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

7 ignal transduction pathways initiated by the PDGF receptor.

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

9 ctural element for its binding with the beta-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 hat blocks the activity of c-Abl, c-Kit, and PDGF receptors.

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

14 ly members or have translocations activating PDGF receptors.

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

16 inase inhibitor which inhibits both VEGF and 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 Nintedanib targets VEGF receptors 1-3, PDGF receptors alpha and beta, FGF receptors 1-3, and Sr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

73 PDGF receptors also have independent functions in the de

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

124 PDGF receptor beta-positive myofibroblasts isolated from

125 DGFB) plays a crucial role in recruitment of PDGF receptor beta-positive pericytes to blood vessels.

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

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

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

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

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

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

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

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

134 athogenesis of LMNA-related DCM and point to PDGF receptor-beta (PDGFRB) as a potential therapeutic t

135 d TRIM27 knockdown reduced the expression of PDGF receptor-beta (PDGFRbeta) and the phosphorylation o

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

152 716, two drugs that block phosphorylation by PDGF receptors, but not VEGF receptors, had no significa

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

183 ied PTEN dephosphorylates autophosphorylated PDGF receptor in vitro.

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

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

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

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

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

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

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

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

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

193 317, which is perhaps phosphorylated by the PDGF receptor itself).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

231 4825 inhibited PDGF-stimulated activation of PDGF receptor (PDGFR), STAT3, Akt, and Erk2 in rat A10 V

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

250 We find that PDGF receptor phosphorylation exhibits positive cooperat

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

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

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

254 beta PDGF receptor profiling further suggested autocrine sign

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

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

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

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

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

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

261 erulonephritis is associated with overactive PDGF receptor signal transduction.

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

263 Similarly, the PDGF receptor signaling inhibitor imatinib increased del

264 Combined PDGF receptor signaling is required for sufficient recru

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

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

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

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

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

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

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

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

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

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

275 In addition, PDGF receptor stimulation promoted epicardial cell migra

276 ization of actomyosin filaments triggered by PDGF receptor stimulation.

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

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

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

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

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

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

283 The PDGF receptor tyrosine kinase inhibitor imatinib mesylat

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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