1 PDGF-BB activated STAT-5B as measured by its tyrosine ph

2 PDGF-BB also induced cyclin A mRNA levels in VSMC in an

3 PDGF-BB also stimulates the expression of tenascin-C (TN

4 PDGF-BB in a synthetic scaffold matrix promotes long-ter

5 PDGF-BB in a synthetic scaffold matrix promotes long-ter

6 PDGF-BB increased DNA synthesis and up-regulated CSF-1 m

7 PDGF-BB induced cyclic adenosine monophosphate-dependent

8 PDGF-BB induced cyclin D1 expression, CDK4 activity, and

9 PDGF-BB inhibition reduced Shh expression, demonstrating

10 PDGF-BB levels decreased significantly in samples collec

11 PDGF-BB maintained ERK activation in the presence of rux

12 PDGF-BB overexpression enhanced the survival of endothel

13 PDGF-BB overexpression promoted both proliferation and m

14 PDGF-BB stimulated the expression of both chemokine (C-C

15 PDGF-BB stimulation had no significant effect on cell pr

16 PDGF-BB with nanofibers induced PDGFR-beta and Akt phosp

17 PDGF-BB-induced activation of STAT3 occurred also in cel

18 PDGF-BB-induced migration was also compromised in ATF-4

19 ansiently increases with elevation of Ang-2, PDGF-BB, and blood glucose; is rapidly reversed on a tim

20 Akt also co-immunoprecipitated with CaM in a PDGF-BB-dependent manner, suggesting that direct interac

21 MCP-1, MIP-1alpha, IL-12p70, IL-18, VEGF-A, PDGF-BB and IL-1RA significantly correlated with disease

22 F, platelet-derived growth factor (PDGF)-AA, PDGF-BB, PDGF-AB, and transforming growth factor (TGF)-b

23 ed upon JAK2 inhibition in vivo, and PDGF-AA/PDGF-BB production persisted in the setting of JAK inhib

24 Platelet-derived growth factor (PDGF)-AB, PDGF-BB, transforming growth factor-beta1, insulin-like

25 etreatment plasma concentrations of PDGF-AB, PDGF-BB, and vascular endothelial growth factor (VEGF) w

26 e studies, approximately 45% of the adsorbed PDGF-BB was released after 10 days.

27 siRNA, or PKCdelta-R144/145A does not affect PDGF-BB-stimulated activation of p38 mitogen-activated p

28 e PDGF receptor-beta (PDGFR-beta), to affect PDGF-BB-induced chemotaxis.

29 ation of SMA and SM22alpha without affecting PDGF-BB mediated cell proliferation or ERK activation.

30 r, and an enhanced mitogenic response, after PDGF-BB stimulation.

31 Ad sPDGFRbeta was validated in vitro against PDGF-BB and in vivo with near-complete blockade of peric

32 ition to a transient phosphorylation of Akt, PDGF-BB stimulation produces an atypical sustained phosp

33 Although PDGF-BB stimulated the membrane translocation of both Nc

34 , and EMD alone, EMD+PDGF-BB, and amelogenin+PDGF-BB significantly increased PDL cell proliferation i

35 tor-BB (PDGF-BB), EMD+PDGF-BB, or amelogenin+PDGF-BB.

36 IGF and PDGF BB stimulated elongation of keratocytes and extensi

37 UB cells synthesize VEGF-A and PDGF-BB proteins and RNA, whereas the MM cells express t

38 n wounds in diabetic mice with VEGF-A165 and PDGF-BB incorporated within VWF A1 HBD-functionalized fi

39 patients had elevated levels of PDGF-AA and PDGF-BB compared with normal patient controls.

40 Low concentrations of PDGF-AA and PDGF-BB found in bone marrow aspirates, which were detec

41 e also measured plasma levels of PDGF-AA and PDGF-BB in patients and normal patient controls.

42 original members of the family, PDGF-AA and PDGF-BB.

43 e than two decades of studies on PDGF-AA and PDGF-BB.

44 similar observations with EGF, PDGF-AA, and PDGF-BB.

45 myoblasts, previously treated with Dll4 and PDGF-BB, adopt a perithelial position stabilizing newly

46 When exposed to Dll4 and PDGF-BB, but not Dll1, skeletal myoblasts downregulate m

47 data indicate that endothelium, via Dll4 and PDGF-BB, induces a fate switch in adjacent skeletal myob

48 ucated LEC') secrete high amounts of EGF and PDGF-BB, compared to normal LEC.

49 d the presence of NFAT-binding elements, and PDGF-BB induced the binding of NFATs to these regulatory

50 The combination of EMD and PDGF-BB produces greater proliferative and wound-fill ef

51 enin, vascular endothelial growth factor and PDGF-BB in MMP-2 knockdown cells.

52 Both FGF2 and PDGF-BB signal through tyrosine kinase receptors, which

53 n exists between the growth factors FGF2 and PDGF-BB, causing tumors to exhibit increased angiogenesi

54 ulated (17 genes) by both Sonic hedgehog and PDGF-BB in a cyclopamine-dependent manner in CCA cells.

55 Here, we report that both IGF-I and PDGF-BB stimulated VSMC de-differentiation of rat heart-

56 strate the role of ATF-4 in both injury- and PDGF-BB-inducible TN-C expression and cell migration.

57 ytes via the action of Dll4 Notch ligand and PDGF-BB.

58 nhibited PDGFRbeta(+) VSMC proliferation and PDGF-BB signaling, whereas small interfering RNA knockdo

59 phate (S1P) signaling and integrates S1P and PDGF-BB signaling pathways, which are both crucial for m

60 7 following surgery, mean levels of VEGF and PDGF-BB at sites treated with PRGF and PRF were not sign

61 Coexpression of VEGF and PDGF-BB encoded by separate vectors in different cells o

62 30 after therapy for evaluation of VEGF and PDGF-BB levels.

63 lude that coordinated expression of VEGF and PDGF-BB via a single vector constitutes a novel strategy

64 arkers: angiogenin (ANG), angiostatin (ANT), PDGF-BB, VEGF, FGF-2, IL-8, TIMP-1, TIMP-2, GM-CSF, and

65 a significant increase in expression of ANT, PDGF-BB, VEGF, FGF-2, and IL-8 for the LCC group over th

66 of other important angiogenic genes, such as PDGF-BB and PDGF receptors.

67 essed PDGF-mediated proliferation as well as PDGF-BB-induced ERK/CREB and mTOR/4E-BP-p70S6K activatio

68 driven by platelet-derived growth factor B (PDGF-BB) in vascular smooth muscle cells, contributing t

69 ts target, platelet-derived growth factor B (PDGF-BB).

70 oped label-free electrochemical C-MEMS based PDGF-BB aptasensor is highly sensitive, selective, and r

71 pathways-platelet-derived growth factor BB (PDGF BB) and neural precursor-cell-expressed development

72 ee media, platelet derived growth factor BB (PDGF BB), insulin-like growth factor (IGF), TGFbeta1, TG

73 target of platelet-derived growth factor BB (PDGF-BB) and found that SMCs respond to Shh by upregulat

74 can bind platelet-derived growth factor BB (PDGF-BB) and promote adult human dermal fibroblast (AHDF

75 , such as platelet-derived growth factor BB (PDGF-BB) and transforming growth factor beta (TGFbeta),

76 Platelet-derived growth factor BB (PDGF-BB) induced cyclin A expression and CDK2 activity i

77 Platelet-derived growth factor BB (PDGF-BB) is a Food and Drug Administration (FDA)-approve

78 ated with platelet-derived growth factor BB (PDGF-BB).

79 ypoxia or platelet-derived growth factor BB (PDGF-BB).

80 ctors via platelet-derived growth factor BB (PDGF-BB)/platelet-derived growth factor receptor (PDGFR)

81 s such as platelet-derived growth factor-BB (PDGF-BB) and transforming growth factor-beta1 (TGF-beta1

82 with both platelet-derived growth factor-BB (PDGF-BB) and vascular endothelial growth factor (VEGF-16

83 acted as platelet-derived growth factor-BB (PDGF-BB) enhancers to promote cell survival.

84 Platelet-derived growth factor-BB (PDGF-BB) has been reported to provide tropic support for

85 levels of platelet derived growth factor-BB (PDGF-BB) in gingival crevicular fluid (GCF) during early

86 ound that platelet-derived growth factor-BB (PDGF-BB) secreted by preosteoclasts induces CD31(hi)Emcn

87 show that platelet-derived growth factor-BB (PDGF-BB) strongly stimulates membrane translocation and

88 GF-A) and platelet-derived growth factor-BB (PDGF-BB) that were engineered to have a syndecan-binding

89 lpha) and platelet-derived growth factor-BB (PDGF-BB) were reduced.

90 that bind platelet-derived growth factor-BB (PDGF-BB), a potent fibroblast survival and mitogenic fac

91 elogenin, platelet-derived growth factor-BB (PDGF-BB), EMD+PDGF-BB, or amelogenin+PDGF-BB.

92 forms and platelet-derived growth factor-BB (PDGF-BB), mainly through the heparin-binding domain (HBD

93 livery of platelet-derived growth factor-BB (PDGF-BB), which recruits pericytes, could induce normal

94 agonist, platelet-derived growth factor-BB (PDGF-BB)-induced p21Cip1 degradation and HASMC prolifera

95 while the platelet-derived growth factor-BB (PDGF-BB)-signalling pathway promotes a switch to the syn

96 PGZ on i) platelet-derived growth factor-BB (PDGF-BB)-stimulated proliferation of human venous smooth

97 vement in platelet-derived growth factor-BB (PDGF-BB)-stimulated VSMC growth and motility and balloon

98 GF-A) and platelet-derived growth factor-BB (PDGF-BB).

99 ection of platelet-derived growth factor-BB (PDGF-BB).

100 ng surface that mimics the interface between PDGF-BB and its receptor, contrasting sharply with mainl

101 o showed a strong inhibitory effect on bFGF, PDGF-BB, and serum-induced cell migration and proliferat

102 These sites bind PDGF-BB with dissociation constants of 10-100 nM.

103 a or Nckbeta alone in human DFs also blocked PDGF-BB-induced cell migration.

104 c deletion of host IL-33 in mice also blocks PDGF-BB-induced TAM recruitment and metastasis.

105 Instead, inhibition of PKCdelta blocks PDGF-BB-stimulated activation of signal transducer and a

106 Both PDGF-BB and IGF-I activated PI3K/Akt to similar degrees;

107 Although both PDGF-BB and IGF-I stimulation resulted in decreased smoo

108 of VSMC phenotypic modulation and that both PDGF-BB and IGF-I, despite their different abilities to

109 In contrast, cell-bound PDGF-BB delivered via cell-cell contact results in activ

110 Specifically, P12 bound PDGF-BB (KD=200 nM), enhanced adult human dermal fibrobl

111 Induction of miR-146b by PDGF-BB is modulated via MAPK-dependent induction of c-f

112 ) was obtained using a medium conditioned by PDGF-BB and TGF-beta1.

113 Cytoprotection by PDGF-BB was dependent upon Hedgehog (Hh) signaling, beca

114 l role for LOX in regulating MK expansion by PDGF-BB and suggest LOX as a new potential therapeutic t

115 The sustained Akt phosphorylation induced by PDGF-BB was inhibited by pretreatment of the cells with

116 ression by PDGF-AA and miR-146b induction by PDGF-BB.

117 hat regulates cell proliferation mediated by PDGF-BB with implications for therapeutic intervention f

118 nal-regulated kinase (ERK) 1/2, or p38MAP by PDGF-BB.

119 r data suggest that p27 is down-regulated by PDGF-BB in vascular smooth muscle cells through an ERK-d

120 se severity, understanding its regulation by PDGF-BB could aid in the development of therapeutic inte

121 y reduces fibroblast migration stimulated by PDGF-BB and reduced in vivo lung fibrosis in mice.

122 In consequence, the signal from the captured PDGF-BB was amplified via the concatameric RCA product,

123 and platelet-derived growth factor B chain (PDGF-BB), to stimulate MM cell differentiation.

124 uman platelet-derived growth factor B-chain (PDGF-BB) using two screened fluorescent aptamers, respec

125 tect platelet-derived growth factor B-chain (PDGF-BB).

126 We found high levels of circulating PDGF-BB in platelet-poor plasma samples from LGL leukemi

127 pter proteins, Nckalpha and Nckbeta, connect PDGF-BB signaling to the actin cytoskeleton and cell mot

128 long-term (72 hours) concentration dependent PDGF-BB chemotaxis response of human bone marrow derived

129 (hypoxia inducible factor)-1alpha depletion, PDGF-BB neutralizing antibody, or the PDGF-BB receptor a

130 lusion, we report a dual role for EC-derived PDGF-BB and HB-EGF in controlling pericyte recruitment t

131 MFB-derived PDGF-BB protects CCA cells from TRAIL cytotoxicity by a

132 losure in mice far more effectively than did PDGF-BB.

133 , we found that in vivo inhibition of either PDGF-BB or Shh signaling reduces NG2(+) MC recruitment i

134 In addition, EMD+PDGF-BB had additive effects on the ALK PHOS (-) cell li

135 (-) cell line (P<0.001), and EMD alone, EMD+PDGF-BB, and amelogenin+PDGF-BB significantly increased

136 elet-derived growth factor-BB (PDGF-BB), EMD+PDGF-BB, or amelogenin+PDGF-BB.

137 However, the combination of EMD+PDGF-BB additively increased wound fill for both ALK PHO

138 Compared to the control, only EMD+PDGF-BB significantly increased PDL cell proliferation i

139 an ALK PHOS (+) cell line (P<0.001) with EMD+PDGF-BB showing a trend for greater proliferation than e

140 Treatment with exogenous PDGF-BB or inhibition of cathepsin K to increase the num

141 e biopsy samples from DMD patients expressed PDGF-BB.

142 ate that in the absence of K-Ras expression, PDGF-BB fails to induce significant AKT activation, alth

143 activated, insensitive to the growth factor PDGF-BB, but show differential sensitivity of their cons

144 cells (SMCs) by the potent migratory factor PDGF-BB through PDGFR-beta.

145 VEGF) and 2) platelet-derived growth factor (PDGF-BB) in gingival crevicular fluid (GCF) from localiz

146 complex for platelet-derived growth factor (PDGF-BB) oncoprotein detection is reported.

147 or (NGF) and platelet-derived growth factor (PDGF-BB), but the functional implications of these inter

148 Expression of Fer was dispensable for PDGF-BB-induced proliferation and migration but essentia

149 eover, we demonstrate that the receptors for PDGF-BB and TGFbeta interact physically in primary derma

150 thermore, we show that ATF-4 is required for PDGF-BB-inducible SMC migration in response to injury.

151 A role for PDGF-BB in vasculogenesis in the 3D MM/UB co-culture sys

152 ion strategies provided high selectivity for PDGF-BB and high stability of 90.34% after 10 days.

153 inistered neutralizing antibody specific for PDGF-BB as well as in Egr-1(-/-) mice.

154 Furthermore, PDGF-BB induced cyclin A promoter-luciferase reporter ge

155 Furthermore, PDGF-BB induction was regulated by activation of ERK1/2

156 Moreover, we generate PDGF-BB- and VEGFA-hypersecreting hMSC lines as short-te

157 ovessel formation while platelet-derived GF (PDGF-BB) is needed later to stabilize the neovessels.

158 However, PDGF-BB stimulated MM cell proliferation, migration, and

159 Recombinant human PDGF-BB (rhPDGF-BB) reduces Parkinsonian symptoms and in

160 membrane (CM) treated with recombinant human PDGF-BB (rhPDGF-BB).

161 -mediated gene transfer of recombinant human PDGF-BB upregulated messenger RNA expression of anti-mes

162 To date, becaplermin (recombinant human PDGF-BB) is the only US FDA-approved growth factor thera

163 ed serum-induced proliferation, and impaired PDGF-BB-directed migration.

164 receptor-beta cell interactions to implicate PDGF-BB as a primary effector of MM cell vasculogenesis.

165 eptor potential canonical (TRPC) channels in PDGF-BB-mediated proliferation.

166 roliferation and migration and is crucial in PDGF-BB pathway in VSMCs.

167 h activation of SOX7 transcription factor in PDGF-BB-stimulated pericytes.

168 Our data suggest a critical role of Fer in PDGF-BB-induced STAT3 activation and cell transformation

169 for the first time, that Shh is involved in PDGF-BB-induced SMC migration and recruitment of MCs int

170 y side, the roles of Nckalpha and Nckbeta in PDGF-BB-stimulated DF migration.

171 stained Akt phosphorylation did not occur in PDGF-BB-stimulated normal human Schwann cells or ST88-14

172 cate that STAT-5B plays an important role in PDGF-BB-induced VSMC growth and motility in vitro and ba

173 Thus, pharmacotherapies that increase PDGF-BB secretion from preosteoclasts offer a new therap

174 interfering RNA (siRNA) completely inhibited PDGF-BB-stimulated DF migration.

175 f FRS2 in VSMC by RNA interference inhibited PDGF-BB-mediated down-regulation of SMA and SM22alpha wi

176 vascular SMCs, and ATF-4 knockdown inhibited PDGF-BB-inducible TN-C expression in vitro and injury-in

177 FATc1 by its small interfering RNA inhibited PDGF-BB-induced cyclin A expression and DNA synthesis bo

178 Thus, miR-125a-5p in this context inhibits PDGF-BB pathway and is therefore a potential regulator o

179 ted the reappearance of PDGF-betar after its PDGF-BB-dependent degradation.

180 nd cortical bone mass, serum and bone marrow PDGF-BB concentrations, and fewer CD31(hi)Emcn(hi) vesse

181 ferent dose levels of PDGF (0.3 or 1.0 mg/mL PDGF-BB) in patients possessing one localized periodonta

182 how that in mouse fibroblasts LRP1 modulates PDGF-BB signaling by controlling endocytosis and ligand-

183 ermal growth factor receptor (EGFR) as a new PDGF-BB target.

184 The assay allows detection of PDGF BB down to 0.5 pM, with linearity of the Raman sign

185 The chemotactic activity of PDGF-BB was significantly enhanced in the presence of a

186 nchymal cells was rescued by the addition of PDGF-BB.

187 th PD and show that i.c.v. administration of PDGF-BB is safe and well tolerated.

188 igh affinity and capacity for the binding of PDGF-BB by cells containing oxidized PDGFR-beta was dimi

189 inhibition of RAC1 and loss of constraint of PDGF-BB-induced cell migration.

190 12 slowed internalization and degradation of PDGF-BB, augmented its survival signals, and promoted ce

191 Mice with depletion of PDGF-BB in the tartrate-resistant acid phosphatase-posit

192 7 down-regulation, we examined the effect of PDGF-BB on p27 promoter activity as well as mRNA stabili

193 mpletely inhibited the stimulatory effect of PDGF-BB, -CC, and -DD; in contrast, this mixture stimula

194 ta-R144/145A) partially mimics the effect of PDGF-BB.

195 tro experiments to understand the effects of PDGF-BB on myoblasts involved in the pathophysiology of

196 vide evidence that anti-apoptotic effects of PDGF-BB on serum-deprived ST88-14 cells can be inhibited

197 d on days 3, 7, 14, and 30 for evaluation of PDGF-BB levels and alkaline phosphatase (ALP) levels.

198 We analyzed the expression of PDGF-BB in muscle biopsy samples from controls and patie

199 Constitutive expression of PDGF-BB led to malignant transformation in nude mice.

200 ting ultimately into increased expression of PDGF-BB.

201 beads on the surface varied as a function of PDGF-BB concentration.

202 ation induced by v-Sis, a viral homologue of PDGF-BB, as well as PDGF-induced mitogenesis and signali

203 Co-implantation of PDGF-BB-overexpressing endothelial cells with 10T1/2 cel

204 e demonstrated cocaine-mediated induction of PDGF-BB in human brain microvascular endothelial cells t

205 Combined inhibition of PDGF-BB and HB-EGF-induced signaling in quail embryos le

206 odel of DMD with repeated i.m. injections of PDGF-BB.

207 Notably, the plasma level of PDGF-BB was inversely correlated with time to treatment

208 mouse model, serum and bone marrow levels of PDGF-BB and numbers of CD31(hi)Emcn(hi) vessels are sign

209 Levels of PDGF-BB and VEGF were higher in the PRGF-treated group,

210 ys 3 and 7 following surgery, mean levels of PDGF-BB at sites treated with PRF membrane or CM incorpo

211 th rhPDGF-BB showed comparable GCF levels of PDGF-BB initially with PRF showing more sustained levels

212 rease in low ploidy MKs, augmented levels of PDGF-BB, and an extensive matrix of fibers.

213 teoclasts, and thus the endogenous levels of PDGF-BB, increases CD31(hi)Emcn(hi) vessel number and st

214 d [Ca(2+) ] levels, affecting mRNA levels of PDGF-BB, RICTOR, and MIR17HG as mediators of Ca(2+) -sig

215 Given the known role of overexpression of PDGF-BB and PDGF-DD on glomerular and tubulointerstitial

216 We hypothesized that overexpression of PDGF-BB in colorectal cancer (CRC) and pancreatic cancer

217 optosis at 72 hours, even in the presence of PDGF-BB.

218 Production of PDGF-BB by leukemic LGLs was demonstrated by immunocytoc

219 Understanding the regulation of PDGF-BB expression may provide insights into the develop

220 The role of PDGF-BB in muscle regeneration in humans has not been st

221 uating the effect and long-term stability of PDGF-BB treatment in patients with localized severe peri

222 ssion, demonstrating that Shh is a target of PDGF-BB, confirming in vitro experiments.

223 These results suggest that targeting of PDGF-BB, a pivotal regulator for the long-term survival

224 Treatment of PDGF-BB-overexpressing tumors with imatinib mesylate (PD

225 heart-derived SMCs in culture, although only PDGF-BB was capable of inducing proliferation.

226 d PI3K/Akt to similar degrees; however, only PDGF-BB concomitantly stimulated an inhibitory signaling

227 Keratocytes cultured in IGF or PDGF BB maintain a quiescent mechanical phenotype over a

228 E-1-binding molecules, such as hyaluronan or PDGF-BB.

229 nofibers with PDGF-BB, but not nanofibers or PDGF-BB alone, decreased cardiomyocyte death and preserv

230 In animal models of PD, PDGF-BB has been shown to restore/protect against dopami

231 F-AA:R2 KD = 530 nM, PDGF-AB:R2 KD = 110 pM, PDGF-BB:R2 KD = 40 nM, and PDGF-CC:R2 KD = 70 pM.

232 , a chemokine expressed by HSC could prevent PDGF-BB-mediated proliferation and migration of cultured

233 BMP-2/BMP-RII signaling prevented PDGF-BB-induced proliferation of human and murine pulmon

234 cells revealed that melanoma cells produced PDGF-BB and TGFbeta, which blocked PEDF production in fi

235 , where the radioactive PDGF/non-radioactive PDGF-BB treated beta-TCP or CaSO(4) sample was inserted

236 Based on our results, PDGF-BB may play a protective role in muscular dystrophi

237 LEC-secreted PDGF-BB induces pericyte infiltration and angiogenesis.

238 in which Fer was down-regulated using siRNA, PDGF-BB was unable to induce phosphorylation of STAT3, w

239 own-regulation of cyclin A levels suppressed PDGF-BB-induced VSMC DNA synthesis.

240 by cyclosporin A (CsA) and VIVIT suppressed PDGF-BB-induced cyclin A expression and CDK2 activity, r

241 ious contexts of infection, and suggest that PDGF BB and NEDD9 play important roles in this interacti

242 show in rat aortic smooth muscle cells that PDGF-BB down-regulated p27 protein and mRNA in an ERK-de

243 these data provides the first evidence that PDGF-BB is a mitogen for MEOE-3M and increases CSF-1 pro

244 We found that PDGF-BB induced AKT binding to actin, and that Tbeta4 pr

245 w molecular weight inhibitors, we found that PDGF-BB-induced Fer activation is dependent on PDGFRbeta

246 Moreover, we found that PDGF-BB-induced SMC migration involves Shh-mediated moti

247 In this study, we found that PDGF-BB-induced synthetic SMCs suppressed EC proliferati

248 proliferation, raising the possibility that PDGF-BB enhances expansion of MSC in the vicinity of the

249 In addition, we show that PDGF-BB and FGF2 act synergistically to induce cell prol

250 Here we show that PDGF-BB induces microRNA-24 (miR-24), which in turn lead

251 Furthermore, we show that PDGF-BB induces tyrosine phosphorylation of FGFR1 and th

252 and randomized study in 52 rats showed that PDGF-BB delivered with nanofibers decreased infarct size

253 etic mobility shift assay (EMSA) showed that PDGF-BB stimulated protein binding to this motif that wa

254 We next showed that PDGF-BB-induced SMC migration was reduced after inhibiti

255 We demonstrate in this study that PDGF-BB induces phosphorylation of Smad2, a downstream m

256 Mechanistically, our evidence suggests that PDGF-BB-bearing cells preferentially stimulate the non-l

257 The PDGF-BB-mediated Smad2 phosphorylation was dependent on

258 However, the PDGF-BB-expressing vessel network failed to establish pa

259 ells can be inhibited by W7, implicating the PDGF-BB-induced activation of calcium/CaM in promoting c

260 ved marked inhibition of tumor growth in the PDGF-BB-overexpressing clones.

261 In the PDGF-BB-overexpressing tumors, we observed an increase i

262 of reperfusion, indicating activation of the PDGF-BB/PDGFR-beta pathway.

263 etion, PDGF-BB neutralizing antibody, or the PDGF-BB receptor antagonist Imatinib.

264 ty of the TbetaRI kinase greatly reduced the PDGF-BB-dependent migration in dermal fibroblasts.

265 several proteins, including human thrombin, PDGF-BB, Avidin, and His-tagged recombinant protein, wer

266 Neutralizing antibody to PDGF-BB inhibited PKB/AKT phosphorylation induced by LGL

267 Exposure of astrocytes to PDGF-BB in turn led to increased proliferation and the r

268 dentified aptamers that specifically bind to PDGF-BB protein with K(d) < 3 nM within 3 rounds.

269 d tissue survival by acting as a cofactor to PDGF-BB.

270 this effect was abrogated in mice exposed to PDGF-BB neutralizing antibody, thus underscoring its rol

271 inds to the cyclin A promoter in response to PDGF-BB in a VIVIT-sensitive manner.

272 s well as with the PDGFRbeta, in response to PDGF-BB stimulation.

273 enuates PDGFRalpha activation in response to PDGF-BB, and reduced phosphorylation of extracellular si

274 ntracellular calcium increase in response to PDGF-BB.

275 Nckbeta all failed to migrate in response to PDGF-BB.

276 itivity of these cells toward LOX and toward PDGF-BB.

277 and Cbl-b were more prone to migrate toward PDGF-BB, whereas no reproducible effect on cell prolifer

278 yte content compared with those in untreated PDGF-BB-overexpressing tumors.

279 ion and CAF-induced tumor cell invasion upon PDGF-BB stimulation.

280 ulate the regenerative potential of MSCs via PDGF-BB/PDGFR-beta signaling.

281 In vitro, PDGF-BB attracted myoblasts and activated their prolifer

282 In vivo PDGF-BB release from beta-TCP and CaSO(4) was evaluated

283 However, whether PDGF-BB regulates neurogenesis, especially in the contex

284 ligament fibroblasts (PDLFs) alone and with PDGF-BB for promoting PDLF growth and migration; 2) to d

285 ll as reduced tumour growth (associated with PDGF-BB delivery) and vascular permeability (triggered b

286 Stimulation of S2-013.MUC1F cells with PDGF-BB increased nuclear colocalization of MUC1CT and b

287 TGF-beta1 alone or combined with PDGF-BB in serum-free medium induces a temporally correc

288 In human skin injected with PDGF-BB and in tissue reparative processes PDGF beta-rec

289 In contrast, in human skin injected with PDGF-BB-bearing tumor cells and in colorectal adenocarci

290 em was validated by direct interference with PDGF-BB or PDGF receptor-beta cell interactions to impli

291 6 rats showed that injecting nanofibers with PDGF-BB, but not nanofibers or PDGF-BB alone, decreased

292 campal neuronal progenitor cells (NPCs) with PDGF-BB restored proliferation that had been impaired by

293 Consistently, in VSMCs pretreated with PDGF-BB, calpastatin induction and calpains inhibition s

294 was rapidly up-regulated by stimulation with PDGF-BB (a known inducer of phenotypic switch in VSMCs)

295 Simultaneous stimulation with PDGF-BB and epidermal growth factor promoted macropinocy

296 dermal fibroblasts and that stimulation with PDGF-BB induces internalization not only of PDGFRbeta bu

297 osteoblasts in response to stimulation with PDGF-BB, which could be attributed to a defect in PDGF s

298 -to-mesenchymal transition when treated with PDGF-BB and TGFbeta1, resulting in vascular SMCs that di

299 sis of muscles from the animals treated with PDGF-BB showed an increased population of satellite cell

300 FBD survived without, and proliferated with, PDGF-BB.