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 signaling may contribute to BBB impairment v

7 PDGFR-alpha suppression prevented neurological deficits,

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

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

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

11 PDGFR-beta inhibition selectively eliminates morphine to

12 PDGFR-beta inhibitors are widely used and well tolerated

13 PDGFR-beta promotes growth of mesenchymal cells, includi

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

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

16 Both a PDGFR inhibitor (CP-673451) and a Wnt/ beta-catenin inhi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

39 expression and inhibition of SDF-1/CXCR4 and PDGFR pathways blocks distant metastasis of human PD/S-S

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

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

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

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

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

45 3 as well as inhibition of PI3K, mTORC2, and PDGFR abrogated the induction of GLS1 by TGF-beta.

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 gulation of differentiation pathways such as PDGFR signaling.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

83 s indicate that functional crosstalk between PDGFR/SDF-1 signaling regulates tumor cell invasion and

84 These data show that both PDGFRs are cell-autonomous inhibitors of adipocyte diffe

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

86 transforming potential that was reversed by PDGFR blockade.

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

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

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

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

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

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

93 ing CDRs as a robust visual readout of early PDGFR signaling, we have identified several contradictor

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

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

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

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

98 an adult epicardial-derived cells expressing PDGFR (platelet-derived growth factor receptor)-alpha we

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

100 addition to the widely accepted function for PDGFR-beta in CDR formation, PDGFR-alpha is also clearly

101 ed function for PDGFR-beta in CDR formation, PDGFR-alpha is also clearly capable of eliciting CDRs.

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

103 Furthermore, PDGFR regulates SDF-1 expression and inhibition of SDF-1

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

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

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

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

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

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

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

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

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

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

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

115 Western blot analysis of immunoprecipitated PDGFRs.

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

117 rmined the NMR structure of the dGMP-fill-in PDGFR-beta vG4 in K(+) solution.

118 The G-quadruplexes (G4s) formed in PDGFR-beta gene promoter are transcriptional modulators

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

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

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

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

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

124 tilbene resveratrol targets PTP1B to inhibit PDGFR mitogenic signaling.

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

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

127 observed after other types of liver injury, PDGFR-alpha loss in HSCs led to a significant albeit tra

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

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

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

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

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

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

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

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

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

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

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

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 PDGF-AB ligand in the vigorous activation of PDGFR-beta homodimers to produce CDRs.

144 f PTP1B, leading to pronounced activation of PDGFR.

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

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

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

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

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

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

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

152 Aberrant expression of PDGFR-beta is associated with a number of diseases.

153 fate that could be reversed by inhibition of PDGFR activity.

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

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

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

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

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 r our findings support a profibrotic role of PDGFR-alpha in HSCs during chronic liver injury in vivo

170 To examine the role of PDGFR-alpha in HSCs, Lrat-Cre recombinase and Pdgfra-flo

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

172 ous experimental design in future studies of PDGFR signaling and its contributions to development and

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

174 hich are required for enduring activation of PDGFRs.

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

176 promotes fibrosis; however, the function of PDGFRs in APs remains unclear.

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

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

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

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

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

182 advanced SCCs, and suggest that CXCR4 and/or PDGFR inhibitors could be used to block metastasis of th

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

184 purified from control SMC contained oxidized PDGFR-beta.

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

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

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

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

189 A series of potent PDGFR inhibitors has been identified.

190 derived growth factor receptor-like protein (PDGFR) alpha and beta, and c-KIT tyrosine kinases.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

205 Platelet Derived Growth Factor Receptor (PDGFR) signaling is a central mitogenic pathway in devel

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

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

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

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

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

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

212 Platelet-derived growth factor receptor (PDGFR)-alpha plays roles in cell survival, proliferation

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

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

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

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

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

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

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

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

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

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

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

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

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

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

229 the platelet-derived growth factor receptor(PDGFR)-beta signaling system is both necessary and suffi

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

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

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

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

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

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

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

237 ss platelet-derived growth factor receptors (PDGFRs), PDGFRalpha and PDGFRbeta.

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 29 family members, which, in turn, repressed PDGFR expression to promote dedifferentiation of wild-ty

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

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

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

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

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

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

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

261 Importantly, the PDGFR-specific inhibitor crenolanib significantly reduce

262 The major G4 formed in the PDGFR-beta gene promoter was previously shown to have a

263 ium of 3'- and 5'-end vG4s is present in the PDGFR-beta promoter sequence, and dGMP favors the 5'-end

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

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

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

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

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

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

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

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

272 e rational design of ligands that target the PDGFR-beta vG4.

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

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

275 Herein, we report that the PDGFR-beta gene promoter sequence forms a vacancy G-quad

276 administering morphine or fentanyl with the PDGFR-beta inhibitor imatinib.

277 dation for the future testing of therapeutic PDGFR-alpha inhibition in hepatic fibrosis, especially i

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

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

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

281 pro-fibrogenic pathways including TNFRSF12A, PDGFR and NOTCH signalling.

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

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

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

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

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

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

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

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

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

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

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

293 Whereas PDGFRs are essential for TGFbeta-stimulated ErbB ligand

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

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

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

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

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

299 Interference with PDGFR activation or PDGF neutralization inhibited invado

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