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 overexpression enhanced the survival of endothel

11 PDGF-BB overexpression promoted both proliferation and m

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

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

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

15 PDGF-BB, tumor necrosis factor-alpha, and insulin-like g

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

32 IGF and PDGF BB stimulated elongation of keratocytes and extensi

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

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

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

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

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

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

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

40 yrosine kinase activity was derepressed, and PDGF-BB-induced endocytosis and degradation of PDGFRbeta

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

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

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

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

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

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

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

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

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

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

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

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

53 actor beta-receptor (PDGFR-beta) kinase- and PDGF-BB-stimulated autophosphorylation of PDGFR-beta in

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

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

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

57 7 following surgery, mean levels of VEGF and PDGF-BB at sites treated with PRGF and PRF were not sign

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

59 30 after therapy for evaluation of VEGF and PDGF-BB levels.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

101 ccompanied by rapid uptake of receptor-bound PDGF-BB into the cells and by attenuated ERK activation

102 f-assembling peptide nanofibers, which bound PDGF-BB in vitro, sustained delivery of PDGF-BB to the m

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

132 s were transduced with a retrovirus encoding PDGF-BB.

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

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

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

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

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

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

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

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

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

142 Steady state mRNA for PDGF-BB decreased significantly 6 weeks after surgery.

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

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

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

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

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

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

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

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

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

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

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

154 0 minutes, and the amount of adsorbed (125)I-PDGF-BB was measured using a gamma counter.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

171 R-beta phosphorylation, selectively inhibits PDGF-BB-stimulated angiogenesis in vivo, and causes sign

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

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

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

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

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

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

178 iogenesis model, CP-673,451 inhibited 70% of PDGF-BB-stimulated angiogenesis at a dose of 3 mg/kg (q.

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

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

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

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

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

184 12 slowed internalization and degradation of PDGF-BB, augmented its survival signals, and promoted ce

185 ound PDGF-BB in vitro, sustained delivery of PDGF-BB to the myocardium at the injected sites for 14 d

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

187 7 down-regulation, we examined the effect of PDGF-BB on p27 promoter activity as well as mRNA stabili

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

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

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

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

192 asal migration and a ninefold enhancement of PDGF-BB-stimulated migration.

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

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

195 Steady state mRNA expression of PDGF-BB was reduced, suggesting a mechanism for the loss

196 ting ultimately into increased expression of PDGF-BB.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

224 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.

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

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

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

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

229 For the adsorption studies, the radiolabeled PDGF-BB/ non-radioactive PDGF solutions with resultant P

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

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

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

233 In the beta-TCP studies, PDGF-BB adsorption and release were accomplished using (

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

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

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

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

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

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

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

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

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

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

244 The absorption studies revealed that PDGF-BB was absorbed in a concentration and time-depende

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

267 ined the 3'-untranslated region responded to PDGF-BB with reduced expression.

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

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

270 by attenuated ERK activation in response to PDGF-BB stimulation.

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

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

273 ntracellular calcium increase in response to PDGF-BB.

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

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

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

277 riments demonstrate the feasibility of using PDGF-BB in combination with alloplastic materials such a

278 endothelial cells protect cardiomyocytes via PDGF-BB signaling and that this in vitro finding can be

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

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

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

282 ed in the nuclear exclusion of FoxO, whereas PDGF-BB alone down-regulated the FoxO target gene, p27(k

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

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

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

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

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

290 6 rats showed that injecting nanofibers with PDGF-BB, but not nanofibers or PDGF-BB alone, decreased

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

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

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

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

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

296 Stimulation with PDGF-BB significantly shortened the half-life of p27 mRN

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.