ライフサイエンスコーパス: VEGF receptor

1 gnificantly inhibited phosphorylation of the VEGF receptor.

2 incorporate antiangiogenesis drugs targeting VEGF receptor.

3 oma has been revolutionised by inhibitors of VEGF receptor.

4 otic and minimally angiogenic mechanisms via VEGF receptors.

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

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

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

8 py for tumors expressing different levels of VEGF receptors.

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

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

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

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

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

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

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

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

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

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

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

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

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

24 negative regulator of angiogenesis, soluble VEGF receptor 1, compared with the untreated mice.

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

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

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

28 ib is an oral antiangiogenic agent targeting VEGF receptors 1, 2, and 3, platelet-derived growth fact

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

30 Nintedanib targets VEGF receptors 1-3, PDGF receptors alpha and beta, FGF r

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

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

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

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

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

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

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

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

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

40 VEGF receptor-1 modulates amyloid beta 1-42 oligomer-ind

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

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

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

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

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

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

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

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

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

50 00-b, a potential anti-angiogenic factor, on VEGF receptor 2 (VEGFR-2) expression and to determine th

51 ascular endothelial growth factor A (VEGF-A)/VEGF receptor 2 (VEGFR-2) signaling pathway mediates lym

52 VEGF and VEGF receptor 2 (VEGFR-2)-mediated signalling and angiog

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

54 tion of VEGF ligand on one of its receptors, 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 ascular endothelial growth factor-A (VEGF-A)/VEGF receptor 2 (VEGFR2) pathway.

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

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

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

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

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

78 4 knockdown inhibited VEGF signaling through VEGF receptor 2 (VEGFR2), Akt, and ERK pathways in lungs

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

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

81 models representing different steps in VEGFA/VEGF receptor 2 (VEGFR2)-induced vascular permeability,

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

83 lial cadherin (VE-cadherin), which increases VEGF receptor 2 (VEGFR2)-Src-VE-cadherin complex formati

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

85 iates most of its angiogenic effects through VEGF receptor 2 (VEGFR2).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

102 ascular endothelial growth factor (VEGF) and VEGF receptor 2 protein were diminished substantially on

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

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

105 romoting decidual vascular expansion through VEGF receptor 2 signaling.

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

107 argeting VEGF signaling with an anti-VEGFR2 (VEGF receptor 2) antibody.

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

109 locks its binding to its signaling receptor, VEGF receptor 2, and is used to treat patients with a va

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

111 odestly enhanced tyrosine phosphorylation of VEGF receptor 2, promotion of vascular permeability by A

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

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

114 ctor (Vegf) receptor 3 signaling, but not on Vegf receptor 2.

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

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

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

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

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

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

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

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

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

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

125 Using a Vegf-receptor 2 (VegfR2) inhibitor (cabozantinib; CBZ) v

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

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

128 dence suggests that simultaneous blockade of VEGF receptor-2 (VEGFR-2) and PD-1 or PD-L1 enhances ant

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

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

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

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

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

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

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

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

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

138 VEGF signaling via VEGF receptor-2 (VEGFR2) is a major regulator of endothe

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

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

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

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

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

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

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

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

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

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

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

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

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

152 cts with vascular endothelial growth factor (VEGF) receptor-2 and activates the downstream signaling

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

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

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

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

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

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

159 ndent on vascular endothelial growth factor (Vegf) receptor 3 signaling, but not on Vegf receptor 2.

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

161 Interference with VEGF receptor-3 and LTbeta receptor signaling pathways a

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

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

164 ated fat pad neovascularization and restored VEGF receptor activation.

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

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

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

168 velopment of diabetic nephropathy, prevented VEGF receptor alterations in the diabetic glomerulus, an

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

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

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

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

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

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

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

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

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

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

179 1 (rAAV.sFLT-1), the extracellular domain of VEGF receptor, and analyzed the morphology and functions

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

181 ated analysis identified the PI3K/mTOR, VEGF/VEGF receptor, and HDAC6/HSP90 pathways as specific vuln

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

183 very of BMP2 and soluble VEGFR1 (sVEGFR1), a VEGF receptor antagonist, in a hydrogel skewed different

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

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

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

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

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

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

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

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

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

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

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

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

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

197 fenestrations and protected against altered VEGF receptor expression.

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

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

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

201 abducens internuclear neurons expressed the VEGF receptor Flk1.

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

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

204 1, and fms-related tyrosine kinase 1/soluble VEGF receptor genes were upregulated five-, seven-, and

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

206 FA mRNA expression, yet increased glomerular VEGF receptor heterodimerization, indicating differentia

207 genesis-associated factors, i.e. CD31, VEGF, VEGF receptor II, phosphor-ERK and HIF-1alpha.

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

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

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

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

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

213 urbed vascular normalization associated with VEGF receptor inhibition.

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

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

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

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

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

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

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

221 nib, a tyrosine kinase inhibitor that blocks VEGF receptors, into a non-inflammatory biodegradable po

222 icate that tyrosine kinase inhibition of the VEGF receptors is preferentially associated with glomeru

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

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

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

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

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

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

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

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

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

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

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

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

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

236 We demonstrated that the RTK PDGF/VEGF receptor (Pvr) and its ligands (Pvfs 2 and 3) are r

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

254 -869 resulted in decreased activation of the VEGF receptor, the epidermal growth factor receptor and

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

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

257 Pharmacological inhibition of VEGF receptor Type 2 (VEGFR-2) signaling attenuated mech

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

259 Importantly, pharmacological inhibition of VEGF receptor Type 2 signaling in rats causes analgesia

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

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

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

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

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

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

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

267 We aimed to assess the activity of the VEGF receptor tyrosine-kinase inhibitor axitinib plus th

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

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

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

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

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

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

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

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

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

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

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

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

280 studies have suggested that treatment with a VEGF receptor (VEGFR) tyrosine kinase inhibitor might be

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

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

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

284 derm-derived VEGF3 and its cognate receptor, VEGF receptor (VEGFR)-10-Ig, is also essential for the d

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

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

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

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

289 VEGF receptor (VEGFR)1 or VEGFR2 blockade prevented the

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

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

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

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

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

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

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

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

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