ライフサイエンスコーパス: PDGF

1 PDGF receptor alpha mRNA correlated with CCN2 and other

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

3 PDGF receptor beta-positive myofibroblasts isolated from

4 PDGF-alpha-syn transgenic (tg) male and female mice were

5 PDGF-CC neutralization had no effects on renal microvasc

6 PDGF-CC neutralization or deficiency was not associated

7 PDGF-DD engagement of NKp44 triggered NK cell secretion

8 nhibitor with an IC50 value of 0.02 muM in a PDGF-Rbeta enzymatic assay also showing activity against

9 Molecular modeling studies on a PDGF-Rbeta homology model using prediction of water ther

10 igration (IC(5)(0) congruent with 1 nM) to a PDGF gradient and reduced TNF-alpha-stimulated p65 trans

11 Using a PDGF-B-driven proneural glioma mouse model, we assessed

12 its ligand platelet-derived growth factor A (PDGF-A) are co-expressed in migrating cranial NC.

13 retion of platelet-derived growth factor AA (PDGF-AA).

14 adient of platelet-derived growth factor-AB (PDGF-AB) expedites migration through native tissue.

15 , or Notch1 and Notch2 receptors accelerates PDGF-driven glioma growth in mice.

16 Active PDGF-AA/alphaalpha signaling results in phosphorylation

17 nzymatic assay also showing activity against PDGF-R dependent cancer cells.

18 romising hit showing strong activity against PDGF-Rbeta in the kinase assay (IC50 = 0.5 muM).

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

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

21 n and inhibit senescence of MSCs; TNF-alpha, PDGF-beta, Wnt1, 4, 6, 7a and 10a, sFRP-3 and sFRP-5 are

22 actors, including IGF-1, FGF2, IL-1beta, and PDGF-A, was altered in TLR4-deficient injured spinal cor

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

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

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

26 rough a specific interaction between Apt and PDGF in a fashion of 2:1, leading to concentration of th

27 t, the controlled release of collagenase and PDGF-AB increases cellularity at the interface and withi

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

29 EGF (vascular endothelial growth factor) and PDGF (platelet derived growth factor).

30 mbrane proteins, and members of ERK, FGF and PDGF signaling pathways, which play key roles in glandul

31 GF and PDGF, we embed VEGF in fibrin gel and PDGF in a heparin-based coacervate that is distributed i

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

33 y between the serine protease matriptase and PDGF-D.

34 B:R2 KD = 110 pM, PDGF-BB:R2 KD = 40 nM, and PDGF-CC:R2 KD = 70 pM.

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

36 f pro-regenerative factors including OSM and PDGF-AA.

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

38 e collagenase (to increase ECM porosity) and PDGF-AB (to attract endogenous cells) in a localized and

39 Dexamethasone, VEGF and PDGF prevent the FBR, increase angiogenesis and promote

40 inase inhibitor which inhibits both VEGF and PDGF receptors.

41 he relative doses of dexamethasone, VEGF and PDGF were adjusted.

42 To achieve sequential release of VEGF and PDGF, we embed VEGF in fibrin gel and PDGF in a heparin-

43 7 following surgery, mean levels of VEGF and PDGF-BB at sites treated with PRGF and PRF were not sign

44 30 after therapy for evaluation of VEGF and PDGF-BB levels.

45 nhanced autocrine signaling through VEGF and PDGF.

46 beta antibody, iii) by administering an anti-PDGF-AB/BB aptamer, and iv) by using small chemical inhi

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

48 mTORC1 rescues PDGFRalpha levels as well as PDGF-AA-dependent phosphorylation of Akt(S473) and Akt(T

49 Because platelet-derived growth factor B (PDGF-B) signaling has a pivotal role in mesangial cell p

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

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

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

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

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

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

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

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

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

59 a], and platelet-derived growth factor-beta [PDGF-beta]) and blood-brain barrier (BBB) occludin and z

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

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

62 difference in capillary rarefaction between PDGF-CC-neutralized mice and mice with intact PDGF-CC.

63 The Apt/MBA-Au NPs bind PDGF through a specific interaction between Apt and PDGF

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

65 the level of cofactor activation: while both PDGF and FGF target gene promoters show enriched genome-

66 Furthermore, FGF promotes proliferation but PDGF favors differentiation.

67 When PDGFRs are activated by PDGF, reactive oxygen species (ROS) and Src family kinas

68 ts appropriate ligand-mediated activation by PDGF-AA.

69 gs indicate that apoptotic priming of CAF by PDGF occurs via Puma-mediated Bak activation, which can

70 iferation and its expression is decreased by PDGF-B.

71 tion and receptor expression is increased by PDGF-B.

72 This function is likely to be mediated by PDGF signaling.

73 nt malignant cell heterogeneity modulated by PDGF-DD signaling in pancreatic neuroendocrine tumors (P

74 h was delayed in the absence of signaling by PDGF-DD.

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

76 HSV carrying PDGF siRNA was established and intrathecally injected in

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

78 Sunitinib also inhibited chronic PDGF-A and -B and VEGF-A and -B expressions.

79 Conversely, continuous PDGF-B infusion in healthy rats induced DbpA expression

80 site through which matriptase can deactivate PDGF-D.

81 , we define a unique role for stroma-derived PDGF signaling in maintaining tumor homeostasis within t

82 Stromal-derived PDGF-CC was crucial for the recruitment and activation o

83 While it is widely believed that direct (PDGF-mediated) activation is the primary mode of activat

84 oskeleton and lamellipodium formation during PDGF stimulation.

85 We made similar observations with EGF, PDGF-AA, and PDGF-BB.

86 GFR activation loop that involved endogenous PDGF.

87 s (SFKs) act downstream of PDGFRs to enhance PDGF-mediated tyrosine phosphorylation of various signal

88 ference among these three TRMs (for example, PDGF increases fibrosis), the relative doses of dexameth

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

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

91 olled the dissemination of tumors expressing PDGF-DD more effectively than control mice, an effect en

92 yrosine kinase, PDGFRbeta, which facilitates PDGF ligand-dependent, ephrin ligand-independent activat

93 Platelet-derived growth factor (PDGF) acts through two conserved receptor tyrosine kinas

94 response to platelet-derived growth factor (PDGF) and fibroblast growth factor (FGF) signaling in mo

95 sion of both platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) is i

96 ride-induced platelet-derived growth factor (PDGF) and Wnt signaling pathways.

97 York, NY), a platelet-derived growth factor (PDGF) antagonist, administered in combination with the a

98 The Platelet Derived Growth Factor (PDGF) family of ligands have well established functions

99 Platelet-derived growth factor (PDGF) is a mitogen and chemoattractant for vascular smoo

100 tative being platelet-derived growth factor (PDGF) isoforms (PDGF-AA, -BB, and -AB), insulin-like gro

101 Platelet derived growth factor (PDGF) plays a pivotal role in the remodeling of connecti

102 l model of a platelet-derived growth factor (PDGF) protein and its DNA aptamer, which was selected in

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

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

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

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

107 to enhanced platelet-derived growth factor (PDGF) signaling are commonly observed in the proneural s

108 A) targeting platelet-derived growth factor (PDGF) was used to alleviate bone cancer pain.

109 Platelet-derived growth factor (PDGF), a potent mitogen for cells of mesenchymal origin,

110 gradient of platelet-derived growth factor (PDGF), together with other spatial cues.

111 In vitro platelet-derived growth factor (PDGF)- and tumor necrosis factor-alpha (TNF-alpha)-induc

112 , including platelet- derived growth factor (PDGF)-AA/alphaalpha, are linked to primary cilia.

113 we show that platelet-derived growth factor (PDGF)-B/PDGF receptor beta (PDGFRbeta) signalling is cri

114 Platelet-derived growth factor (PDGF)-BB belongs to a family of growth factors that regu

115 rand factor, platelet-derived growth factor (PDGF)-BB, angiopoietin-1, and lysyl oxidase-2 and the ce

116 treated with platelet-derived growth factor (PDGF)-BB.

117 ta 2 (FOG2), platelet-derived growth factor (PDGF)-beta, and phosphatidic acid phosphatase 2b (PPAP2B

118 e identified platelet-derived growth factor (PDGF)-CC as a potent profibrotic mediator in kidney fibr

119 r PDGFRbeta, platelet-derived growth factor (PDGF)-DD, opened the possibility of a previously unident

120 mors produce platelet-derived growth factor (PDGF)-DD, which promotes cellular proliferation, epithel

121 ivation in a platelet-derived growth factor (PDGF)-dependent manner.

122 nt two novel platelet-derived growth factor (PDGF)-driven mouse models of pediatric supratentorial HG

123 on basal and platelet-derived growth factor (PDGF)-induced proliferation and migration; and underlyin

124 es and mice, platelet-derived growth factor (PDGF)-like signaling induced mesencephalic astrocyte-der

125 gradients of platelet-derived growth factor (PDGF).

126 detection of platelet-derived growth factor (PDGF).

127 ombined VEGF/platelet-derived growth factor (PDGF)/FGF receptor inhibitors, paracrine ERK activation

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

129 that the presence of fibrotic growth factor, PDGF-AA, results in increased proliferation of PDGFRalph

130 Platelet-derived growth factors (PDGF) have an ambiguous role in this deleterious cascade

131 Platelet-derived growth factors (PDGFs) and their receptors (PDGFRs) make profound contri

132 We computationally predict that cross-family PDGF binding could contribute up to 96% of VEGFR2 ligati

133 (341)GR(343)A within the GFD is critical for PDGF-D deposition and binding to the ECM.

134 hese results show that CRMP2 is required for PDGF-directed cell migration in vitro.

135 ion, consistent with an instructive role for PDGF signaling.

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

137 Furthermore, 2 was shown to be selective for PDGF-Rbeta in a panel of 24 therapeutically relevant pro

138 f TGF-beta upregulated invadosome formation, PDGF-B mRNA expression, and phosphorylation of PDGFR.

139 ipitated Akt phosphorylation substrates from PDGF-AA-treated primary mouse embryonic palatal mesenchy

140 tly bound to and activated Usp1 Furthermore, PDGF-mediated expression of USP1 led to the stabilizatio

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

142 On one hand, PDGF may exert vascular stabilizing and antiapoptotic ac

143 osstalk in the heart; and on the other hand, PDGF signaling mediates neointimal formation and exacerb

144 However, PDGF-B/PDGFRbeta signalling is expendable for maintainin

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

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

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

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

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

150 sphatase inhibitor okadaic acid, implicating PDGF-induced activation of protein phosphatase 1 (PP1) i

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

152 c small interfering RNA induced apoptosis in PDGF-activated fibroblasts, but not in quiescent fibrobl

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

154 PC, insofar as mice genetically deficient in PDGF-CC phenocopied the glioma/vascular defects observed

155 a large (Bcl-xL) as a key survival factor in PDGF-activated human and mouse fibroblasts.

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

157 xpanding the range of proteins implicated in PDGF signalling pathways.

158 cytes, PI3Kalpha was selectively involved in PDGF-B expression, whereas both PI3Kalpha and PI3Kdelta

159 We found that Prx2 becomes oxidized in PDGF-treated fibroblasts, but only when TrxR1 has first

160 vity by ciliary transport plays key roles in PDGF-AA/alphaalpha signaling.

161 Heparin, which binds ligands including PDGF and SCF, and imatininib which blocks downstream tyr

162 However, both increased PDGF ligand abundance and enhanced PDGFRalpha pathway ac

163 r proneural glioblastoma featuring increased PDGF signaling.

164 ing regeneration, acts as a decoy to inhibit PDGF signalling and to prevent FAP over-activation.

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

166 Our results indicate that NOTCH2 inhibits PDGF-B-dependent proliferation and its expression is dec

167 DGF-CC-neutralized mice and mice with intact PDGF-CC.

168 In this study, we investigated PDGF-AA/alphaalpha signaling via P-Akt(T308) and P-Akt(S

169 telet-derived growth factor (PDGF) isoforms (PDGF-AA, -BB, and -AB), insulin-like growth factor bindi

170 Latent full-length PDGF-D (FL-D) consists of a CUB domain, a growth factor

171 factor receptor], in complex with its ligand PDGF-B.

172 rowth factor], sCD40L [soluble CD40 ligand], PDGF [platelet-derived growth factor], RANTES [regulated

173 ce plasmon resonance to identify and measure PDGF-to-VEGFR binding rates, establishing cut-offs for b

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

175 We discovered new PDGF:VEGFR2 interactions with PDGF-AA:R2 KD = 530 nM, PD

176 R2 interactions with PDGF-AA:R2 KD = 530 nM, PDGF-AB:R2 KD = 110 pM, PDGF-BB:R2 KD = 40 nM, and PDGF-

177 ors outside the PDGF family but little or no PDGFs, promoted formation of a unique SFK-PDGFRalpha com

178 Surprisingly, ablation of PDGF-DD did not affect the vasculature or stroma of PanN

179 This does not occur in the absence of PDGF or on uniformly coated fibronectin substrates.

180 reased Akt phosphorylation in the absence of PDGF-AA stimulation, which we show is due to impaired de

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

182 proteomics study, using a SILAC approach, of PDGF-stimulated mouse embryonic fibroblasts (MEFs).

183 signal of 4-MBA against the concentration of PDGF over 1-50 pM.

184 he biological function and ECM deposition of PDGF-D and provide molecular insight into the dynamic fu

185 ptase processing regulates the deposition of PDGF-D dimer species into the extracellular matrix (ECM)

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

187 nally, we demonstrate overlapping domains of PDGF-PI3K signaling and osteoblast differentiation in th

188 RhoG is activated by Trio downstream of PDGF in a PI3K- and Src-dependent manner.

189 s describe a signaling cascade downstream of PDGF that sustains proneural glioblastoma cells and sugg

190 gial cells confirmed a stimulatory effect of PDGF-B on DbpA transcript numbers and protein levels.

191 ration, we examined the regulatory effect of PDGF-B on DbpA.

192 Independent of the effect of PDGF-CC neutralization on renal fibrosis, we found no di

193 e is known about the downstream effectors of PDGF signaling in glioblastoma.

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

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

196 ing no significant pro-angiogenic effects of PDGF-CC during renal fibrosis.

197 ical perspective, the profibrotic effects of PDGF-CC outweigh the pro-angiogenic effects and, thus, d

198 The expression of PDGF-AA and BMP2 was positively regulated by the p38 MAP

199 cells, likely due to decreased expression of PDGF-AA and BMP2.

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

201 However, the precise function of PDGF-DD in tumor growth and invasion remains elusive.

202 Depletion of CRMP2 resulted in impairment of PDGF-mediated cell migration in an in vitro wound healin

203 Our data indicate that inhibition of PDGF signaling presents an attractive therapeutic approa

204 Inhibition of PDGF-A/PDGFRalpha blocks NC migration by inhibiting N-ca

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

206 Intrathecal injection of PDGF siRNA and morphine reversed thermal and mechanical

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

208 PDE levels of PDGF-AA, platelet glycoprotein VI, integrin-linked kinas

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

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

211 synoviocytes that involves the production of PDGF-B induced by TGF-beta.

212 Here we show that endothelial production of PDGF-CC during white adipose tissue (WAT) angiogenesis r

213 Thus, while cancer cell production of PDGF-DD supports tumor growth and stromal reaction, it c

214 b axis in osteoclasts, with the promoters of PDGF-AA and BMP2 having Creb binding sites.

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

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

217 The oncogenic roles of PDGF-D and its proteolytic activator, matriptase, have b

218 A distinctive transcriptional signature of PDGF-DD-induced cytokines and the downregulation of tumo

219 based on the published crystal structure of PDGF-B predicted that the matriptase cleavage site R(340

220 ults indicate that DbpA is a novel target of PDGF-B signaling and a key mediator of mesangial cell pr

221 do not limit a potential therapeutic use of PDGF-CC inhibition in renal fibrosis.

222 nderlying collagen and migrated dependent on PDGF or serum.

223 ing imaginal disc by activating the oncogene PDGF/VEGF-receptor (Pvr).

224 Among the PDGF-A-D isoforms, only PDGF-B was found both significantly elevated in FLS line

225 Interference with PDGFR activation or PDGF neutralization inhibited invadosome formation in RA

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

227 bone morphogenetic protein 4 (BMP4), EGF, or PDGF was unaffected by the TAT-SNX9 peptide.

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

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

230 genome-wide overlap with SRF ChIP-seq peaks, PDGF selectively activates a network of MRTF-dependent c

231 F-AA:R2 KD = 530 nM, PDGF-AB:R2 KD = 110 pM, PDGF-BB:R2 KD = 40 nM, and PDGF-CC:R2 KD = 70 pM.

232 GF receptor-alpha, suggesting that potential PDGF-CC effects would have to be indirect.

233 as a dominant-negative ligand that prevents PDGF-B-mediated beta-PDGF receptor activation in fibrobl

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

235 Our results lead us to propose PDGF-A/PDGFRalpha signalling as a tissue-autonomous regu

236 ive platelet-derived growth factor receptor (PDGF-R) beta-inhibitors.

237 binding, e.g., VEGFs bind to VEGF receptors, PDGFs bind to PDGF receptors, etc.

238 cells and innate lymphoid cells, recognizes PDGF-DD.

239 t of senescence-free wounds with recombinant PDGF-AA rescued the delayed wound closure and lack of my

240 which was recently identified as a requisite PDGF-gradient-sensing pathway, with the goal of identify

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

242 t once NC cells have undergone EMT, the same PDGF-A/PDGFRalpha works as an NC chemoattractant, guidin

243 vation, normal T cell expressed and secreted PDGF and RESISTIN.

244 only weakly amplifies signaling in a shallow PDGF gradient, but it synergizes with other feedback mec

245 has to be administered at higher doses than PDGF; c) an increase in dexamethasone dosing must be acc

246 These results demonstrate that PDGF siRNA can effectively treat pain induced by bone ca

247 parative transcriptomics, we determined that PDGF signaling upregulated ubiquitin-specific peptidase

248 Mechanistically, we found that PDGF signaling regulated the expression of the E2F trans

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

250 or stroma of PanNET; instead, we found that PDGF-DD stimulated bulk tumor cell proliferation by indu

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

252 We further show that PDGF-CC stimulation upregulates UCP1 expression and acqu

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

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

255 Our results suggest that PDGF-B signaling may play a role in endothelial and card

256 in zebrafish pdgfra mutants, suggesting that PDGF signaling steers cardiomyocytes toward the midline

257 The PDGF receptor tyrosine kinase inhibitor imatinib mesylat

258 Among the PDGF-A-D isoforms, only PDGF-B was found both significan

259 e (PD) that expresses GFP-ASYN driven by the PDGF-beta promoter, we investigated how accumulation of

260 us uncover a novel mode of signaling for the PDGF family during vertebrate development.

261 ngitudinal live imaging of the retina in the PDGF-alpha-syn::GFP mice might represent a useful, non-i

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

263 oma cells and suggest that inhibition of the PDGF-E2F-USP1-ID2 axis could serve as a therapeutic stra

264 s, which contains growth factors outside the PDGF family but little or no PDGFs, promoted formation o

265 onstrate that, after ligand stimulation, the PDGF beta receptor (PDGFRbeta) becomes ubiquitinated in

266 anNET characterized by signaling through the PDGF-DD/PDGFRbeta axis.

267 the FGF response is MEK dependent, while the PDGF response is PI3K dependent.

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

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

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

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

272 The results suggest that, in response to PDGF stimulation, PDGFR activity is evenly distributed a

273 gulated and 45 down-regulated in response to PDGF stimulation.

274 showed decreased P-Akt(S473) in response to PDGF-AA upon anterograde transport disruption.

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

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

277 PI3K/AKT signaling and dampened response to PDGF-induced mitochondrial fission and reactive oxygen s

278 Our results identify distinct responses to PDGF and FGF and provide insight into the mechanisms enc

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

280 s (PHH3(+) mitotic cells, YAP translocation, PDGF secretion) or increase collagen presence.

281 increase in P-Akt(S473) or P-Akt(T308) upon PDGF-AA stimulation.

282 increased toxicity reflective of known VEGF/PDGF inhibitory effects.

283 vation, and that combined inhibition of VEGF/PDGF/FGF receptors is sufficient to inhibit mitogenic si

284 erse events known to be associated with VEGF/PDGF inhibition.

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

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

287 FOG2 regulates VEGF expression, whereas PDGF-beta and PPAP2B regulate Akt activity.

288 sive capillary rarefaction, we asked whether PDGF-CC neutralization in fibrosis might have detrimenta

289 The mechanism by which PDGF regulates pain was also investigated by comparing t

290 discovered new PDGF:VEGFR2 interactions with PDGF-AA:R2 KD = 530 nM, PDGF-AB:R2 KD = 110 pM, PDGF-BB:

291 To interfere with PDGF-B signaling, we injected nephritic rats with PDGF-B

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

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

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

295 B signaling, we injected nephritic rats with PDGF-B neutralizing aptamers or the MEK/ERK inhibitor U0

296 In response to stimulation with PDGF, CRMP2 was dephosphorylated on Thr514, an event kno

297 In wild-type cells treated with PDGF-AA, c-Cbl becomes enriched in the cilium, and the r

298 -to-mesenchymal transition when treated with PDGF-BB and TGFbeta1, resulting in vascular SMCs that di

299 sis of muscles from the animals treated with PDGF-BB showed an increased population of satellite cell

300 pillary rarefaction in mice with and without PDGF-CC neutralization (using genetically deficient mice