ライフサイエンスコーパス: VEGFR-2

1 nd on one of its receptors, VEGF receptor 2 (VEGFR-2).

2 -1, and VEGF receptors-1 and -2 (VEGFR-1 and VEGFR-2).

3 scular Endothelial Growth factor Receptor-2 (VEGFR-2).

4 ts receptor tyrosine kinase VEGF receptor-2 (VEGFR-2).

5 to be mediated primarily by VEGF receptor-2 (VEGFR-2).

6 l cells (GEnC) that express VEGF receptor-2 (VEGFR-2).

7 mainly mediated through its VEGF receptor 2 (VEGFR-2).

8 y blocking VEGF-C-induced phosphorylation of VEGFR-2.

9 essential for VEGF to recognize and activate VEGFR-2.

10 anomolar inhibition of enzymatic activity of VEGFR-2.

11 rough PKA/p38 MAPK controls the stability of VEGFR-2.

12 mimic the VEGF-binding site to its receptor VEGFR-2.

13 er1191 is required for the ubiquitination of VEGFR-2.

14 9, and its phosphorylation requires Y1173 of VEGFR-2.

15 diates the ubiquitination and degradation of VEGFR-2.

16 not levels of NRP2, gp130, CD31, VEGFR-1, or VEGFR-2.

17 elial growth factor (VEGF) and its receptor, VEGFR-2.

18 98), is required for binding VEGFR-3 but not VEGFR-2.

19 ctions with its major receptors, VEGFR-1 and VEGFR-2.

20 crine growth in melanoma is mediated through VEGFR-2.

21 animals, we found markedly increased soluble VEGFR-2.

22 phosphorylation of key tyrosine residues in VEGFR-2.

23 ween the level of expression of miR200-b and VEGFR-2.

24 enable the selective imaging of VEGFR-1 and VEGFR-2.

25 ody that targets the extracellular domain of VEGFR-2.

26 was obtained by targeting both Tie1 and VEGF/VEGFR-2.

27 after infection was reduced 68% by blocking VEGFR-2, 83% by blocking VEGFR-3, and 99% by blocking bo

28 scular endothelial growth factor receptor 2 (VEGFR-2), a potent angiogenic receptor tyrosine kinase,

29 Upregulation of VEGFR-2 abundance at the protein level contributes in pa

30 , tip cell formation, vascular permeability, VEGFR-2 accumulation, and Akt phosphorylation could be p

31 ration, we observed reduced endothelial cell VEGFR-2 activation and a concomitant increase in BMP4 ex

32 an in sparse cells; (2) cell density affects VEGFR-2 activation by reducing its affinity for VEGF in

33 inhibition of melanoma by blocking autocrine VEGFR-2 activation, and (c) a possible therapeutic role

34 mic signaling proteins that are activated by VEGFR-2, activation of PLCgamma1 is considered to have a

35 VEGF-MPs prolong VEGFR-2 and Akt phosphorylation in cord blood-derived la

36 Immunohistochemical analysis of VEGFR-2 and CD31 supported SPECT and autoradiographic im

37 e the expression of endothelial cell markers VEGFR-2 and CD31.

38 PDCL3 binds to the juxtamembrane domain of VEGFR-2 and controls the abundance of VEGFR-2 by inhibit

39 P-1 increases VEGF binding and activation of VEGFR-2 and ERK1/2 in endothelial cells and that these e

40 ) coincides with expression of Brachyury and VEGFR-2 and identifies endothelial precursors in murine

41 tors with improved selectivity profiles over VEGFR-2 and IGF-1R that could serve as useful tools to p

42 ) and maintains a basal expression level for VEGFR-2 and its downstream signaling activation.

43 of combined therapeutic blockade of VEGF or VEGFR-2 and JAK2/STAT3.

44 quitin E3 ligase is recruited to S1188/S1191 VEGFR-2 and mediates the ubiquitination and degradation

45 Transcriptional down-regulation of VEGFR-2 and NRP-1 was mediated by a lack in stability of

46 VEGFR)-1, NRP-1, and VEGF165 in complex with VEGFR-2 and NRP-1.

47 neuropilin-1 in the HemSCs demonstrate that VEGFR-2 and NRP1 are not needed for VEGF-A- or VEGF-B-in

48 ast mechanotransduction, most likely through VEGFR-2 and NRP1.

49 Cs from Pkd2KO mice increased phosphorylated VEGFR-2 and phosphorylated mitogen signal-regulated kina

50 Finally, we found that ESDN associates with VEGFR-2 and regulates its complex formation with negativ

51 , we reveal a novel association of CD36 with VEGFR-2 and spleen tyrosine kinase (Syk).

52 taining for the endothelial markers CD31 and VEGFR-2 and terminal deoxynucleotidyl transferase-mediat

53 In contrast, no differences were observed in VEGFR-2 and tumor necrosis factor-alpha expression.

54 Further, we show that VEGFR-2 and VEGFR-1 blocking antibodies displayed opposi

55 orneal LG and whether a combined blockade of VEGFR-2 and VEGFR-3 effectively suppresses early-, middl

56 acts in vascular homeostasis by fine-tuning VEGFR-2 and VEGFR-3 signaling in ECs, suggesting its rel

57 ove lymphatic growth in adult mice, but both VEGFR-2 and VEGFR-3 were required for the development of

58 hey exhibit structural homology and activate VEGFR-2 and VEGFR-3, receptors on endothelial cells that

59 espite the dependence of lymphangiectasia on VEGFR-2 and VEGFR-3, the condition was not reversed by b

60 D (Phe(93)-Arg(108)) is critical for binding VEGFR-2 and VEGFR-3.

61 ough a mechanism involving signaling of both VEGFR-2 and VEGFR-3.

62 receptor-1 (VEGFR-1(+/-)), VEGF receptor-2 (VEGFR-2(+/-)), and overexpressing (VEGF(hi/+)) and under

63 the corresponding receptor VEGF receptor 2 (VEGFR-2) and local differences in endothelial cells prol

64 d that it is complexed with VEGF receptor 2 (VEGFR-2) and maintains a basal expression level for VEGF

65 scular endothelial growth factor receptor-2 (VEGFR-2) and platelet-derived growth factor receptor-bet

66 osphorylation status of the VEGF-receptor-2 (VEGFR-2) and the downstream signaling pathways were eval

67 F-A-dependent activation of VEGF receptor-2 (VEGFR-2), and subsequent TSAd-mediated activation of Src

68 The activation of p38 stabilizes VEGFR-2, and its inactivation accelerates VEGFR-2 downre

69 We further show that VEGF165, VEGFR-2, and monomeric NRP-1 bind weakly to heparin alon

70 acity of fluorescein isothiocyanate-RamAb to VEGFR-2, and no difference in VEGFR-2 binding affinity w

71 cular cell adhesion molecule PECAM1, but not VEGFR-2, and participate in a PECAM1-dependent form of v

72 rentiated human embryonic stem cells express VEGFR-2, and VEGFR-2 expression persists on differentiat

73 tivate 3 receptor tyrosine kinases, VEGFR-1, VEGFR-2, and VEGFR-3, promoting angiogenic and lymphangi

74 gs, revealing the corresponding depletion of VEGFR-2- and CD31-positive endothelial cells from tumor

75 during therapy and the rapid reemergence of VEGFR-2- and CD31-positive vasculature at the tumor edge

76 scular endothelial growth factor receptor 2 (VEGFR-2), angiogenesis, and the prognosis of ischemia.

77 d whether ramucirumab, a monoclonal antibody VEGFR-2 antagonist, in combination with paclitaxel would

78 s whether ramucirumab, a monoclonal antibody VEGFR-2 antagonist, prolonged survival in patients with

79 cetaxel plus either ramucirumab-a human IgG1 VEGFR-2 antagonist-or placebo in this patient population

80 islets and highlights a novel application of VEGFR-2 antagonists for the therapeutic treatment of T1D

81 ound that RTK inhibitors (RTKIs) and VEGF or VEGFR-2 antibodies reversed diabetes when administered a

82 In this study, VEGFR-2 antibody (DC101) inhibited growth of RenCa renal

83 de by short hairpin RNA against VEGF or anti-VEGFR-2 antibody (DC101) reduced tumor blood vessel dens

84 ombination therapy using GW2580 with an anti-VEGFR-2 antibody synergistically suppresses tumor growth

85 Anti-VEGF, but not anti-VEGFR-2, antibody significantly increased infiltration o

86 Therefore drugs targeting VEGFA/VEGFR-2 are being presently used in the clinics for trea

87 echniques, we demonstrate that VEGFA-165 and VEGFR-2 are expressed in identified phrenic motor neuron

88 a new approach for early diagnosis of DR and VEGFR-2 as a molecular marker.

89 NPs significantly reduced protein levels of VEGFR-2 as revealed by western blot and markedly suppres

90 thase (eNOS), phosphorylation of PECAM-1 and VEGFR-2, as well as activation of SRC and AKT.

91 ptor scV/Zr was mediated by both VEGFR-1 and VEGFR-2 at an approximately 2:1 ratio.

92 R-1 knockout led to abundant accumulation of VEGFR-2 at the protein level, increased VEGFR-2 tyrosine

93 Overall, these data show that inhibition of VEGFR-2 augmented CS-induced oxidative stress and inflam

94 r vasculature through disruption of the VEGF/VEGFR-2 axis can increase extravasation of adoptively tr

95 oscopy studies were performed to compare the VEGFR-2 binding affinity of RamAb and NOTA-RamAb.

96 anate-RamAb to VEGFR-2, and no difference in VEGFR-2 binding affinity was seen between RamAb and NOTA

97 he percent reduction of HA is greater in the VEGFR-2 blockade group.

98 This proliferation is inhibited by VEGF-A/VEGFR-2 blockade.

99 uvant therapy, a group that may benefit from VEGFR-2 blockade.

100 are the most affected in response to VEGF or VEGFR-2 blockades.

101 Treatment with VEGF or VEGFR-2 blocking antibodies similarly reduced tumor angi

102 VEGF-C phosphorylated VEGFR-2 but not VEGFR-3, myosin light chain-2, or VE-cad

103 VEGFR-2- but not VEGFR-1-specific blockade led to the sa

104 Inhibition of VEGFR-2 by a specific kinase inhibitor (NVP-AAD777) enha

105 ain of VEGFR-2 and controls the abundance of VEGFR-2 by inhibiting its ubiquitination and degradation

106 vel protein involved in the stabilization of VEGFR-2 by serving as a chaperone.

107 peptide demonstrated the highest affinity to VEGFR-2 by surface plasmon resonance assay.

108 T cells transduced with VEGFR-2 CAR showed durable and increased tumor infiltrat

109 A single dose of VEGFR-2 CAR-engineered mouse T cells plus exogenous IL-2

110 se and human T cells expressing the relevant VEGFR-2 CARs mediated specific immune responses against

111 scular endothelial growth factor receptor 2 (VEGFR-2), CD133, and CD34 were examined by flow cytometr

112 scular endothelial growth factor receptor-2 (VEGFR-2), -CD146, -CD45, and -von Willebrand factor (vWF

113 creased adhesion to antibodies against CD34, VEGFR-2, CD31, and CD146 compared to CD45, consistent wi

114 tic patients (n=7) showed significantly more VEGFR-2 compared to nondiabetic controls (n=5) or periph

115 cal angiogenic signaling axes, integrins and VEGFR-2, converge at Shc to regulate postnatal angiogene

116 VEGFR-2 could become a key diagnostic target, one that m

117 wth factor (VEGF), VEGFR-1, VEGFR-2, phospho-VEGFR-2, cyclooxygenase (COX)-1, COX-2, and endothelial

118 Myocardial Vegf-a or endocardial Vegfr-2 deletion inhibited coronary angiogenesis and art

119 endothelial growth factor (VEGF) receptor-2 (VEGFR-2)-dependent proliferation and migration, coupled

120 tyrosine phosphorylation and is required for VEGFR-2-dependent endothelial capillary tube formation a

121 factor-A/VEGFR-2 signaling and suggest that VEGFR-2-dependent lymphangiogenesis is a mechanism that

122 the structure of the ligand-bound wild-type VEGFR-2 dimer.

123 Endothelial cell specific Vegfr-2 disruption in newborn mice not only blocked reti

124 d by tumor endothelial cells, which leads to VEGFR-2 down-regulation, endothelial cell apoptosis, and

125 es VEGFR-2, and its inactivation accelerates VEGFR-2 downregulation.

126 Ab blockade of VEGFR-2 during infection led to a reduction in lymphatic

127 on molecule-2), but not all (eg, VEGFR-1 and VEGFR-2), EC-enriched genes.

128 A model of the VEGF-E/VEGFR-2 ECD complex derived from small-angle scattering

129 assays with endothelial cells overexpressing VEGFR-2 established that sunitinib does not inhibit VEGF

130 responses against VEGFR-2 protein as well as VEGFR-2-expressing cells in vitro.

131 GFR-3 that was concomitant with increases in VEGFR-2 expression and downstream signaling.

132 he molecular mechanism by which it regulates VEGFR-2 expression and function.

133 The level of CD31 and p-VEGFR-2 expression has demonstrated that the excellent e

134 Immunohistochemistry showed VEGFR-2 expression in capillaries of diabetic animals bu

135 scesses was specific and directly related to VEGFR-2 expression in the neovasculature of the angiogen

136 ction as a PET imaging agent for visualizing VEGFR-2 expression in vivo, which may also find potentia

137 ibody-based imaging agent for PET imaging of VEGFR-2 expression in vivo.

138 d miR200-b delivery has negatively regulated VEGFR-2 expression in vivo.

139 an embryonic stem cells express VEGFR-2, and VEGFR-2 expression persists on differentiation.

140 CS down-regulated VEGFR-2 expression, eNOS levels, and VEGF-induced VEGFR-

141 Caspase-1 activation inhibits VEGFR-2 expression.

142 anti-angiogenic factor, on VEGF receptor 2 (VEGFR-2) expression and to determine the underlying angi

143 scular endothelial growth factor receptor-2 (VEGFR-2) expression can be used for detecting VEGFR-2-po

144 scular endothelial growth factor receptor 2 (VEGFR-2) expression identifies endothelial precursors.

145 nhibitors of the tyrosine kinase activity of VEGFR-2 (fetal liver kinase 1, kinase insert domain-cont

146 ies of amino acid ester prodrugs of the dual VEGFR-2/FGFR-1 kinase inhibitor 1 (BMS-540215) was prepa

147 FRET and biochemical analysis, we show that VEGFR-2 forms dimers also in the absence of ligand when

148 VEGFR-2 gene expression was abundant in adjacent liver p

149 VEGFR-2 has a role in gastric cancer pathogenesis and pr

150 VEGFR-2 has been hypothesized to be monomeric in the abs

151 lial growth factor (VEGF) with its receptor (VEGFR-2) has been reported to "normalize" tumor vasculat

152 itor SU1498, anti-VEGF-A, or introduction of Vegfr-2(+/-) heterozygosity into Vegfr-1 somatic knockou

153 rming that these functions are controlled by VEGFR-2 homodimers.

154 d liver defects; their LCECs expressed VEGF, VEGFR-2, hypoxia-inducible factor (HIF)-1alpha, phosphor

155 scular endothelial growth factor receptor-2 (VEGFR-2) immunoreactivity in tumor endothelial cells, wi

156 ressed in 100% of vestibular schwannomas and VEGFR-2 in 32% of tumor vessels on immunohistochemical a

157 Targeting soluble VEGFR-2 in atherosclerosis may provide a new strategy fo

158 Additive effects of an antibody against VEGFR-2 in conjunction with ACT were seen in this model

159 rmed to elucidate the expression patterns of VEGFR-2 in different tissues and organs to validate in v

160 ase in the expression of membrane-associated VEGFR-2 in endothelial cells of Timp-3(156/156) mutant m

161 VEGF induced greater phosphorylation of VEGFR-2 in lung ECs and of VEGFR-1 in liver ECs.

162 More than 80% of the VEGFR-2 in the diabetic retina was in the capillaries, c

163 co-receptor functions of CD44v6 for MET and VEGFR-2 in tumors and metastases grown from cells that e

164 scular endothelial growth factor receptor 2 (VEGFR-2) in retinal and choroidal vessels of diabetic an

165 VEGFR-1 or VEGFR-2 inhibition decreased tumor burden not by prevent

166 e formation in vitro were suppressed more by VEGFR-2 inhibition for lung EC and more by VEGFR-1 inhib

167 VEGFR-2 inhibition increases caspase-1 activation in HAE

168 than the MET inhibitor crizotinib and/or the VEGFR-2 inhibitor pazopanib in reducing xenograft tumor

169 Pkd2KO but not Pkd1KO mice, exposure to the VEGFR-2 inhibitor SU5416 significantly reduced liver cys

170 gs of mice exposed to CS and/or treated with VEGFR-2 inhibitor were decreased.

171 r cells resistant to cabozantinib, a Met and VEGFR-2 inhibitor, reside in a "resistance niche" adjace

172 Identification of VEGFR-2 inhibitors with optimal ADME properties for an o

173 on and iterative compound design to identify VEGFR-2 inhibitors with potential to benefit wet AMD pat

174 M-EPC), having the phenotype (CD133+, CD34+, VEGFR-2+), initiate neovascularization in response to TG

175 vations, we demonstrate that in normal liver VEGFR-2 is activated and BMP4 expression is suppressed.

176 The degradation and ubiquitination of VEGFR-2 is controlled by its PEST domain, and the phosph

177 F-E binding to D23 or the full-length ECD of VEGFR-2 is dominated by favorable entropic contribution

178 the complex formed by endogenous VEGF-A with VEGFR-2 is localized within the EEA1 (early endosome ant

179 VEGFR-2 is the primary regulator of angiogenesis, the de

180 Here, we show that VEGFR-2 is ubiquitinated in response to VEGF, and Lys 48

181 VEGF rapidly stimulated VEGFR-2/JAK2/STAT3 binding and activated STAT3 to bind M

182 d and found to yield nanomolar inhibitors of VEGFR-2 (KDR) with an improved selectivity profile again

183 between VEGF receptor-1 (VEGFR-1; Flt-1) and VEGFR-2 (KDR; Flk-1) (VEGFR(1-2)) in endothelial cells w

184 Compound 2 also inhibited Flt-3 and VEGFR-2 kinases with IC50 values of 4 and 27 nM, respect

185 VEGFR-2 knockdown or inhibition abrogated VEGF-mediated

186 tory effect of bevacizumab was eliminated by VEGFR-2 knockdown with small interfering RNA, showing th

187 ompanied by increased pulmonary VEGF-A and p-VEGFR-2 levels, with VEGF-A staining in accumulated intr

188 ainst Src, B-Raf wt, B-Raf V600E, EGFRs, and VEGFR-2, making it a good lead for novel anticancer prog

189 al growth factor (VEGF) and VEGF receptor-2 (VEGFR-2)-mediated signalling and angiogenesis can contri

190 The VEGFR-2-mediated activation of p38 is established throug

191 established that sunitinib does not inhibit VEGFR-2-mediated uptake of scVEGF-based tracers.

192 nti-VEGF antibody, inhibits proliferation of VEGFR-2(+) melanoma cell lines by an average of 41%; how

193 show (a) an autocrine growth loop active in VEGFR-2(+) melanoma, (b) a nonangiogenic mechanism for i

194 that patients with high pre-treatment plasma VEGFR-2 might benefit from the addition of bevacizumab (

195 ls of activated endothelium in livers in the VEGFR-2 MoAB group.

196 VEGFR-2 MoAB therapy decreased the levels of the cell cy

197 We further show that the pathogenic C482R VEGFR-2 mutant, linked to infantile hemangioma, promotes

198 wever, it failed to inhibit proliferation of VEGFR-2(neg) melanoma cell lines.

199 on; n = 4) and significantly lower uptake in VEGFR-2-negative A549 tumors (4.3 +/- 0.2 percentage inj

200 th factor (VEGF) and three of its receptors, VEGFR-2, neuropilin-1, and neuropilin-2, in paraffin-emb

201 However, VEGFR-2 neutralization had no effect on RenCa liver meta

202 VEGFR-2 neutralizing antibody, in contrast, inhibited bo

203 receptor 3 (VEGFR-3) neutralizing antibody, VEGFR-2 neutralizing antibody, or isotype IgG.

204 When sorted and differentiated, VEGFR-2(+)NRP-1(+) cells form endothelial-like colonies

205 and its binding to the VEGFR-2 promoter and VEGFR-2, NRP-1 expression, VEGF-dependent proliferation,

206 nesis of endothelial cells, the abundance of VEGFR-2 on the surface of endothelial cells is essential

207 VEGF receptor-2 (VEGFR-2 or kinase insert domain receptor; KDR) is a know

208 ical to these processes is signaling through VEGFR-2 or the kinase insert domain receptor (KDR) upon

209 est that disrupting endocan interaction with VEGFR-2 or VEGF-A could offer a novel rational strategy

210 ere also assessed after antibody blockade of VEGFR-2 or VEGFR-3 RESULTS: Although high-dose bFGF stim

211 Blockade of either VEGFR-2 or VEGFR-3 signaling reduces both HA and LA; how

212 e VEGF-C did not influence binding to either VEGFR-2 or VEGFR-3, indicating distinct determinants of

213 ereas expression of VEGF receptors (VEGFR-1, VEGFR-2, or NRP1) is unaffected.

214 eptor (VEGFR)-1 (P = 0.04 and P < 0.001) and VEGFR-2 (P < 0.001 for both analysis) showed a strong in

215 These receptors, in particular VEGFR-2, participate in PFSS-induced VEGF release.

216 el vascular endothelial growth factor (VEGF)/VEGFR-2 pathway, likely functioning in the formation and

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

218 r endothelial growth factor (VEGF), VEGFR-1, VEGFR-2, phospho-VEGFR-2, cyclooxygenase (COX)-1, COX-2,

219 -2 expression, eNOS levels, and VEGF-induced VEGFR-2 phosphorylation in HMVEC-Ls, resulting in impair

220 Inhibition of VEGFR-2 phosphorylation in PBMC was detected in eight of

221 Studies of VEGFR-2 phosphorylation status and down-regulation of ne

222 All VEGF mimics inhibited VEGFR-2 phosphorylation with VEGF-P3(CYC) showing the hi

223 ion and thereby, angiogenesis by suppressing VEGFR-2 phosphorylation.

224 scular endothelial growth factor receptor 2 (VEGFR-2) phosphorylation in peripheral blood mononuclear

225 and prominent uptake of (64)Cu-NOTA-RamAb in VEGFR-2-positive HCC4006 tumors (9.4 +/- 0.5 percentage

226 EGFR-2) expression can be used for detecting VEGFR-2-positive malignancies and subsequent monitoring

227 ng of the signalling protein to its receptor VEGFR-2, preventing receptor phosphorylation and downstr

228 ctor A (VEGF-A) by way of a VEGF receptor-2 (VEGFR-2) primed activation of p38 MAPK.

229 s restored Sp1 levels and its binding to the VEGFR-2 promoter and VEGFR-2, NRP-1 expression, VEGF-dep

230 s mediated specific immune responses against VEGFR-2 protein as well as VEGFR-2-expressing cells in v

231 nsduce downstream the upstream difference in VEGFR-2 protein level and activation; and (5) the mathem

232 , we found that: (1) cell density influences VEGFR-2 protein level, as receptor number is 2-fold high

233 ding mode of this molecule in both c-Met and VEGFR-2 proteins led to a novel strategy for designing m

234 s and HRECs expressed functional PDGFB-R and VEGFR-2, respectively.

235 ly by the corresponding receptor, VEGFR-1 or VEGFR-2, respectively.

236 ng manipulations, including injection of the VEGFR-2 selective inhibitor SU1498, anti-VEGF-A, or intr

237 Compared to wild-type mice, VEGFR-2(+/-) showed similar: ischemic scores, recovery o

238 nhanced vascular endothelial growth factor-A/VEGFR-2 signaling and suggest that VEGFR-2-dependent lym

239 ngiogenesis was strictly dependent on VEGF-A/VEGFR-2 signaling but not on VEGFR-3 ligands.

240 sought to determine whether disrupting VEGF/VEGFR-2 signaling could enhance the effectiveness of ACT

241 g blockade of migration, tube formation, and VEGFR-2 signaling in response to fibroblast growth facto

242 reveals a previously unappreciated role for VEGFR-2 signaling in the pathogenesis of T1D by controll

243 for TSP-1 and CD36 in the activation of the VEGFR-2 signaling pathway that requires Syk.

244 Blockade of VEGFR-2 signaling suppressed these vascular abnormalitie

245 esponses in vivo and attenuated VEGF-induced VEGFR-2 signaling without altering VEGF receptor or neur

246 had increased dimerization, induced elevated VEGFR-2 signaling, and caused aberrant angiogenesis in v

247 umor angiogenesis through regulation of VEGF/VEGFR-2 signaling, suggesting COUP-TFII as a candidate t

248 al therapeutic target to the existing VEGF-A/VEGFR-2 signaling-based antiangiogenesis strategies.

249 ty at the same concentrations by suppressing VEGFR-2 signaling.

250 rols HIF-1alpha-dependent VEGF secretion and VEGFR-2 signaling.

251 helial growth factor (VEGF)/VEGF receptor-2 (VEGFR-2) signaling by transcriptionally repressing the e

252 These data validate inhibition of VEGFR-2 signalling as a potential new therapeutic treatm

253 Our findings validate VEGFR-2 signalling as an important therapeutic target in

254 Interestingly, the blockade of VEGFR-2 significantly suppressed BV and LV.

255 The dimeric ligand comprises one VEGFR-2-specific monomer (VEGF-E) and a VEGFR-1-specific

256 h histology analysis, further confirming the VEGFR-2 specificity of (64)Cu-NOTA-RamAb.

257 y has identified a unique mechanism in which VEGFR-2 stability and degradation is modulated.

258 cell (CSC) self-renewal via VEGF receptor-2 (VEGFR-2)/STAT3-mediated upregulation of Myc and Sox2.

259 s tumor-initiating cell self-renewal through VEGFR-2/STAT3 signaling.

260 nantly by forming heterodimer receptors with VEGFR-2 subunits and such heterodimers regulate endothel

261 eted form of the protein, designated soluble Vegfr-2 (sVegfr-2), that inhibits developmental and repa

262 ions in monitoring the treatment response of VEGFR-2-targeted cancer therapy.

263 equent monitoring of therapeutic response to VEGFR-2-targeted therapies.

264 We hypothesized that the elevated soluble VEGFR-2 that was found in the aortas of apoE(-/-) mice w

265 scular endothelial growth factor receptor-2 (Vegfr-2) that encodes a secreted form of the protein, de

266 thelial growth factor receptors, VEGFR-1 and VEGFR-2, that play important and distinct roles in tumor

267 1 binding and neither requires nor activates VEGFR-2, the cognate receptor for VEGF-A.

268 The PEST domain acts as a dual modulator of VEGFR-2; the phosphorylation of S1188/S1191 controls ubi

269 Anti-VEGFR-2 therapy slightly impaired liver regeneration in

270 at were hypersensitive to anti-VEGF and anti-VEGFR-2 therapy, leading to dormancy of a substantial nu

271 to 10 days compared with the CG, whereas for VEGFR-2, these values were 252% and 60%, respectively, f

272 PKA is recruited to VEGFR-2 through AKAP1/AKAP149, and its phosphorylation r

273 of key endothelial specific genes including VEGFR-2, Tie-2, and vascular endothelial cadherin.

274 ght prevent ligand-independent activation of VEGFR-2 to evade the deleterious consequences for blood

275 differs from exogenous VEGF-A by regulating VEGFR-2 transcription through mediation of FoxC2 binding

276 VEGF specific binding to VEGF receptor-2 (VEGFR-2) triggers different signaling pathways, includin

277 n of VEGFR-2 at the protein level, increased VEGFR-2 tyrosine phosphorylation transiently, and enhanc

278 scular endothelial growth factor receptor 2 (VEGFR-2) tyrosine kinase inhibitors.

279 Immunostaining revealed that VEGFR-2 (VEGF receptor) colocalized with CD31 (endotheli

280 ly the result of the increased expression of VEGFR-2, VEGF-A, VEGF-C, and VEGF-D.

281 dothelial growth factor receptor (VEGFR) -1, VEGFR-2, VEGFR-3, and c-kit.

282 Inhibition of VEGFR-2/VEGFR-3 did not prevent the formation of BALT.

283 VEGFR-2/VEGFR-3 heterodimers were more abundant in the d

284 is required for VEGF-D to drive formation of VEGFR-2/VEGFR-3 heterodimers which have recently been sh

285 ncreata from patients with T1D revealed that VEGFR-2 was confined to the islet vascularity, which was

286 Loss of VEGFR-2 was followed by increased activated caspase-3 in

287 r metastases, inhibition of both VEGFR-1 and VEGFR-2 was required to induce growth delay.

288 utralizing antibodies against VEGFR-3 and/or VEGFR-2 were administrated systemically with the treatme

289 elective PET tracers for imaging VEGFR-1 and VEGFR-2 were constructed and successfully validated in a

290 g endothelial cells expressed high levels of VEGFR-2 were highly susceptible to blockade by VEGF Trap

291 Both VEGFR-3 and VEGFR-2 were involved in corneal suture-induced inflamma

292 s, FAs, and DVs that expressed low levels of VEGFR-2 were largely resistant.

293 The mRNA levels of VEGF and VEGFR-2 were quantified by qRT-PCR and showed significan

294 secretion and phosphorylation of ERK1/2 and VEGFR-2 were significantly increased in cultured LCECs f

295 tor (VEGF)-A, and phospho-VEGF receptor-2 (p-VEGFR-2) were compared and monocyte accumulation was ass

296 scular endothelial growth factor receptor-2 (VEGFR-2) were overexpressed in ccRCCs relative to normal

297 anced affinity to, respectively, VEGFR-1 and VEGFR-2, were constructed.

298 is by increasing phosphorylation of Y1175 in VEGFR-2, which is a major tyrosine for promoting VEGF-A-

299 eric antigen receptor (CAR) targeted against VEGFR-2, which is overexpressed in tumor vasculature and

300 hrough the phosphorylation and activation of VEGFR-2, which was required to promote cell migration an

301 tion) of signaling molecules downstream from VEGFR-2 within the phrenic motor nucleus, including ERK