ライフサイエンスコーパス: PDGF receptor

1 inhibition causes the down-regulation of the PDGF receptor.

2 orylate PDGF-induced tyrosine phosphorylated PDGF receptor.

3 ession increases tyrosine phosphorylation of PDGF receptor.

4 domains of PTEN contribute to binding to the PDGF receptor.

5 ion of tyrosine phosphorylated and activated PDGF receptor.

6 ctural element for its binding with the beta-PDGF receptor.

7 that LRP is found in caveolae along with the PDGF receptor.

8 ignal transduction pathways initiated by the PDGF receptor.

9 olin 2 and GLUT4 with very low levels of the PDGF receptor.

10 erminal SH2 domain was disabled bound to the PDGF receptor.

11 ludes a deletion of the alpha subunit of the PDGF receptor.

12 inase inhibitor which inhibits both VEGF and PDGF receptors.

13 hat blocks the activity of c-Abl, c-Kit, and PDGF receptors.

14 at adult neural stem cells (B cells) express PDGF receptors.

15 ly members or have translocations activating PDGF receptors.

16 PS-/- cells are due to reduced expression of PDGF receptors.

17 factor domain of PDGF CC and DD to activate PDGF receptors.

18 DGFRbeta) in HEK293 cells lacking endogenous PDGF receptors.

19 lls of mesenchymal origin, signaling through PDGF receptors.

20 ss platelet-derived growth factor (PDGF) and PDGF receptors.

21 tat3 interacts with and is phosphorylated by PDGF receptors.

22 ortant angiogenic genes, such as PDGF-BB and PDGF receptors.

23 inase-linked platelet-derived growth factor (PDGF) receptor.

24 Src and the platelet-derived growth factor (PDGF) receptor.

25 PDGF-receptor activated signaling pathways for the "slow

26 cytoplasmic domain in a process dependent on PDGF receptor activation and c-Src family kinase activit

27 ve ligand that prevents PDGF-B-mediated beta-PDGF receptor activation in fibroblasts.

28 st a role for the EGF receptor downstream of PDGF receptor activation in the signaling events that le

29 PAR-1, ATP, and PDGF receptor activation resulted in prominent nuclear C

30 Stimuli such as PDGF receptor activation that also induce recruitment of

31 glomerular manifestations likely result from PDGF receptor activation.

32 F receptor function and negatively regulates PDGF receptor activation.

33 F depletion were not attributable to altered PDGF receptor activity or alterations in activation of A

34 es revealed co-localization of LRP1 with the PDGF receptor after PDGF treatment within endosomal comp

35 his mutant has greatly reduced activity as a PDGF receptor agonist.

36 They signal through cell membrane receptors, PDGF receptor alpha (PDGF-Ralpha) and receptor beta (PDG

37 ic nerve, there are glial cells that express PDGF receptor alpha (PDGFR alpha) [1] and divide in resp

38 The pdgf receptor alpha (pdgfra) 3' UTR contained a Mirn140

39 cell lines showed that either IGF-1R or the PDGF receptor alpha (PDGFRA) can mediate intrinsic resis

40 had mutations in the KIT-related kinase gene PDGF receptor alpha (PDGFRA), which occurred in either e

41 make only a minor contribution to activating PDGF receptor alpha (PDGFRalpha) and driving experimenta

42 To assess the combined role of PDGF receptor alpha (PDGFRalpha) and PDGFRbeta, we gener

43 ndirectly and chronically activate monomeric PDGF receptor alpha (PDGFRalpha) in the setting of a bli

44 Increased PDGF receptor alpha and beta protein levels were associa

45 y podosome regulators as targets of miR-143 (PDGF receptor alpha and protein kinase C epsilon) and mi

46 PDGF receptor alpha mRNA correlated with CCN2 and other

47 shRNA-expressing cells remained PDGF receptor alpha positive, olig2(+), or NG2(+) or bec

48 increased expression of Foxf1, PDGFa, PDGFb, PDGF receptor alpha, and myocardin.

49 PDGF A, PDGF B, PDGF receptor alpha, and PDGF receptor beta mRNAs were d

50 eta receptors I and II, PDGFalpha, PDGFbeta, PDGF receptor alpha, and PDGF receptor beta was performe

51 elial cell adhesion molecule, Megsin, Thy-1, PDGF receptor alpha, and vascular alpha-actin) and induc

52 vant to PVR pathogenesis because they act on PDGF receptor alpha, which is required for experimental

53 These PDGF receptor alpha-positive cells co-localized with PDG

54 In mice challenged with angiotensin II, PDGF receptor alpha-positive cells were increased in the

55 ated neural cell adhesion molecule-positive, PDGF receptor alpha-positive, and beta-tubulin-negative

56 s, inhibited non-PDGF-mediated activation of PDGF receptor alpha.

57 profibrotic genes, including type beta1 TGF, PDGF receptors alpha and beta, and tissue inhibitors of

58 xpression of platelet-derived growth factor (PDGF) receptor alpha (PDGFRalpha) dramatically increases

59 While platelet-derived growth factor (PDGF) receptor alpha (PDGFRalpha) has well-documented fu

60 ctivation of platelet-derived growth factor (PDGF) receptor alpha (PDGFRalpha) via PDGF, indirect act

61 e found that platelet-derived growth factor (PDGF) receptor alpha is overexpressed in 67% of pediatri

62 We studied the signaling properties of the PDGF receptor, alpha polypeptide (PDGFRA) isoforms (V561

63 erging data indicate the distinctive role of PDGF receptor-alpha (PDGFRalpha) in this process.

64 Large numbers of PDGF receptor-alpha (PDGFRalpha)-expressing stromal cell

65 bind and signal through two known receptors, PDGF receptor-alpha and PDGF receptor-beta, which are co

66 b mesylate and a monoclonal antibody against PDGF receptor-alpha enhanced myocardial damage evidenced

67 nity binding of recombinant GFD (PDGF-CC) to PDGF receptor-alpha homodimers and PDGF receptor-alpha/b

68 Capillary endothelium did not express PDGF receptor-alpha, suggesting that potential PDGF-CC e

69 GF-CC) to PDGF receptor-alpha homodimers and PDGF receptor-alpha/beta heterodimers.

70 eceptor-beta, and fibronectin, and increased PDGF-receptor-alpha and PDGF-C mRNA).

71 Since the PDGF receptor also activates the Src tyrosine kinase, it

72 PDGF receptors also have independent functions in the de

73 ncluding the platelet-derived growth factor (PDGF) receptor, although the extent to which this occurs

74 ar Abl tyrosine kinase activity but also the PDGF receptor and c-Kit tyrosine kinases at similar conc

75 SH2 domain was impaired did not bind to the PDGF receptor and consequently was neither phosphorylate

76 kinase activation that occurs in response to PDGF receptor and insulin/IGF-1 receptor stimulation.

77 the leading edge, where it colocalized with PDGF receptor and Rac1, in migrating VSMCs.

78 led significant associations between stromal PDGF receptor and STC1 expression.

79 which can induce phosphorylation of the beta-PDGF receptor and stimulates LNCaP cell proliferation in

80 composed of the extracellular domain of the PDGF receptor and the transmembrane and intracellular do

81 that a kinase inhibitor that blocks VEGF and PDGF receptors and several isoforms of protein kinase C

82 uble mutant did not associate with activated PDGF receptors and was not tyrosine phosphorylated.

83 ociated with platelet-derived growth factor (PDGF) receptor and that PDGF causes its dissociation fro

84 tes with the platelet-derived growth factor (PDGF) receptor and undergoes tyrosine phosphorylation in

85 by VEGF and platelet-derived growth factor (PDGF) receptors and several isoforms of protein kinase C

86 iogenesis inhibitor targeting VEGF receptor, PDGF receptor, and c-KIT, was evaluated in patients with

87 h inactive Stat3 pre-assembles with inactive PDGF receptors, and in response to ligand binding and in

88 ptor, blocked phosphorylation of the EGF and PDGF receptors, and inactivated several signaling pathwa

89 h factor and platelet-derived growth factor (PDGF) receptors, and multiple phosphorylated tyrosine re

90 There is no expression of the PDGF-receptor, and the Abl kinase is not activated by SC

91 -negative PDGF-A (88%) or treatment with the PDGF receptor antagonist CT52923 (50%).

92 were also treated for up to 50 weeks with a PDGF receptor antagonist that blocks all three PDGF rece

93 for the PDGFRbeta, we hypothesized that both PDGF receptors are involved in NCC formation.

94 ctivated by tyrosine phosphorylation, and as PDGF receptors are ligand-activated tyrosine kinases, we

95 In NSCLC alterations in PDGF receptors are markers of worst prognosis and effici

96 hanced, and prolonged the phosphorylation of PDGF receptor at Tyr857 with a corresponding inhibition

97 appear to result from a gross dysfunction of PDGF receptors, because ligand-stimulated tyrosine phosp

98 Clinical studies have shown that both PDGF receptor beta (beta-PDGFR) and its ligand PDGF D ar

99 let-derived growth factor (PDGF) B-chain and PDGF receptor beta (PDGFR beta) are essential for glomer

100 Nckbeta binds at Tyr-1009 in human PDGF receptor beta (PDGFR-beta) which is different from

101 d expression of LRP6 and colocalization with PDGF receptor beta (PDGFR-beta).

102 However, the direct effects of PDGF receptor beta (PDGFRbeta) activation on VSMCs have

103 PDGF receptor beta (PDGFRbeta) is highly expressed in ac

104 tability of growth factor receptors, such as PDGF receptor beta (PDGFRbeta) known to be important in

105 Activation of the PDGF receptor beta (PDGFRbeta) leads to tyrosine phospho

106 vec were used to block PDGF-D expression and PDGF receptor beta (PDGFRbeta) signaling.

107 that platelet-derived growth factor (PDGF)-B/PDGF receptor beta (PDGFRbeta) signalling is critical in

108 Their expression of Arf overlapped with Pdgf receptor beta (Pdgfrbeta), which is essential for p

109 e composed of both wild-type (WT) and marked PDGF receptor beta (PDGFRbeta)-deficient cells, and dete

110 is and ligand-induced down-regulation of the PDGF receptor beta (PDGFRbeta).

111 pacities and reveal diminished expression of PDGF receptor beta and JAGGED1 ligand.

112 Biochemically, LRP-6 interacts closely with PDGF receptor beta and TGF-beta receptor 1 at the cell m

113 s, which was partially mediated via elevated PDGF receptor beta expression on such cells.

114 Immune complex tyrosine kinase assay of PDGF receptor beta immunoprecipitates from lysates of me

115 erived growth factor (PDGF)-BB, PDGF-DD, and PDGF receptor beta in association with immature glomerul

116 By in situ hybridization, PDGF receptor beta is expressed in the cranial ectoderm

117 es using isolated Flk-1, FGF receptor 1, and PDGF receptor beta kinases revealed that SU6668 has comp

118 PDGF A, PDGF B, PDGF receptor alpha, and PDGF receptor beta mRNAs were detected in corneal epithe

119 , we further studied signaling properties of PDGF receptor beta subunit (PDGFRbeta) in HEK293 cells l

120 DGFalpha, PDGFbeta, PDGF receptor alpha, and PDGF receptor beta was performed in 19 SSc patients, 76

121 essive reduction of pericytes, identified by PDGF receptor beta, NG2, desmin, or alpha-smooth muscle

122 eptor alpha-positive cells co-localized with PDGF receptor beta, procollagen, and periostin.

123 PDGF receptor beta-positive myofibroblasts isolated from

124 rotein alpha, alpha smooth muscle actin, and PDGF receptor beta.

125 cal role for platelet-derived growth factor (PDGF) receptor beta (beta-PDGFR) signaling in prostate c

126 ted forms of platelet-derived growth factor (PDGF) receptor beta (PDGFRbeta), hepatocyte growth facto

127 involves the platelet-derived growth factor (PDGF) receptor beta and phosphoinositide 3-kinase.

128 The mechanism of PDGF-receptor beta (PDGFRbeta) activation was explored b

129 Additionally, NRP-1 colocalized with PDGF-receptor beta (PDGFRbeta) in HSCs both in the injur

130 sphorylation of VEGF receptor 2 (VEGFR2) and PDGF receptor-beta (PDGFR-beta) were blunted in diabetic

131 t study of ours showed that LOX oxidizes the PDGF receptor-beta (PDGFR-beta), leading to amplified do

132 oxidize cell surface proteins, including the PDGF receptor-beta (PDGFR-beta), to affect PDGF-BB-induc

133 and that this phosphorylation is mediated by PDGF receptor-beta (PDGFRbeta), but not c-Src.

134 ral nerve sheath tumors (MPNSTs) overexpress PDGF receptor-beta and generate an aberrant intracellula

135 h mesangial cell markers alpha8-integrin and PDGF receptor-beta but not with endothelial, podocyte, o

136 dated by direct interference with PDGF-BB or PDGF receptor-beta cell interactions to implicate PDGF-B

137 This signaling cascade leads to PDGF receptor-beta dephosphorylation and a reduction in

138 gs emphasize the importance of engagement of PDGF receptor-beta in transducing mesangial cell prolife

139 resulting from stimulation of overexpressed PDGF receptor-beta may contribute to the survival and tu

140 he lung and as smooth muscle actin (SMA) and PDGF receptor-beta positive cells in the walls of pulmon

141 (e.g., collagen I, ecto-5'-nucleotidase, and PDGF receptor-beta).

142 In mouse cardiac allografts PDGF receptor-beta, but not -alpha intragraft messenger

143 two known receptors, PDGF receptor-alpha and PDGF receptor-beta, which are constitutively expressed i

144 ts (reduced transcription of PDGF-B, PDGF-D, PDGF-receptor-beta, and fibronectin, and increased PDGF-

145 Thus, inhibition of VEGF and PDGF receptor binding with a synthetic molecule results

146 inhibitory effect, but less so than the VEGF/PDGF receptor blocker.

147 od, especially since PDGF not only activates PDGF receptor but also binds directly to LRP.

148 drug that blocks phosphorylation by VEGF and PDGF receptors, but not PKC, completely inhibited retina

149 716, two drugs that block phosphorylation by PDGF receptors, but not VEGF receptors, had no significa

150 Blockade of phosphorylation by PDGF receptors, but not VEGF receptors, had no significa

151 e C (PKC) or platelet-derived growth factor (PDGF) receptor by seemingly independent pathways.

152 he c-kit and platelet-derived growth factor (PDGF) receptors by autocrine/paracrine mechanisms follow

153 In vitro phosphorylation assays showed that PDGF receptor, calcium-dependent tyrosine kinase (CADTK/

154 Blockade of phosphorylation by VEGF and PDGF receptors caused dramatic, almost complete inhibiti

155 mediated by the association of two 1:1 PDGF/PDGF receptor complexes.

156 Together, these data demonstrate that PDGF receptors cooperate in the yolk sac mesothelium to

157 related transcription factor, was reduced in PDGF receptor-deficient epicardial cells, and overexpres

158 ceptor tyrosine kinase inhibitor of VEGF and PDGF receptors, demonstrates antitumor activity in metas

159 GF receptor antagonist that blocks all three PDGF receptor dimers.

160 e formation of a ternary complex between the PDGF receptor, DOCK4, and Dynamin, which is formed at th

161 PDGF-B from circulating cells or blockade of PDGF receptors does not appear sufficient to prevent smo

162 s PDGF-dependent cell migration by promoting PDGF receptor endocytosis and Rac1 activation at the cel

163 ctor, and Dynamin regulate cell migration by PDGF receptor endocytosis.

164 nism by which cell migration is regulated by PDGF receptor endocytosis.

165 VEGFs bind to VEGF receptors, PDGFs bind to PDGF receptors, etc.

166 The rescue of PDGF receptor expression and activation by PS2 is facili

167 geneous population of cells, and the lack of PDGF receptor expression in the GLUT4-positive cell popu

168 ignal transduction pathways initiated by the PDGF receptor from endosomes.

169 unction where it acts as an effector for the PDGF receptor function and negatively regulates PDGF rec

170 phox to regulate NOX activity, which affects PDGF receptor function for cell proliferation.

171 lcin-1 (STC1) as a mediator of metastasis by PDGF receptor function in the setting of colorectal canc

172 Both PDGF receptor genes (PDGFRA and PDGFRB) also showed no d

173 In addition, coexpression of PDGF and PDGF receptors has been demonstrated in human gliomas, i

174 r (VEGF) and platelet-derived growth factor (PDGF) receptors, has single-agent activity in non-small-

175 g the interaction between the enzyme and the PDGF receptor have now been investigated by functionally

176 est the effect of blocking the output of the PDGF receptor in an experimental model of PVR.

177 -JNK, P-ERK1/2, P-Akt, P-p38, p47phox, and P-PDGF receptor in cell lysates were detected by Western b

178 studies reveal that LRP1 associates with the PDGF receptor in endosomal compartments and modulates it

179 Furthermore, transfection of the PDGF receptor in the insulin receptor-, GLUT4-, and cave

180 ied PTEN dephosphorylates autophosphorylated PDGF receptor in vitro.

181 of platelet-derived growth factor (PDGF) and PDGF receptors in the human cornea and to study the effe

182 ted that the platelet-derived growth factor (PDGF) receptor in adipocytes can activate PI 3-kinase ac

183 mbryos that do not express either of the two PDGF receptors induced PVR poorly when injected into the

184 er, the authors evaluated the effects of the PDGF receptor inhibitor STI571 in 2 different animal mod

185 In a pilot study, imatinib, a c-kit/PDGF-receptor inhibitor, induced partial regression of A

186 form of the platelet-derived growth factor (PDGF) receptor involves recognition of a unique sequence

187 Signaling through both PDGF receptors is necessary for epicardial EMT and forma

188 The platelet-derived growth factor (PDGF) receptor is a cell surface receptor on fibroblasts

189 ccount for functional specificity of the two PDGF receptor isoforms.

190 317, which is perhaps phosphorylated by the PDGF receptor itself).

191 It is possible to model the PDGF receptor juxtamembrane domain as a short alpha-heli

192 for Src in STAT activation, we found that a PDGF receptor juxtamembrane tyrosine residue required fo

193 retreatment with 1 microM AG1295 (a specific PDGF receptor kinase inhibitor), EGFR transactivation wa

194 , with both inhibited by AG1296, a selective PDGF receptor kinase inhibitor.

195 the ATP binding pockets of the FIk-1/KDR and PDGF receptor kinases provided insight to explain the re

196 olin-2-ones to inactivate the VEGF, FGF, and PDGF receptor kinases.

197 oth VEGF and platelet-derived growth factor (PDGF) receptor kinases; a drug that inhibits PDGF, but n

198 Mouse embryo fibroblasts derived from PDGF receptor knock-out embryos that do not express eith

199 enib inhibits VEGF receptors 1, 2, and 3 and PDGF receptors like other anti-angiogenic tyrosine-kinas

200 onstrate that inhibition of the c-kit and/or PDGF receptors may represent an effective strategy for t

201 Following activation of PDGF receptors, MCP-1 mRNA does not begin to accumulate

202 Analysis of the model suggests that PDGF receptor-mediated endocytosis and degradation of PD

203 n the cytoplasm via the FF domains, but upon PDGF receptor-mediated phosphorylation of an FF domain,

204 results support the hypothesis that VEGF and PDGF receptor-mediated signaling is an effective therape

205 ther isoforms, results in down-regulation of PDGF receptor mRNA and protein, suggesting a direct effe

206 Single-agent therapy targeting PDGF receptor must be used with caution in tumors when P

207 or was fused to the IgG(1) Fc domain, and to PDGF receptors on NIH 3T3 cells.

208 Elevated expression of PDGF receptors on stromal CAFs is associated with metast

209 ased (125)I-PDGF maximum binding (B(max)) to PDGF receptors on VSMCs without altering the binding con

210 nt effect on tyrosine phosphorylation of the PDGF receptors or activation of extracellular signal-reg

211 kbeta was required for the activation of the PDGF receptor, p21-activated protein kinase (Pak1), AKT,

212 Inhibition of the PDGF-CC-PDGF receptor pathway for different clinical purposes sh

213 thelial cell platelet-derived growth factor (PDGF) receptor (PDGF-R) by PDGF has been implicated in n

214 he activated platelet-derived growth factor (PDGF) receptor (PDGFbetaR) to the actin cytoskeleton.

215 elet-derived growth factor (PDGF) B chain or PDGF receptor (PDGFR) beta lack mesangial cells.

216 that these cells express functionally active PDGF receptor (PDGFR) beta.

217 litated the identification of novel PDGF and PDGF receptor (PDGFR) family members in C. elegans, Dros

218 peptides in that it redirected ligand-bound PDGF receptor (PDGFR) from the clathrin-dependent endocy

219 as consisting of the extracellular domain of PDGF receptor (PDGFR) fused to the transmembrane and cyt

220 Activation of PDGF receptor (PDGFR) in rat aortic vascular smooth musc

221 The PDGF receptor (PDGFR) is a receptor tyrosine kinase that

222 document that ErbB ligand induction requires PDGF receptor (PDGFR) mediation and engages a positive a

223 PDGF receptor (PDGFR) signaling appears to be required f

224 stochemical and immunoblot studies to detect PDGF receptor (PDGFR) subtypes and (2) immunoprecipitati

225 thway, platelet-derived growth factor (PDGF)/PDGF receptor (PDGFR) that regulates glycolysis in gliom

226 d -D, that signal through the alpha and beta PDGF receptor (PDGFR) tyrosine kinases.

227 Phosphorylation of the PDGF receptor (PDGFR) was monitored by antiphosphotyrosi

228 4825 inhibited PDGF-stimulated activation of PDGF receptor (PDGFR), STAT3, Akt, and Erk2 in rat A10 V

229 fibrogenic effects through interactions with PDGF receptor (PDGFR)-alpha and PDGFR-beta.

230 nd Ang-2 and its receptor, Tie-2, as well as PDGF receptor (PDGFR)-alpha.

231 vation of Akt, but not ERK, was blocked by a PDGF receptor (PDGFR)-specific inhibitor, AG1296, sugges

232 elanoma cells express abundant levels of the PDGF receptor (PDGFR).

233 e we show that LRP1 forms a complex with the PDGF receptor (PDGFR).

234 We investigated the response of KS to the PDGF receptor (PDGFR)/c-kit inhibitor, imatinib mesylate

235 s associated with increased ERK1/2, Src, and PDGF receptor (PDGFR)beta phosphorylation, without alter

236 ve for PDGF-A and -D, whereas CAFs expressed PDGF receptor (PDGFR)beta.

237 rs including platelet-derived growth factor (PDGF) receptor (PDGFR) beta, hepatocyte growth factor re

238 The platelet-derived growth factor (PDGF) receptor (PDGFR) family of receptor tyrosine kinas

239 Platelet-derived growth factor (PDGF) receptors (PDGFR) and their ligands play critical

240 Furthermore, PDGF receptors (PDGFRs) are present and activated in epi

241 not due to differences in the expression of PDGF receptors (PDGFRs) during the cell cycle.

242 e dimers capable of activating their cognate PDGF receptors (PDGFRs).

243 The platelet-derived growth factor (PDGF) receptors (PDGFRs) are central to a spectrum of hu

244 f a truncated platelet-derived growth factor PDGF receptor (PDGFXR) to investigate whether antagonism

245 sensitivity of PDGF gradient sensing through PDGF receptor/phosphoinositide 3-kinase-mediated signal

246 es Tyr-439 and Tyr-494 in SH2-Bbeta and that PDGF receptor phosphorylates SH2-Bbeta on Tyr-439.

247 We find that PDGF receptor phosphorylation exhibits positive cooperat

248 ly observed increases in PTP1B oxidation and PDGF receptor phosphorylation in TrxR1 knockout cells.

249 d in cells that possessed mutations in their PDGF receptor-PI 3-K interaction domain.

250 To quantitatively assess the kinetics of PDGF receptor/PI 3-kinase/Akt signaling in fibroblasts,

251 beta PDGF receptor profiling further suggested autocrine sign

252 t circumvents the embryonic lethality of the PDGF receptor (R)beta-/- genotype and minimizes the tend

253 m led to reduced expression and signaling of PDGF-receptor (R)-alpha- and PDGFR-beta-chains.

254 arkers (KIT, platelet-derived growth factor [PDGF] receptor [-R], AKT2, phosphorylated AKT [p-AKT], s

255 phorylated and recruited to activated EGF or PDGF receptors, respectively.

256 Furthermore, conditional mutations of both PDGF receptors revealed a requirement in steroid-produci

257 AG1296, a PDGF receptor selective tyrosine kinase inhibitor, marke

258 erulonephritis is associated with overactive PDGF receptor signal transduction.

259 eport that 3' PI turnover is not affected by PDGF receptor signaling in our cells, allowing us to foc

260 Similarly, the PDGF receptor signaling inhibitor imatinib increased del

261 Combined PDGF receptor signaling is required for sufficient recru

262 CC lineage tracing, we observed that loss of PDGF receptor signaling resulted in reduced NCCs in the

263 Correspondingly, Gleevec, which blocks PDGF receptor signaling, and PDGF-Rbeta-neutralizing ant

264 tic potential of crenolanib, an inhibitor of PDGF receptor signaling, in cultured fibroblasts and in

265 angiogenesis inhibitor that targets VEGF and PDGF receptor signaling, in two GEMMs of pancreatic canc

266 Coincident with loss of PDGF receptor signaling, we found a reduction in collage

267 We therefore tested the effect of largeT on PDGF receptor signaling.

268 the study of platelet-derived growth factor (PDGF) receptor signaling in an angiomyolipoma cell model

269 Platelet-derived growth factor (PDGF) receptor signaling is a major functional determina

270 lete loss of platelet-derived growth factor (PDGF) receptor signaling results in embryonic lethality

271 Blockade of the PDGF receptors similarly delays, but does not prevent, a

272 In addition, PDGF receptor stimulation promoted epicardial cell migra

273 ization of actomyosin filaments triggered by PDGF receptor stimulation.

274 Moreover, an interaction between EGF and PDGF receptor systems is supported by the observation th

275 gamma1) binds to the tyrosine-phosphorylated PDGF receptor through one or both of its Src homology 2

276 accounts for the inability of the endogenous PDGF receptor to activate GLUT4 translocation.

277 Moreover, mutation of tyrosine-1021 of the PDGF receptor to phenylalanine, which impairs its associ

278 s1 represents a novel signaling pathway from PDGF receptor to the actin cytoskeleton via Src-related

279 wever, the nature of the pathways connecting PDGF receptors to AP-1 is still poorly defined.

280 rich syndrome protein (N-WASP) to facilitate PDGF receptor traffic and directed motility.

281 The PDGF receptor tyrosine kinase inhibitor imatinib mesylat

282 In terms of PDGF activation of PDGF receptor tyrosine phosphorylation as well as the mi

283 PDGF showed no inhibitory effect of BMP2 on PDGF receptor tyrosine phosphorylation.

284 osine kinase requires phosphorylation of the PDGF receptor tyrosine residue responsible for binding o

285 r (VEGF) and platelet-derived growth factor (PDGF) receptor tyrosine kinases.

286 ities underlie restenosis, inhibition of the PDGF-receptor tyrosine kinase (PDGFr-TK) is postulated t

287 t hippocampal slices, which was abolished by PDGF receptor-tyrosine kinase inhibitor STI-571.

288 nd SM22, induction of FGF-2, VEGF, PDGF, and PDGF receptors, upregulation of integrins alpha3 and alp

289 lable, ATP-competitive inhibitor of VEGF and PDGF receptors used clinically to suppress angiogenesis

290 transphosphorylation of the EGFR, ErbB2, or PDGF receptor was not required for its antiapoptotic eff

291 In contrast, the PDGF receptor was only expressed in approximately 10% of

292 itor with high binding affinity for VEGF and PDGF receptors, was tested for clinical activity in pati

293 ice with epicardial-specific deletion of the PDGF receptors, we found that epicardial epithelial-to-m

294 iple phosphorylated tyrosine residues on the PDGF receptor were able to mediate Vav2 tyrosine phospho

295 ing HUVECs, with diminished recruitment when PDGF receptors were neutralized.

296 ctively, and platelet-derived growth factor (PDGF) receptors were expressed only in activated PSC (aP

297 Furthermore, pharmacologic inhibition of the PDGF receptor, which is expressed by submesothelial fibr

298 ing and largely diminished the activation of PDGF receptor with no inhibition of LMW-PTP.

299 ation of the platelet-derived growth factor (PDGF) receptor within 1 h of treatment and increasing re

300 The mutant PDGF receptor Y708F/Y719F but not Y977F/Y989F showed sig