ライフサイエンスコーパス: VEGF receptor

1 incorporate antiangiogenesis drugs targeting VEGF receptor.

2 gnificantly inhibited phosphorylation of the VEGF receptor.

3 otic and minimally angiogenic mechanisms via VEGF receptors.

4 F) signaling with activity against all three VEGF receptors.

5 n of microvessels, and altered expression of VEGF receptors.

6 -alpha also increased expression of VEGF and VEGF receptors.

7 py for tumors expressing different levels of VEGF receptors.

8 r the study of interactions between VEGF and VEGF receptors.

9 oplasmic staining for active, phosphorylated VEGF receptor 1 (pVEGFR1) and phosphorylated VEGF recept

10 mation and secreted higher levels of soluble VEGF receptor 1 (sFlt), an antagonizing factor to VEGF.

11 ss production of the VEGF-scavenging soluble VEGF receptor 1 (soluble fms-like tyrosine kinase 1; sFl

12 secrete high levels of a soluble form of the VEGF receptor 1 (sVEGFR-1), which neutralizes VEGF and i

13 rt, increases the expression of cell surface VEGF receptor 1 (VEGFR1) and VEGF receptor 2 (VEGFR2) by

14 sensitivity through selective activation of VEGF receptor 1 (VEGFR1) expressed in sensory neurons in

15 acizumab and growth factors, including VEGF, VEGF receptor 1 (VEGFR1), VEGFR2, Tie2, erythropoietin,

16 s role likely involves signaling mediated by VEGF receptor 1 (VEGFR1), which is highly expressed in e

17 fs120 tumor-bearing mice and a dependence on VEGF receptor 1 activity for metastasis to the lung, B20

18 -A) isoforms, expression of neuropilin-1 and VEGF receptor 1 in tumors or plasma, and genetic variant

19 but further demonstrate that VEGF and other VEGF receptor 1 ligands promote CNV-associated inflammat

20 Osteoblast differentiation was reduced when VEGF receptor 1 or 2 was knocked down but was unaffected

21 y, blockade of VEGF-A activity using soluble VEGF receptor 1 resulted in significantly lower levels o

22 This occurs via the reprogramming of VEGF receptor 1(+)/IL-1R1(+) cells to express hypoxia in

23 ugh interactions between bone marrow-derived VEGF receptor 1(+)/IL-1R1(+) immature myeloid cells and

24 addition of cediranib (an oral inhibitor of VEGF receptor 1, 2, and 3) to cisplatin and gemcitabine

25 , matrix metalloproteinase (MMP) -2, soluble VEGF receptor 1, stromal cell-derived factor-1alpha, and

26 but not of FMS-like tyrosine kinase 1 (FLT1)/VEGF receptor 1.

27 /kinase insert domain receptor (KDR) but not VEGF receptor 1/FLT1.

28 ses portions of the extracellular domains of VEGF receptors 1 and 2 and that binds all isoforms of VE

29 bind directly and with high affinity to both VEGF receptors 1 and 2, in a region that differs from VE

30 Regorafenib inhibits VEGF receptors 1, 2, and 3 and PDGF receptors like other

31 multitargeted kinase inhibitor that inhibits VEGF receptors 1, 2, and 3.

32 D34) and vascular endothelial growth factor (VEGF) receptors 1 and 2 was measured by fluorescence-act

33 bitor of vascular endothelial growth factor (VEGF) receptors 1, 2, and 3.

34 ors slowed tumor growth by secreting soluble VEGF receptor-1 (sVEGFR-1) that binds and inactivates VE

35 actor (GM-CSF) produce a soluble form of the VEGF receptor-1 (sVEGFR-1), which neutralizes VEGF biolo

36 eded by being bound to a soluble form of the VEGF receptor-1 (sVR-1).

37 ysiological function of heterodimers between VEGF receptor-1 (VEGFR-1; Flt-1) and VEGFR-2 (KDR; Flk-1

38 ar translocation of a C-terminal fragment of VEGF receptor-1 (VEGFR1) and (b) inhibition of VEGF-indu

39 vels, VEGF-A upregulation, decreased soluble VEGF receptor-1 (VEGFR1), and increased VEGFR2 phosphory

40 oth muscle cells, we observed stimulation of VEGF receptor-1 and fibroblast growth factor receptor-3.

41 nd showed that the motif Arg-Pro-Leu targets VEGF receptor-1 and neuropilin-1.

42 VEGF-A) and increased the mRNA expression of VEGF receptor-1 and placental growth factor (PLGF) in HE

43 -A), protein expression of neuropilin-1, and VEGF receptors-1 and -2 (VEGFR-1 and VEGFR-2).

44 e effects were observed with EE treatment in VEGF receptor 2 (Flk-1) knock-out mice.

45 mural-like tumor cells that strongly express VEGF receptor 2 (Flk-1).

46 VEGF receptor 1 (pVEGFR1) and phosphorylated VEGF receptor 2 (pVEGFR2), and by western blotting we fo

47 found that CCN1 activity is integrated with VEGF receptor 2 (VEGF-R2) activation and downstream sign

48 endothelial growth factor (VEGF)-A, -C, and VEGF receptor 2 (VEGF-R2) in VECs was assessed by real-t

49 -A and its family of receptors, particularly VEGF receptor 2 (VEGF-R2).

50 overexpression of the corresponding receptor VEGF receptor 2 (VEGFR-2) and local differences in endot

51 We found that it is complexed with VEGF receptor 2 (VEGFR-2) and maintains a basal expressi

52 00-b, a potential anti-angiogenic factor, on VEGF receptor 2 (VEGFR-2) expression and to determine th

53 tion of VEGF ligand on one of its receptors, VEGF receptor 2 (VEGFR-2).

54 ogenic action is mainly mediated through its VEGF receptor 2 (VEGFR-2).

55 ls, increased VEGF-A levels led to increased VEGF receptor 2 (VEGFR2) activation and subsequent alter

56 tudy, we investigated the effect of R-Ras on VEGF receptor 2 (VEGFR2) activation by VEGF, the key mec

57 levels of VEGF and expressed high levels of VEGF receptor 2 (VEGFR2) and its phosphorylated forms as

58 Furthermore, phosphorylation of VEGF receptor 2 (VEGFR2) and PDGF receptor-beta (PDGFR-b

59 alectin-1 prolongs cell-surface retention of VEGF receptor 2 (VEGFR2) and stimulates VEGF-independent

60 vascular endothelial growth factor (VEGF) to VEGF receptor 2 (VEGFR2) and that both VEGFR2 and an imm

61 ntivascular/antiangiogenic doses, of an anti-VEGF receptor 2 (VEGFR2) antibody results in a more homo

62 We show that tyrosine phosphorylation of VEGF receptor 2 (VEGFR2) at Y951 facilitates binding of

63 of cell surface VEGF receptor 1 (VEGFR1) and VEGF receptor 2 (VEGFR2) by translocating to the nuclei

64 a PDZ-dependent interaction between NRP1 and VEGF receptor 2 (VEGFR2) complex and synectin, which del

65 CM-immobilized VEGF can bind to and activate VEGF receptor 2 (VEGFR2) directly, with a different patt

66 This also acts on VEGF receptor 2 (VEGFR2) expressed in PD prolactin-produ

67 ponsive to VEGF, caused by downregulation of VEGF receptor 2 (VEGFR2) expression after reduced Vegfr2

68 Mechanistically, decorin interacted with VEGF receptor 2 (VEGFR2) in a region overlapping with it

69 er heightened when therapeutic inhibition of VEGF receptor 2 (VEGFR2) is utilized in combination with

70 othelial growth factor (VEGF) acting through VEGF receptor 2 (VEGFR2) on endothelial cells (ECs) is a

71 (VEGF) stimulates angiogenesis by binding to VEGF receptor 2 (VEGFR2) on endothelial cells (ECs).

72 cle-associated protein (GIV)/girdin mediates VEGF receptor 2 (VEGFR2) signaling and compensates for n

73 n consistently led to significantly impaired VEGF receptor 2 (VEGFR2) signaling and decreased levels

74 de cyclic stretch (18% CS) rapidly activates VEGF receptor 2 (VEGFR2) signaling by dissociating VEGFR

75 protracted autophagic program downstream of VEGF receptor 2 (VEGFR2) signaling that requires paterna

76 rough S1P receptors 1 and 3 (S1P1/S1P3), and VEGF receptor 2 (VEGFR2) stimulates migration.

77 4 knockdown inhibited VEGF signaling through VEGF receptor 2 (VEGFR2), Akt, and ERK pathways in lungs

78 inding of soluble and immobilized ligands to VEGF receptor 2 (VEGFR2), the endosomal trafficking of V

79 f angiogenesis and vascular permeability via VEGF receptor 2 (VEGFR2), whereas lymphangiogenesis sign

80 We report here that both VEGF receptor 2 (VEGFR2)-positive and -negative cells de

81 ity, and that this required signaling by the VEGF receptor 2 (VEGFR2).

82 n osteoblast differentiation are mediated by Vegf receptor 2 (Vegfr2).

83 Pharmacological inhibitors for VEGF receptor 2 and Akt/PKB as well as MG scavenger amin

84 d phosphorylation of proangiogenic mediators VEGF receptor 2 and endothelial nitric oxide synthase.

85 t was highly specific, as flow activation of VEGF receptor 2 and NF-kappaB was normal.

86 This effect correlates with reduced VEGF receptor 2 and PI3K/AKT signalling, and can be mimi

87 knockdown of TRIM28 inhibited expression of VEGF receptor 2 and suppressed VEGF-induced proliferatio

88 ious studies have demonstrated that blocking VEGF receptor 2 attenuates VEGFA-induced vascular permea

89 Re-expression of LKB1 or knockdown of VEGF receptor 2 decreased the overproliferation and -mig

90 Mechanistically, it increases VEGF receptor 2 expression both in vivo and in vitro and

91 ascular endothelial growth factor (VEGF) and VEGF receptor 2 expression were similar in both groups.

92 A-containing microparticles, which activated VEGF receptor 2 in ECs and largely mediated their proang

93 by retaining expression of TNFR-1 and -2 and VEGF receptor 2 in ECs.

94 ular permeability through phosphorylation of VEGF receptor 2 in glomerular endothelial cells, and rev

95 kinase insert domain protein receptor (KDR)/VEGF receptor 2 in these regions.

96 Interestingly, the ability of VEGF receptor 2 inhibition to antagonize filopodia forma

97 d hydrogen peroxide (H2O2), which attenuates VEGF receptor 2 phosphorylation and establishes a link f

98 l membrane by inhibiting IGF-1 signaling and VEGF receptor 2 phosphorylation.

99 eloid cells or pharmacological inhibition of VEGF receptor 2 signaling prevents this angiogenic respo

100 n into the retina through over-activation of VEGF receptor 2 signaling, the importance of targeting d

101 romoting decidual vascular expansion through VEGF receptor 2 signaling.

102 ly we found that ADAM17 is important for the VEGF receptor 2 stimulated processing of several recepto

103 Mechanistically, LECT2 reduced VEGF receptor 2 tyrosine phosphorylation and its downstr

104 e relationship between CHIP and VEGF-VEGFR2 (VEGF receptor 2) pathway in RCC.

105 mulates expression of Kdr, the gene encoding VEGF receptor 2, in murine embryonic gonads.

106 ation and protease production in vitro via a VEGF receptor 2-dependent mechanism.

107 e, pretreatment of mesenteric vessels with a VEGF receptor 2-neutralizing antibody significantly atte

108 ree receptor tyrosine kinases Axl, Tie2, and VEGF receptor 2.

109 genic response is abolished by inhibition of VEGF receptor 2.

110 herosclerosis: a regulatory role for soluble VEGF receptor 2.

111 ody that targets the extracellular domain of VEGF receptor 2.

112 r-1 receptor (IGF-1R) and the interaction of VEGF receptor 2/kinase insert domain receptor (VEGFR2/KD

113 Although vascular endothelial growth factor (VEGF) receptor 2 (VEGFR2) is traditionally regarded as a

114 and the vascular endothelial growth factor (VEGF) receptor 2 (VEGFR2) on endothelial cells.

115 ation of vascular endothelial growth factor (VEGF) receptor 2 and its downstream target Akt/protein k

116 nhibited vascular endothelial growth factor (VEGF) receptor 2-dependent vascularization of Matrigel p

117 ation of vascular endothelial growth factor (VEGF) receptor 2/kinase insert domain receptor (KDR) but

118 ed by endothelial cells can actually repress VEGF-receptor 2 (Flk-1) expression.

119 scular endothelial growth factor (VEGF), and VEGF receptor-2 (KDR/Flk-1), Peroxisome proliferator-act

120 VEGF receptor-2 (VEGFR-2 or kinase insert domain recepto

121 thelial growth factor A (VEGF-A) by way of a VEGF receptor-2 (VEGFR-2) primed activation of p38 MAPK.

122 ed vascular endothelial growth factor (VEGF)/VEGF receptor-2 (VEGFR-2) signaling by transcriptionally

123 VEGF specific binding to VEGF receptor-2 (VEGFR-2) triggers different signaling p

124 Upon VEGF-A-dependent activation of VEGF receptor-2 (VEGFR-2), and subsequent TSAd-mediated

125 ascular endothelial growth factor (VEGF) and VEGF receptor-2 (VEGFR-2)-mediated signalling and angiog

126 s by activating its receptor tyrosine kinase VEGF receptor-2 (VEGFR-2).

127 nesis is thought to be mediated primarily by VEGF receptor-2 (VEGFR-2).

128 lung cancer stem cell (CSC) self-renewal via VEGF receptor-2 (VEGFR-2)/STAT3-mediated upregulation of

129 more potent mechanism by which TSP1 inhibits VEGF receptor-2 (VEGFR2) activation through engaging its

130 receptors that mediate angiogenesis, such as VEGF receptor-2 (VEGFR2) and alpha(v)beta(3) integrin.

131 combination of a HER2 inhibitor with an anti-VEGF receptor-2 (VEGFR2) antibody significantly slows tu

132 tyrosine kinase inhibitors (TKI) that target VEGF receptor-2 (VEGFR2) have not been effective as adju

133 in adherens junctions, which is regulated by VEGF receptor-2 (VEGFR2) responses.

134 VEGFxxxa isoforms and decrease activation of VEGF receptor-2 (VEGFR2), hereunto considered the domina

135 showed that in vivo nephrin associates with VEGF receptor-2 (VEGFR2), the signaling receptor for VEG

136 ng a chimeric antigen receptor targeting the VEGF receptor-2 (VEGFR2; KDR) that is overexpressed on t

137 VEGF revealed differences in the kinetics of VEGF receptor-2 activation and endocytosis, downstream k

138 iogenic factor that triggers a novel mode of VEGF receptor-2 activation, promoting less vessel leakin

139 ascular endothelial growth factor-A (VEGF-A)/VEGF receptor-2 and activated protein C systems, among o

140 ietin-1 (VA1) chimeric protein bound to both VEGF receptor-2 and Tie2 and induced the activation of b

141 s a recombinant IgG1 monoclonal antibody and VEGF receptor-2 antagonist.

142 EGF accumulation in SKO mice with aggravated VEGF receptor-2 degradation and blunted in vivo signalin

143 inhibitory eNOS phosphorylation and enhanced VEGF receptor-2 degradation with attenuated VEGF signali

144 of cultured murine brown adipocytes and that VEGF receptor-2 is phosphorylated, indicating VEGF signa

145 VEGF receptor-2 signaling via the phosphoinositide-3-kin

146 VEGF and VEGF receptor-2-mediated angiogenesis contribute to hepa

147 ncreased vascular endothelial growth factor (VEGF) receptor-2 (VEGFR-2)-dependent proliferation and m

148 TIMP-3 on the phosphorylation status of the VEGF-receptor-2 (VEGFR-2) and the downstream signaling p

149 otype, with the expression of podoplanin and VEGF receptor 3 (VEGFR-3) but not of LYVE-1 and prospero

150 mbinant fibulin-3 also significantly reduced VEGF receptor 3 expression.

151 We also found elevated levels of VEGF receptor 3 together with reduced levels of ephrin-B

152 ed essential tip cell genes, including Dll4, VEGF receptor 3, and ephrin-B2, and stimulated VEGF resp

153 ion after periodontal infection, we used K14-VEGF receptor 3-Ig (K14) mice that lack lymphatics in gi

154 h factor-C (VEGF-C) and its cognate receptor VEGF receptor-3 (VEGFR3) in lymphatic endothelial cells

155 nfected explants, whereas VEGF-A and soluble VEGF receptor-3 increased in those infected with AD169.

156 e metastatic process and identify the VEGF-C/VEGF receptor-3 pathway as the target not only for preve

157 vascular endothelial growth factor (VEGF)-C/VEGF receptor-3 signaling in lymphangiogenesis, signific

158 b to be ineffective in blocking MV-dependent VEGF receptor activation.

159 ated fat pad neovascularization and restored VEGF receptor activation.

160 lator of vascular endothelial growth factor (VEGF) receptor activation.

161 Finally, chemical inhibition of VEGF receptor activity in zebrafish resulted in angiobla

162 cted with adenoviral vector encoding a decoy VEGF receptor (Ad-Flk) or a control adenovirus (Ad-C), a

163 t is distinct from the epitopes of a natural VEGF receptor and six different anti-VEGF Fabs.

164 Our data suggest that both the VEGF/VEGF receptor and the BMP9/ALK1 pathways are essential f

165 In endothelial cells (ECs), VEGF binds VEGF receptors and activates ERK1/2 through the phosphol

166 ents were found to induce phosphorylation of VEGF receptors and promote proangiogenic behavior in end

167 Our study aimed to determine to what extent VEGF receptors and their subtypes are expressed on selec

168 f EVs, called microvesicles (MVs), activates VEGF receptors and tumour angiogenesis through a unique

169 ting the vascular endothelial growth factor (VEGF) receptor and bevacizumab, a monoclonal antibody ta

170 ction as vascular endothelial growth factor (VEGF) receptors and contribute to the development of oth

171 through vascular endothelial growth factor (VEGF) receptors and the tyrosine kinase with IgG and EGF

172 del exhibited increased levels of cyclin D1, VEGF receptor, and Akt phosphorylation, and divided sign

173 d vascular endothelial growth factor (VEGF), VEGF receptor, and CD34/CD31 (hematopoietic progenitor c

174 DPSCs resulted in down-regulation of Vegfa, Vegf receptors, and EphrinB2 and decreased angiogenic in

175 ications for the use of VEGF antagonists and VEGF receptor antagonists in patients for which inhibiti

176 hat drugs targeting extracellular domains of VEGF receptors are active, affect signal transduction, a

177 nt, showing a lower IC50 than aflibercept in VEGF receptor binding assays (RBAs) and retaining activi

178 ranibizumab for VEGF binding, inhibition of VEGF receptor binding assays (RBAs), and VEGF-driven in

179 ion protein with binding domains from native VEGF receptors, binds VEGF-A, VEGF-B, and placental grow

180 d in rats with neointima formation following VEGF receptor blockade and chronic hypoxia.

181 Vascular endothelial growth factor (VEGF) receptor blockade, which resulted in EC hyperproli

182 that binding of immobilized growth factor to VEGF receptors, both on endothelial cells and soluble VE

183 ealed that quininib does not directly target VEGF receptors but antagonizes cysteinyl leukotriene rec

184 All cells expressed tyrosine kinase VEGF receptors, but these were not active/activatable su

185 luence molecular interactions of VEGF-D with VEGF receptors, co-receptors, and heparin, and its effec

186 nd VEGF(121), suggesting that the functional VEGF receptor complex contains heparan sulfate.

187 speridone, and of kinase drugs targeting the VEGF receptor, demonstrates how underlying molecular mec

188 hanism of VEGF-A action via interaction with VEGF receptors does not mediate these events, as these c

189 e some PVR-associated cellular responses via VEGF receptors expressed on the retinal pigment epitheli

190 t partly by increasing endothelial cell VEGF/VEGF receptor expression through PI3K/Akt and Erk/MAPK p

191 reatment shows a nonlinear dependence on the VEGF receptor expression.

192 eedback loop regulating E2F1 acetylation and VEGF receptor expression.

193 This effect was blocked by inhibitors of the VEGF receptor flk-1 and Src kinase, but not by inhibitor

194 in RVD, restoring expression levels of VEGF, VEGF receptor Flk-1, and downstream angiogenic mediators

195 This response depends on expression of the VEGF receptor Flk1, driven by Fli1 and Gata2.

196 abducens internuclear neurons expressed the VEGF receptor Flk1.

197 cking the activity of the mesoderm-localized VEGF receptor, FLK1, recapitulates both the mesoderm and

198 sflt1), an alternatively spliced form of the VEGF receptor Flt1 encoding a potent secreted decoy.

199 tylation of histones and E2F1; this required VEGF receptor function, as seen in ChIP-re-ChIP experime

200 1, and fms-related tyrosine kinase 1/soluble VEGF receptor genes were upregulated five-, seven-, and

201 rosine kinase inhibitors and a soluble decoy VEGF receptor have demonstrated nominal benefit among pa

202 hat it occurs independently of KDR, the main VEGF receptor in blood vessels.

203 VEGF) antibody, and secretoneurin stimulated VEGF receptors in these cells.

204 express vascular endothelial growth factor (VEGF) receptors, including neuropilins (NRPs), which reg

205 bitor of vascular endothelial growth factor (VEGF) receptors, inhibited proliferation of GBM cells th

206 elops in response to either monocrotaline or VEGF receptor inhibition combined with chronic hypoxia.

207 urbed vascular normalization associated with VEGF receptor inhibition.

208 tance to vascular endothelial growth factor (VEGF) receptor inhibition is caused by hypoxia-driven re

209 ith either a c-Met inhibitor (PHA-665752) or VEGF receptor inhibitor (semaxanib) and compared with sh

210 formation was not only resistant to an anti-VEGF receptor inhibitor in mouse GBMs but it led to an i

211 ompare the mTOR inhibitor everolimus and the VEGF receptor inhibitor sunitinib in patients with non-c

212 VEGF) receptors, with sorafenib, an approved VEGF receptor inhibitor, as second-line therapy in patie

213 f tumor perfusion as early as 5 days in both VEGF receptor inhibitor-naive and -refractory patients.

214 Unexpectedly, we found that VEGF receptor inhibitors blocked both innate immune cell

215 dual EGFR and HER2 inhibitors, other VEGF or VEGF-receptor inhibitors, and agents that alter crucial

216 that the vascular endothelial growth factor (VEGF) receptor KDR is expressed on subsets of mitogen-ac

217 , VEGFA, vascular endothelial growth factor (VEGF) receptor KDR, and genes involved in angiogenesis (

218 g of the endoglin and VEGF pathway, with the VEGF receptor kinase inhibitor SU5416, increased antiang

219 melanoma model with acquired resistance to a VEGF receptor kinase inhibitor, anti-ALK1 also delayed t

220 elet-derived growth factor receptor beta and VEGF receptors, known in vivo targets of sorafenib.

221 lation of Akt serine-473 phosphorylation and VEGF receptor levels.

222 ote cell growth through interaction with the VEGF receptor neuropilin-1 (NRP-1).

223 ciated with both beta1 integrin and the main VEGF receptor on ECs, VEGFR2.

224 omplexes that together activate integrin and VEGF receptors on adjacent endothelial cells thereby sti

225 F-induced VEGFR-2 signaling without altering VEGF receptor or neuropilin expression.

226 s VEGF-stimulated permeability downstream of VEGF receptor or Src tyrosine kinase activation in vivo.

227 ay for genetic interactions between the Vegf/Vegf-receptor pathway and SoxF transcription factors and

228 bitor of fibroblast growth factor receptors, VEGF receptors, PDGFR-beta, and c-KIT, as second-line th

229 ligand-receptor binding, e.g., VEGFs bind to VEGF receptors, PDGFs bind to PDGF receptors, etc.

230 ed that both the bone marrow vasculature and VEGF receptor-positive hematopoietic cells could be impa

231 maginal disc by activating the oncogene PDGF/VEGF-receptor (Pvr).

232 In vivo molecular imaging revealed higher VEGF receptor (R)-2 in angiogenic tips compared with nor

233 Soluble VEGF receptors R1 and R2 were detected in all samples wi

234 an sulfate suggested that it interacted with VEGF receptors rather than the ligand.

235 Tivozanib, a pan-inhibitor of VEGF receptors, reduced proliferation of the chemoresist

236 In this study, we uncovered the PDGF- and VEGF-receptor related (Pvr) pathway as an essential regu

237 The PDGF/VEGF-receptor related (Pvr) protein is implicated in the

238 ursal injection of axitinib, an inhibitor of VEGF receptors, retarded neo-angiogenesis that was assoc

239 were treated over a range of doses with the VEGF receptor-selective tyrosine kinase inhibitors axiti

240 f vascular endothelial growth factor (VEGF), VEGF receptors, semaphorin 3F, neuropilin 1, neuropilin

241 n smaller blood vessels in zebrafish via the VEGF receptor signaling cascade, thereby describing a ne

242 on of FGF2/FGF receptor (FGFR) and VEGF(165)/VEGF receptor signaling complexes.

243 by integrating the insulin-mediated and PDGF-VEGF receptor signaling pathways.

244 unlike other anticancer agents that inhibit VEGF receptor signaling, PT2385 exhibited no adverse eff

245 ha is a previously unidentified component of VEGF receptors signaling.

246 lated by vascular endothelial growth factor (VEGF) receptor signaling.

247 signaling utilizes Pvr (the Drosophila PDGF/VEGF receptor), STAT92E, and adenosine deaminase-related

248 inhibition of signaling events triggered by VEGF-receptor stimulation that are upstream of c-kit act

249 secrete high levels of a soluble form of the VEGF receptor (sVEGFR-1), which neutralizes VEGF and inh

250 receptor 2 (VEGFR2), the primary functional VEGF receptor that mediates endothelial cell vasculariza

251 -869 resulted in decreased activation of the VEGF receptor, the epidermal growth factor receptor and

252 cy, and so their responsiveness to anti-VEGF/VEGF receptor therapy.

253 ted expression of VEGF and activation of the VEGF receptor through phosphorylation promoted an increa

254 scriptional activity, secretion of VEGF, and VEGF receptor type 2 phosphorylation and down-regulated

255 owth but requires the activation of multiple VEGF receptor types.

256 Inhibition of VEGF receptor tyrosine kinase (axitinib, 4 mg/kg/d, 14 d

257 M patients who had been treated with the pan-VEGF receptor tyrosine kinase inhibitor cediranib versus

258 hanisms of nGBM response to cediranib, a pan-VEGF receptor tyrosine kinase inhibitor, using MRI techn

259 Cediranib, an oral pan-VEGF receptor tyrosine kinase inhibitor, was administere

260 e undergoing treatment with cediranib, a pan-VEGF receptor tyrosine kinase inhibitor.

261 As a class, VEGF receptor tyrosine kinase inhibitors (VEGFR TKIs) ha

262 Adjuvant treatment with the VEGF receptor tyrosine kinase inhibitors sorafenib or su

263 oral pan-vascular endothelial growth factor (VEGF) receptor tyrosine kinase inhibitor, either as mono

264 Several vascular endothelial growth factor (VEGF) receptor tyrosine kinase inhibitors and a soluble

265 VEGF directly stimulates VEGF-receptor tyrosine kinases on endothelial cell surfa

266 with the vascular endothelial growth factor (VEGF) receptor, VEGF-R2, is important for maintaining th

267 as suppressed by neutralizing antibodies for VEGF receptor (VEGFR) 1 and 2 or neuropilin receptor 1 o

268 anti-angiogenic agent with activity against VEGF receptor (VEGFR) 1, VEGFR2, and VEGFR3.

269 nalysis demonstrated increased expression of VEGF receptor (VEGFR) 2 as well as VEGF signaling molecu

270 in vascular endothelial growth factor (VEGF)/VEGF receptor (VEGFR) 2 pathways, despite similar Vegfa

271 The role of CD34(+)/VEGF receptor (VEGFR) 2(+) progenitor cells (PCs) in vas

272 Anti-VEGF/VEGF receptor (VEGFR) drugs treat cancer, but the underl

273 Angiogenesis inhibitors that block VEGF receptor (VEGFR) signaling slow the growth of many

274 in vivo Moreover, EPAC activation inhibited VEGF receptor (VEGFR) signaling through the Ras/MEK/ERK

275 n-2 (Ang-2) compromises the benefits of anti-VEGF receptor (VEGFR) treatment in murine GBM models and

276 shed to determine whether the high levels of VEGF receptor (VEGFR) within the tumor vasculature could

277 er square millimeter and mRNA expression for VEGF receptor (VEGFR)-1 (P = 0.04 and P < 0.001) and VEG

278 en vascular endothelial growth factor (VEGF)/VEGF receptor (VEGFR)-1 autocrine loop modulating hypoxi

279 A subpopulation of CD3+ T cells expressed VEGF receptor (VEGFR)-1 by immunostaining and FACS analy

280 ial growth factor (VEGF)-B selectively binds VEGF receptor (VEGFR)-1, a receptor that does not mediat

281 equirements for heparin/HS interactions with VEGF receptor (VEGFR)-1, NRP-1, and VEGF165 in complex w

282 re potentiated by decreased transcription of VEGF receptor (VEGFR)-2 and neuropilin (NRP)-1, the prim

283 and lymphangiogenesis through signaling via VEGF receptor (VEGFR)-2 and VEGFR-3, respectively.

284 systemic delivery of an anti-VEGF or an anti-VEGF receptor (VEGFR)-2 neutralizing antibody caused glo

285 ion and biological significance of the VEGFC/VEGF receptor (VEGFR)-3 pathway in ovarian cancer growth

286 dynes/cm(2) at 1 Hz), whereas expression of VEGF receptors (VEGFR-1, VEGFR-2, or NRP1) is unaffected

287 The effect of VEGF, PLGF, and VEGF-receptor (VEGFR) activation on BBB permeability was

288 duce VEGF-C signals: neuropilin-2 (Nrp2) and VEGF-receptor (VEGFR)-2/3.

289 xia-induced VEGF and increased levels of the VEGF receptor VEGFR1 in the tumor stroma, decreased leve

290 Notably, RNAi-mediated depletion of VEGF receptor VEGFR1/FLT1 replicated the effects of VEGF

291 D (FIGF), and placental growth factor (PGF); VEGF receptors VEGFR1 (FLT1), VEGFR2 (KDR), and VEGFR3 (

292 VEGF receptors VEGFR1, VEGFR2 and Neuropilin-1 (NRP1) ar

293 tion in situ between heparan sulfate and the VEGF receptor, VEGFR2.

294 ave been developed to target EGFR, VEGF, and VEGF receptors (VEGFRs) and are important additions to C

295 elial growth factor (VEGF) that can activate VEGF receptors (VEGFRs) on or within tumor cells to prom

296 domain, that contains the binding sites for VEGF receptors (VEGFRs), but their biological functions

297 Activation of VEGF receptors (VEGFRs), phosphoinositol 3-kinase (PI-3K

298 s, but VEGFA was lower and the high-affinity VEGF receptor was higher in IUGR islets and ECs, respect

299 Most orbital vascular lesions express VEGF receptors, which may suggest a future target for no

300 bitor of vascular endothelial growth factor (VEGF) receptors, with sorafenib, an approved VEGF recept