ライフサイエンスコーパス: PDGFR

1 PDGFR antagonists may improve potency and efficacy of ot

2 PDGFR is a promising target for anti-cancer therapy beca

3 PDGFR is an important target for novel anticancer therap

4 PDGFR is phosphorylated upon PDGF stimulation, and is de

5 PDGFR-alpha activation led to BBB impairment and this wa

6 PDGFR-alpha and -beta immunoreactivity was observed in r

7 PDGFR-alpha signaling may contribute to BBB impairment v

8 PDGFR-alpha suppression prevented neurological deficits,

9 PDGFR-alpha(+)Sca-1(+) (PalphaS) MSCs have augmented gro

10 PDGFR-BB is an inducer of mitotic proliferation in MKs.

11 PDGFR-beta has become an attractive target for the treat

12 PDGFR-beta inhibition selectively eliminates morphine to

13 PDGFR-beta inhibitors are widely used and well tolerated

14 PDGFR-beta promotes growth of mesenchymal cells, includi

15 of both these single agents against VEGFR-2, PDGFR-beta, and hTS is better than or close to standards

16 A PDGFR antagonist (Gleevec) or agonist (PDGF-AA) was admi

17 rapeutic targeting reduced tumor burden in a PDGFR-dependent manner with effects on cell proliferatio

18 umented secondary cause of eosinophilia or a PDGFR -positive myeloproliferative neoplasm were exclude

19 Additional tissue culture studies showed a PDGFR-dependent regulation of rhabdosphere formation/can

20 t platelet-derived growth factor receptor A (PDGFR-A) may be a mediator of disease progression and me

21 edatolisib and dasatinib was observed in ABL/PDGFR-mutant models (P < .001).

22 As E5 is known to activate PDGFR within the thin membranes of the Golgi compartment

23 activation is the primary mode of activating PDGFRs, the discovery that they can also be activated in

24 relevance of the indirect mode of activating PDGFRs.

25 In addition, PDGFR-alpha and -beta protein expression was observed in

26 s the benefits of targeted therapies against PDGFR-beta in aggressive life-threatening familial forms

27 atelet-derived growth factor receptor alpha (PDGFR-alpha) and stem cell antigen 1 (Sca-1) have recent

28 atelet-derived growth factor receptor alpha (PDGFR-alpha) signaling, resulting in increased apoptosis

29 atelet-derived growth factor receptor alpha (PDGFR-alpha), a tyrosine kinase receptor, was found in p

30 atelet-derived growth factor receptor-alpha (PDGFR-alpha)(+)Sca-1(+)CD45(-)Ter119(-) (PalphaS) cells.

31 atelet-derived growth factor receptor (alpha-PDGFR) signaling, which was shown using the small-molecu

32 olished the aberrant activation of c-Abl and PDGFR and protected against experimental cGvHD.

33 ummary, the combined inhibition of c-Abl and PDGFR is effective for prevention and treatment of exper

34 f imatinib, combined inhibition of c-Abl and PDGFR might be a promising future strategy for treatment

35 e was accompanied by inhibition of c-abl and PDGFR phosphorylation and suppression of TNF-alpha and I

36 mation, and fibrosis by inhibiting c-abl and PDGFR signaling pathways and downstream inflammatory cyt

37 Higher expression of p-AKT and PDGFR-beta were associated with shorter PFS, and higher

38 nd signaling of PDGF-receptor (R)-alpha- and PDGFR-beta-chains.

39 n association between autocrine TGF-beta and PDGFR-mediated invadosome formation in RA synoviocytes t

40 distinguishing between ANCA-negative CSS and PDGFR-negative HES is difficult because of significant o

41 Simultaneous inhibition of both EGFR and PDGFR was necessary for abrogation of PI3 kinase pathway

42 , SMAD family genes, AURKA, EGFR, HSP90, and PDGFR.

43 Because KIT and PDGFR-alpha remain drivers of GIST after resistance to i

44 dothelial growth factor receptor, c-KIT, and PDGFR, and has shown clinical activity in various solid

45 bserved in areas of F4/80(+) macrophages and PDGFR-beta(+) and transgelin(+) fibroblasts, all of whic

46 on of the joint PDGFR/integrin signaling and PDGFR-dependent cell responses.

47 The interaction between tTG and PDGFR reduces cellular levels of the receptor by acceler

48 The inhibition of VEGFR2 and PDGFR-beta activity was associated with increased SHP-1

49 interface is predominantly hydrophobic, and PDGFRs and the PDGF propeptides occupy overlapping posit

50 may explain mixed clinical responses of anti-PDGFR-based approaches and suggest the need for integrat

51 s who might benefit from treatment with anti-PDGFR therapies, such as sunitinib.

52 echanism of cardiotoxicity due to anticancer PDGFR inhibitors.

53 e U.S. Food and Drug Administration-approved PDGFR inhibitor, sunitinib, targets FOXC2-expressing tum

54 zing specific cell surface proteins, such as PDGFR-beta.

55 tes, indicating the presence of an autocrine PDGFR activation loop that involved endogenous PDGF.

56 Pharmacologic inhibition of the PDGF-B/PDGFR-beta signaling axis disrupted the association of m

57 e regenerative potential of MSCs via PDGF-BB/PDGFR-beta signaling.

58 latelet-derived growth factor receptor beta (PDGFR-beta) expression in malignancies, we have cloned a

59 latelet-derived growth factor receptor beta (PDGFR-beta) has been associated with cancers and vascula

60 and colocalization with PDGF receptor beta (PDGFR-beta).

61 latelet-derived growth factor receptor-beta (PDGFR-beta) for antiangiogenic effects and also inhibit

62 latelet-derived growth factor receptor-beta (PDGFR-beta) signaling during MC recruitment.

63 receptor 2 (VEGFR2) and PDGF receptor-beta (PDGFR-beta) were blunted in diabetic Prkcd(+/+) mice but

64 ed that LOX oxidizes the PDGF receptor-beta (PDGFR-beta), leading to amplified downstream signaling.

65 proteins, including the PDGF receptor-beta (PDGFR-beta), to affect PDGF-BB-induced chemotaxis.

66 latelet-derived growth factor receptor-beta (PDGFR-beta)-mediated signaling plays a key role in morph

67 oth PDGF-B and -D were able to activate beta-PDGFR, only PDGF-D was able to induce osteoclastic diffe

68 We found an increase in PDGF D and beta-PDGFR expression levels in PTEN-null tumor cells, accomp

69 the maintenance of increased PDGF D and beta-PDGFR expression.

70 ave shown that both PDGF receptor beta (beta-PDGFR) and its ligand PDGF D are up-regulated in primary

71 ved growth factor (PDGF) receptor beta (beta-PDGFR) signaling in prostate cancer (PCa) progression, t

72 et-derived growth factor receptor-beta (beta-PDGFR) signaling in prostate cancer (PCa).

73 vel signaling axis of matriptase/PDGF-D/beta-PDGFR in PCa, providing new insights into functional int

74 prostate cancer progression via PDGF D/beta-PDGFR signal transduction.

75 However, a ligand responsible for beta-PDGFR activation in PCa was unknown, and recent clinical

76 e, we identified PDGF-D as a ligand for beta-PDGFR in PCa and discovered matriptase as its regulator.

77 fied the PDGF-D isoform as a ligand for beta-PDGFR in PCa and showed that PDGF-D is activated by seri

78 s, whereas PDGF B, a classic ligand for beta-PDGFR, is not frequently detected in clinical samples.

79 (PCa) progression, the precise roles of beta-PDGFR and PDGF isoform-specific cell signaling have not

80 inical studies suggest the potential of beta-PDGFR as a therapeutic target in metastatic PCa.

81 tase colocalization is accompanied with beta-PDGFR phosphorylation in human PCa tissues.

82 Pericyte coverage was determined by PDGFR-beta and alpha-SMA staining.

83 transforming potential that was reversed by PDGFR blockade.

84 These results demonstrate that cardiomyocyte PDGFR-beta is a regulator of the compensatory cardiac re

85 echanistically, we showed that cardiomyocyte PDGFR-beta signaling plays a vital role in stress-induce

86 ifically, we demonstrated that cardiomyocyte PDGFR-beta was an essential upstream regulator of the st

87 antibodies: allophycocyanin (APC)-conjugated PDGFR-alpha, FITC-conjugated Sca-1, phycoerythrin (PE)-c

88 nsitivity to down-regulation of FLT1, CSF1R, PDGFR, ROR1, EPHA4/5, JAK1/3, LMTK3, LYN, FYN, PTK2B, an

89 skin is impaired, correlating with defective PDGFR-beta and transforming growth factor-beta (TGF-beta

90 usion gene was mutually exclusive with EGFR, PDGFR, or MET amplification.

91 Viral entry in cells harbouring endogenous PDGFR-alpha was competitively inhibited by pretreatment

92 e we report that in fibroblasts tTG enhances PDGFR-integrin association by interacting with PDGFR and

93 In this study, we explored PDGFR-regulated microRNAs demonstrating that miR-23b clu

94 R-1, -3, c-Kit and RET, most cells expressed PDGFR-alpha and -beta.

95 s mitogenic for mesenchymal cells expressing PDGFR-beta, and PI3-K is an important regulator of PDGF-

96 othelial HS appears sufficient to facilitate PDGFR-beta activation in trans.

97 ese results establish proof-of-principal for PDGFR-A as a therapeutic target in alveolar rhabdomyosar

98 the redox-regulated signal transduction from PDGFR to STAT3.

99 t oncoproteins such as BCR-ABL, c-Kit, HER2, PDGFR, and EGFR.

100 like Nanog(low)Sox2(low)Lin28(high)CD24(high)PDGFR-alpha(high) population.

101 Targeted human PDGFR-alpha activation in mouse beta-cells stimulated Er

102 telomestatin significantly reduced the human PDGFR-beta basal promoter activity relative to the contr

103 clease hypersensitivity element of the human PDGFR-beta gene promoter have been found to inhibit PDGF

104 d the first functional promoter of the human PDGFR-beta gene, which has been confirmed by luciferase

105 pecific G-quadruplex structures in the human PDGFR-beta promoter can modulate its transcription.

106 region (positions -165 to -139) of the human PDGFR-beta promoter is crucial for basal promoter activi

107 fferent G-quadruplex structures of the human PDGFR-beta promoter.

108 ockade of receptor function with a humanized PDGFR-alpha blocking antibody (IMC-3G3) or targeted inhi

109 Having identified PDGFR-beta to be regulated by FOXC2, we show that the U.

110 h the pericyte marker (immunohistochemistry: PDGFR-beta) and CK19.

111 Western blot analysis of immunoprecipitated PDGFRs.

112 These findings collectively implicate PDGFRs as critical mediators of breast cancer oncogenesi

113 This deficiency in PDGFR phosphorylation resulted in significant inhibition

114 indings indicate p.Arg561Cys substitution in PDGFR-beta as a cause of the dominant form of this disea

115 ndent signal transduction pathway, including PDGFR-beta, SHP2, AKT1, and ERK1/ERK2 (p44/42 MAPK), tur

116 receptor tyrosine kinases (RTKs), including PDGFR, have been validated as therapeutic targets in gli

117 alysis shows that many other RTKs, including PDGFRs, VEGFRs, KIT, CSF1R, FLT3, TEK, and TIE, are also

118 a activation and exogenous PDGF-AA increased PDGFR-alpha activation, regardless of thrombin inhibitio

119 ed by significant upregulation and increased PDGFR-beta signaling.

120 adhesion-mediated and growth factor-induced PDGFR activation, and up-regulates downstream signaling.

121 neutralizing antibodies inhibit HCMV-induced PDGFR-alpha phosphorylation.

122 wever, several anticancer drugs that inhibit PDGFR signaling have been associated with clinical heart

123 tilbene resveratrol targets PTP1B to inhibit PDGFR mitogenic signaling.

124 eta gene promoter have been found to inhibit PDGFR-beta transcriptional activity.

125 Furthermore, resveratrol inhibited PDGFR phosphorylation at the PI 3 kinase and Grb-2 bindi

126 l surface tTG in the regulation of the joint PDGFR/integrin signaling and PDGFR-dependent cell respon

127 At least one target of imatinib (KIT, PDGFR-alpha, or PDGFR-beta) was expressed in all tumors,

128 Sunitinib, which targets KIT, PDGFRs, and several other kinases, has demonstrated effi

129 able expression and mutations within the KIT/PDGFR pathway were observed.

130 edominant ligand involved in the CM-mediated PDGFR activation.

131 controversial at which membrane microdomains PDGFRs reside and how they control such diverse intracel

132 target this secondary structure and modulate PDGFR-beta gene expression.

133 mutations in the genes SMARCA4, EPHA3, MYB, PDGFR-beta, and PIK3CA.

134 pathway with lithium treatment rescued NG2(+)PDGFR-alpha(+) progenitor cell proliferation in BBS muta

135 so known as neuron-glial antigen 2 or NG2)(+)PDGFR-alpha(+) neural progenitors.

136 Here, we developed a novel PDGFR biosensor based on fluorescence resonance energy t

137 > G mutation in exon 12 (amino acid 567) of PDGFR-alpha.

138 tant underlying mechanism for the ability of PDGFR/c-Src signaling to control the stability of COX-2

139 Activation of PDGFR signaling has been described in gastrointestinal s

140 have inhibitory effects on the activation of PDGFR specifically located in lipid rafts but not outsid

141 Activation of PDGFR was monitored by antiphosphotyrosine Western blot

142 cks PDGF-dependent binding and activation of PDGFR, signaling events, and cellular responses.

143 f PTP1B, leading to pronounced activation of PDGFR.

144 Moreover, the association of PDGFR with tTG causes receptor clustering, increases PDG

145 e Pdgf-c gene or pharmacological blockade of PDGFR-alpha impair the WAT-beige transition.

146 However, the discovery of PDGFR activating mutations or gene rearrangements in oth

147 as efficiently as the bona fide TM domain of PDGFR.

148 IFN-gamma treatment led to downregulation of PDGFR-alpha (platelet-derived growth factor receptor-alp

149 Understanding this effect of PDGFR inhibitors has been difficult because the role of

150 are downregulated by increased expression of PDGFR-alpha or PDGFR-beta in NSCLC cells.

151 Consistent with this, inhibition of PDGFR combined with small molecule inactivation of IAPs

152 We found that in vitro inhibition of PDGFR in human GBM cells initiated the intrinsic pathway

153 findings strongly suggest that inhibition of PDGFR is critical to reverse diabetes and highlight a cr

154 Inhibition of PDGFR-A by RNA interference, small molecule inhibitor or

155 ating TPH1 down-regulation via inhibition of PDGFR-beta signaling.

156 esence of Tyrphostin AG1296, an inhibitor of PDGFR kinase.

157 shown using the small-molecule inhibitor of PDGFR signaling AG1296.

158 was blocked by small molecule inhibitors of PDGFR.

159 ukemic cells expressed much higher levels of PDGFR-beta transcripts than purified normal CD8(+) T cel

160 The known ligands of PDGFR, platelet-derived growth factor (PDGF) and vascula

161 ts, thereby enhancing the phosphorylation of PDGFR and synthesis of type I collagen.

162 Phosphorylation of PDGFR-alphabeta was also elevated in RA synovial tissues

163 GF-B mRNA expression, and phosphorylation of PDGFR.

164 e activity of PTP1B, improved the profile of PDGFR phosphorylation, decreased the numbers of tyrosine

165 nd preserving stemness-related properties of PDGFR-beta(+) MSCs, including the ability to repopulate

166 es PDGF signaling in VSMCs via regulation of PDGFR surface levels.

167 itors has been difficult because the role of PDGFR signaling in the heart remains largely unexplored.

168 e present study, we investigated the role of PDGFR-alpha following ICH-induced brain injury in mice,

169 onstituted with the transmembrane segment of PDGFR, it was able to tolerate even the most pronounced

170 PDGF-C(-/-) mice) or even an upregulation of PDGFR-beta and signaling (anti-PDGF-C group).

171 hich are required for enduring activation of PDGFRs.

172 Src family kinases (SFKs) act downstream of PDGFRs to enhance PDGF-mediated tyrosine phosphorylation

173 a (GBM) subtype, we interrogated the role of PDGFRs in intratumoral GBM heterogeneity.

174 harmacologic inhibition or gene silencing of PDGFRs sensitizes mammary epithelial cells to chemothera

175 ker profile of infected cells, NG2+, olig2+, PDGFR-alpha+, nestin+, GFAP-, and CC1-, indicated a clos

176 rylation at tyrosine-751 and tyrosine-716 on PDGFR with concomitant reduction in Akt and Erk1/2 kinas

177 We found that FAP was robustly expressed on PDGFR-alpha(+), Sca-1(+) multipotent bone marrow stromal

178 ed by increased expression of PDGFR-alpha or PDGFR-beta in NSCLC cells.

179 one target of imatinib (KIT, PDGFR-alpha, or PDGFR-beta) was expressed in all tumors, and most tumors

180 ion in GSNOR(-/-) MSCs, whereas NO donors or PDGFR antagonist reduced tube formation approximately 50

181 purified from control SMC contained oxidized PDGFR-beta.

182 ding of PDGF-BB by cells containing oxidized PDGFR-beta was diminished by approximately 2-fold when c

183 te markers in carcinoma cells, in particular PDGFR-beta and N-cadherin, which enabled EMT cells to be

184 mical data together offer insights into PDGF-PDGFR signaling, as well as strategies for PDGF-antagoni

185 These results show that PDGF-PDGFR signaling influences at least the MSC in the micro

186 t that PVR arises at least in part from PDGF/PDGFR-driven events.

187 stimulation by HCMV, tyrosine-phosphorylated PDGFR-alpha associated with the p85 regulatory subunit o

188 A series of potent PDGFR inhibitors has been identified.

189 e shown that PDGF-D and its cognate receptor PDGFR-beta are expressed in prostate tumor tissues, sugg

190 atelet-derived growth factor-alpha receptor (PDGFR-alpha) is specifically phosphorylated by both labo

191 of platelet-derived growth factor receptor (PDGFR) alpha results in spina bifida, but the underlying

192 er, platelet derived growth factor receptor (PDGFR) alpha.

193 R), platelet-derived growth factor receptor (PDGFR) and integrins in multiple cell types including ne

194 as platelet derived growth factor receptor (PDGFR) and integrins is required for effective signal tr

195 een platelet-derived growth factor receptor (PDGFR) and serotonin signaling and investigate the PAH p

196 tes platelet-derived growth factor receptor (PDGFR) beta in a ligand-independent manner by transmembr

197 the platelet-derived growth factor receptor (PDGFR) family, as well as Src and Flt-3 kinases.

198 and platelet-derived growth factor receptor (PDGFR) kinases have been evaluated.

199 and platelet-derived growth factor receptor (PDGFR) kinases.

200 the platelet-derived growth factor receptor (PDGFR) pathway.

201 Platelet-derived growth factor receptor (PDGFR) senses extracellular growth factors and transfer

202 KIT/platelet-derived growth factor receptor (PDGFR) signal transduction pathway.

203 of platelet-derived growth factor receptor (PDGFR) signaling in CMPs.

204 and platelet-derived growth factor receptor (PDGFR) that generate oncogenic fusion tyrosine kinases (

205 the platelet-derived growth factor receptor (PDGFR), and ErbB4 significantly attenuates 5-HT(2A) rece

206 tor platelet derived growth factor receptor (PDGFR), is involved in vessel maturation, stimulation of

207 of platelet-derived growth factor receptor (PDGFR), PDGFRbetaIg, rapidly reversed diabetes.

208 gen platelet-derived growth factor receptor (PDGFR), thereby skewing the PI3K axis toward tumor cell

209 of platelet-derived growth factor receptor (PDGFR), which is known to participate in the development

210 and platelet-derived growth factor receptor (PDGFR), with broad-spectrum anticancer activity in precl

211 ugh platelet-derived growth factor receptor (PDGFR)-beta in associated mural cells.

212 BB)/platelet-derived growth factor receptor (PDGFR)-beta signaling.

213 ABL/platelet-derived growth factor receptor (PDGFR)-mutant models with mean 66.9% (range, 42.0%-87.6%

214 and platelet-derived growth factor receptor (PDGFR).

215 the platelet-derived growth factor receptor (PDGFR)A, although most overexpress KIT.

216 low platelet-derived growth factor receptor (PDGFR)alpha levels, whereas retrograde mutants exhibit n

217 ing platelet-derived growth factor receptor (PDGFR)alpha, MET, insulin receptor/insulin-like growth f

218 of platelet derived growth factor receptor (PDGFR)alpha, which is differentially expressed by OPCs.

219 and platelet-derived growth factor receptor (PDGFR)alpha.

220 of platelet-derived growth factor receptor (PDGFR)beta in development of epicardial-derived vascular

221 at it redirected ligand-bound PDGF receptor (PDGFR) from the clathrin-dependent endocytic pathway to

222 rbB ligand induction requires PDGF receptor (PDGFR) mediation and engages a positive autocrine/paracr

223 immunoblot studies to detect PDGF receptor (PDGFR) subtypes and (2) immunoprecipitation, immunoblot,

224 -derived growth factor (PDGF)/PDGF receptor (PDGFR) that regulates glycolysis in glioma-derived tumor

225 Phosphorylation of the PDGF receptor (PDGFR) was monitored by antiphosphotyrosine Western blot

226 th increased ERK1/2, Src, and PDGF receptor (PDGFR)beta phosphorylation, without altering total PDGFR

227 nd -D, whereas CAFs expressed PDGF receptor (PDGFR)beta.

228 telet-derived growth factor (PDGF) receptor (PDGFR) family of receptor tyrosine kinases (RTK) has bee

229 R], platelet-derived growth factor receptor [PDGFR], Flt3, and c-KIT).

230 rived growth factor (PDGF) and its receptor, PDGFR, promote fibrosis in systemic sclerosis (SSc; scle

231 through activation of PDGF-alpha receptors (PDGFR-alpha) on perivascular astrocytes, and treatment o

232 Platelet-derived growth factor receptors (PDGFR) alpha and beta have been suggested as potential t

233 nd platelet-derived growth factor receptors (PDGFR) in experimental sclerodermatous cGvHD.

234 elet-derived growth factor (PDGF) receptors (PDGFR) and their ligands play critical roles in several

235 growth factor (PDGF) ligands and receptors (PDGFRs) are commonly overexpressed in gliomas and initia

236 Platelet-derived growth factor receptors (PDGFRs) were selectively activated in MSCs by CLL-CM and

237 T, platelet-derived growth factor receptors (PDGFRs), and the discoidin domain receptor.

238 (PDGFs) and their tyrosine kinase receptors (PDGFRs) are known to play important roles during develop

239 Furthermore, PDGF receptors (PDGFRs) are present and activated in epiretinal membrane

240 elet-derived growth factor (PDGF) receptors (PDGFRs) are central to a spectrum of human diseases.

241 growth factors (PDGFs) and their receptors (PDGFRs) are prototypic growth factors and receptor tyros

242 growth factors (PDGFs) and their receptors (PDGFRs) make profound contributions to both physiology a

243 ast growth factor receptors, VEGF receptors, PDGFR-beta, and c-KIT, as second-line therapy both in pa

244 ibition with beta-aminopropionitrile reduces PDGFR-BB binding to cells and downstream signaling, as w

245 raising the possibility that ESDN regulates PDGFR processing.

246 ified Ig from these sera was shown to retain PDGFR binding activity and, at 200-1,000 microg/ml, exhi

247 We demonstrated that, among the common RTKs, PDGFR-alphabeta was specifically phosphorylated in FLS f

248 Furthermore, RGC-5 cells showed PDGFR-alpha/beta tyrosine phosphorylation that induced t

249 ated in cell survival and fate, specifically PDGFR, ERK, JAK STAT, MAPK, and TCR/NF-kappaB signaling;

250 ggest that, in response to PDGF stimulation, PDGFR activity is evenly distributed at different membra

251 nued exploration of the influence of stromal PDGFRs on sarcoma progression.

252 To study subcellular PDGFR activity at membrane microdomains, this PDGFR bios

253 Thrombin inhibition suppressed PDGFR-alpha activation and exogenous PDGF-AA increased P

254 However, the mechanisms of synergistic PDGFR/integrin signaling remain poorly understood.

255 for DSB repair whereby BCR-ABL, Tel-ABL, Tel-PDGFR, FLT3-ITD, and Jak2V617F all increase mutagenic re

256 immunoblotting and immunokinase assays that PDGFR-A and its downstream effectors, mitogen-activated

257 Our findings demonstrate that PDGFR is a critical RTK required for the prodestructive

258 As described herein, we have found that PDGFR-beta expression and activation increase dramatical

259 Taken together, these data indicate that PDGFR-alpha is a critical receptor required for HCMV inf

260 The PDGFR-selective inhibitor CP-673,451 regulated cell prol

261 focal amplification of the gene encoding the PDGFR ligand PDGFC was also detected, and silencing PDGF

262 Furthermore, the PDGFR-beta mRNA level in Daoy cells was significantly de

263 ermined the major G-quadruplex formed in the PDGFR-beta promoter.

264 dulation of MSCs by VEGF-A activation of the PDGFR and illustrate a paradoxical inhibitory role of S-

265 Compound 25 shows 24 h occupancy of the PDGFR kinase domain, after a single i.t. dose and has ef

266 ess, in both the absence and presence of the PDGFR transmembrane segment.

267 thelial cells in vitro via inhibition of the PDGFR-beta pathway.

268 The novel folding of the PDGFR-beta promoter G-quadruplex emphasizes the robustne

269 The novel folding of the PDGFR-beta promoter G-quadruplex may be attractive for s

270 Phosphorylated members of the PDGFR-beta-dependent signal transduction pathway, includ

271 n conclusion, our finding sheds light on the PDGFR signaling and endorses the possibility to employ m

272 e therapeutically exploited by targeting the PDGFR and FGFR1 pathways to block relapse and metastasis

273 The therapeutic interventions targeting the PDGFR-alpha signaling may be a novel strategy to prevent

274 Exposure of chick embryos to the PDGFR inhibitor imatinib mesylate resulted in spina bifi

275 When cells were treated with the PDGFR inhibitor AG1296 in addition to RA or D3, signs of

276 r astrocytes, and treatment of mice with the PDGFR-alpha antagonist imatinib after ischemic stroke re

277 DGFR activity at membrane microdomains, this PDGFR biosensor was further targeted in or outside lipid

278 the potent migratory factor PDGF-BB through PDGFR-beta.

279 nsfer (FRET), which can detect the real-time PDGFR activity in live cells with high spatiotemporal re

280 ients contained detectable autoantibodies to PDGFR, these antibodies were not specific to scleroderma

281 non-stem cells involves a shift from EGFR to PDGFR signaling and results in the PKCalpha-dependent ac

282 e show that bladder wall distension leads to PDGFR activation and identify thrombomodulin (TM) as an

283 The discovery of VEGF-PDGFRs binding challenges this paradigm and calls for in

284 SU14813, an anti-VEGFR, PDGFR-beta, KIT, and FLT3 inhibitor, was also assessed i

285 receptor tyrosine kinases EGFR, HGFR, VEGFR, PDGFR, NGFR and IGF1R, as well as interleukin-2 receptor

286 effective, whereas drugs that target VEGFRs, PDGFR and Tie2 (Linifanib and Cabozantinib) do regress t

287 +) progenitor cells, as well as in human WAT-PDGFR-alpha(+) adipocytes, supporting the physiological

288 beige phenotype in differentiated mouse WAT-PDGFR-alpha(+) progenitor cells, as well as in human WAT

289 After stimulation with PDGF, not only were PDGFR and ERK-1/2 phosphorylated to a greater extent, bu

290 tor must be used with caution in tumors when PDGFR is not the target on the tumor cell itself.

291 When PDGFRs are activated by PDGF, reactive oxygen species (R

292 Whereas PDGFRs are essential for TGFbeta-stimulated ErbB ligand

293 Cells in which PDGFR-alpha was genetically deleted or functionally bloc

294 ls initially enter the thymus at E13.5, with PDGFR-beta(+) mesenchymal cells following at E14.5.

295 a cell-autonomous manner, acting in cis with PDGFR-beta and TGF-beta receptors during induction/polar

296 und that wild-type LRP6 forms a complex with PDGFR-beta and enhances its lysosomal degradation, funct

297 GFR-integrin association by interacting with PDGFR and bridging the two receptors on the cell surface

298 HCMV glycoprotein B directly interacts with PDGFR-alpha, resulting in receptor tyrosine phosphorylat

299 Interference with PDGFR activation or PDGF neutralization inhibited invado

300 However, unlike WT PDGFR that is expressed on the surface of ligand-stimula