ライフサイエンスコーパス: VEGFR

1 VEGFR inhibitors could be beneficial for the treatment o

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

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

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

5 VEGFR-2 inhibition also attenuated morphine analgesic to

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

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

8 VEGFR-2 knockdown or inhibition abrogated VEGF-mediated

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

10 VEGFR-3 neutralization for 2 weeks before mating blocked

11 scular endothelial growth factor receptor-1 (VEGFR-1/sFlt-1), which serves to antagonize VEGF-mediate

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

13 scular endothelial growth factor receptor 2 (VEGFR-2) in endothelial cells.

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

15 al growth factor A (VEGF-A)/VEGF receptor 2 (VEGFR-2) signaling pathway mediates lymphangiogenesis, w

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

17 scular endothelial growth factor receptor 2 (VEGFR-2), contributing to their selective and early prol

18 VEGF and VEGF receptor 2 (VEGFR-2)-mediated signalling and angiogenesis can contri

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

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

21 at simultaneous blockade of VEGF receptor-2 (VEGFR-2) and PD-1 or PD-L1 enhances antigen-specific T-c

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

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

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

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

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

27 ological inhibition of VEGF receptor Type 2 (VEGFR-2) signaling attenuated mechanical nociception in

28 a Pharmaceuticals, LLC), a novel c-MET/TIE-2/VEGFR inhibitor was able to effectively reduce tumor bur

29 endothelial growth factor receptor (VEGFR)-2/VEGFR-3 signaling of lung lymphatics in sustained inflam

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

31 VEGFR-2/VEGFR-3 heterodimers were more abundant in the dilated l

32 scular endothelial growth factor receptor 3 (VEGFR-3) ameliorated aGVHD and improved survival in muri

33 scular endothelial growth factor receptor 3 (VEGFR-3) antibody to block lymphangiogenesis in mice.

34 scular endothelial growth factor receptor 3 (VEGFR-3) are the major lymphatic growth factor and recep

35 xpression of podoplanin and VEGF receptor 3 (VEGFR-3) but not of LYVE-1 and prospero homeobox protein

36 ssess whether the addition of ramucirumab, a VEGFR-2 antagonist monoclonal antibody, to first-line ch

37 reatment of mucosally injured WT mice with a VEGFR inhibitor resulted in the development of penetrati

38 uding at least one previous treatment with a VEGFR inhibitor), measurable disease according to the Re

39 ort 1) or had been treated previously with a VEGFR multikinase inhibitor (cohort 2).

40 patients with DTC previously treated with a VEGFR-targeted therapy had an objective response to cabo

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

42 However, a direct role of the VEGF-A/VEGFR pathway inhibition in this phenomenon is a matter

43 the bone marrow microenvironment and VEGF-A/VEGFR targeting restores bone marrow function.

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

45 r and molecular mediators involved in VEGF-A/VEGFR-2 signaling using a murine model of infection.

46 d miR-150 transfer and miR-150-driven VEGF-A/VEGFR/PI3K/Akt pathway activation, thereby modulating th

47 Previous studies of VEGF-A:VEGFR binding have measured binding kinetics for VEGFA(1

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

49 A, exhibited enhanced potency for activating VEGFR-3, was able to promote increased COX-2 mRNA levels

50 Altered VEGFR expression has been documented in brains of AD pat

51 rs may impair vascular functions by altering VEGFR-1 expression and causing ECs to enter a senescent

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

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

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

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

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

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

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

59 cular homeostasis by fine-tuning VEGFR-2 and VEGFR-3 signaling in ECs, suggesting its relevance in th

60 c growth in adult mice, but both VEGFR-2 and VEGFR-3 were required for the development of lymphangiec

61 structural homology and activate VEGFR-2 and VEGFR-3, receptors on endothelial cells that signal for

62 gh signaling via VEGF receptor (VEGFR)-2 and VEGFR-3, respectively.

63 ependence of lymphangiectasia on VEGFR-2 and VEGFR-3, the condition was not reversed by blocking both

64 rg(108)) is critical for binding VEGFR-2 and VEGFR-3.

65 nism involving signaling of both VEGFR-2 and VEGFR-3.

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

67 ke phenotype of the SC, implicate VEGF-C and VEGFR-3 as critical regulators of SC lymphangiogenesis,

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

69 rapeutic target in therapy-resistant EOC and VEGFR blockade by tivozanib may yield stronger anti-tumo

70 pathways involving MET, paxillin, EPHA2, and VEGFR.

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

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

73 ts, suggesting a conserved role for PDGF and VEGFR-2 signaling in regulating mechanical nociception.

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

75 ox 1-enhanced green fluorescence protein and VEGFR-3 as markers.

76 , such differential apicobasal signaling and VEGFR distribution were found in the microvasculature of

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

78 talk between G protein-coupled receptors and VEGFRs in PAH.

79 static ASPS comparing cediranib with another VEGFR inhibitor, sunitinib.

80 Anti-VEGFR-3 abolished CCL21 gradients around lymphatics, alt

81 Anti-VEGFR-3 prevented migration of CD4 T cells into lymphati

82 Anti-VEGFR-3 therapy had no significant impact on growth of m

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

84 was down-regulated around lymphatics by anti-VEGFR-3 and this was dependent on heparanase-mediated de

85 strategy to overcome the limitations of anti-VEGFR monotherapy in GBM patients by integrating the com

86 The administration of anti-VEGFR-3 antibodies did not interfere with hematopoietic

87 PI3K activator prevented the effects of anti-VEGFR-3.

88 Our data show that anti-VEGFR-3 treatment ameliorates lethal aGVHD and identifie

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

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

91 20 genes that encode proteins acting around VEGFR-3 signaling but also downstream of other tyrosine

92 Competitive binding to VEGF between VEGFR and bevacizumab was monitored in real-time using t

93 e breadth of VEGF's influence extends beyond VEGFR-positive cells and propose a plausible mechanistic

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

95 Phe(93) to Thr(98), is required for binding VEGFR-3 but not VEGFR-2.

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

97 ced 68% by blocking VEGFR-2, 83% by blocking VEGFR-3, and 99% by blocking both receptors.

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

99 of pan-receptor scV/Zr was mediated by both VEGFR-1 and VEGFR-2 at an approximately 2:1 ratio.

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

101 ases was comparable with the one produced by VEGFR inhibition.

102 Vascular endothelial growth factor C/VEGFR-3 signaling through PI3Kalpha regulates the activi

103 The VEGF-C/VEGFR-3 and VEGF-A/VEGF-R2 signaling pathways are two of

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

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

106 y increased VEGFR-1 expression and decreased VEGFR-2 levels.

107 m by which tMUC1 may modulate NRP1-dependent VEGFR signaling in PDA cells.

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

109 not affect VEGF expression but downregulated VEGFR expression, which may cause a delay in the bone re

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

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

112 modulate vascular endothelial growth factor (VEGFR)-2 and epidermal growth factor receptor (EGFR) sig

113 er square millimeter and mRNA expression for VEGFR-1 were, respectively, 89% and 37% lower from 3 to

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

115 Embryos from VEGFR-3-neutralized dams developed normally when transfe

116 4, the receptor tyrosine kinases EGFR, HGFR, VEGFR, PDGFR, NGFR and IGF1R, as well as interleukin-2 r

117 roangiogenesis factors, including HIF1alpha, VEGFR, and MMP-2/MMP-9.

118 During contact hypersensitivity, VEGFR-3, CCL21, and HS expression were all attenuated, a

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

120 ity was found to be more sensitive to IGF1R, VEGFR and ABL inhibitors.

121 antitumour activity of ramucirumab (an IgG1 VEGFR-2 antagonist) combined with pembrolizumab (an IgG4

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

123 t-in-class selective PET tracers for imaging VEGFR-1 and VEGFR-2 were constructed and successfully va

124 esults demonstrate a novel role for ARRB1 in VEGFR regulation and suggest a mechanism for cross talk

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

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

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

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

129 CLEC14A KO resulted in a marked reduction in VEGFR-3 that was concomitant with increases in VEGFR-2 e

130 phosphorylation of key tyrosine residues in VEGFR-2.

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

132 ssion of lymphatic specific genes, including VEGFR-3 and Prox1.

133 FLT4 rs307826 increased VEGFR-3 phosphorylation, membrane trafficking, and recep

134 d these cells showed significantly increased VEGFR-1 expression and decreased VEGFR-2 levels.

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

136 Caspase-1 activation inhibits VEGFR-2 expression.

137 that more than 80% of tracer tumor uptake is VEGFR-mediated, whereas uptake in all major organs is no

138 the lymphangiogenic receptor tyrosine kinase VEGFR-3 in venous endothelial cells in postnatal mice.

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

140 inhibitor of tyrosine kinases including MET, VEGFR, and AXL.

141 ozantinib is a multikinase inhibitor of MET, VEGFR, AXL, and RET, which also has an effect on the tum

142 cule tyrosine kinase inhibitor, targets MET, VEGFR, RET, ROS1, and AXL, which are implicated in lung

143 These studies suggest that modulating VEGFR-1 expression and signaling events could potentiall

144 ase, and previous treatment with one or more VEGFR tyrosine-kinase inhibitors to receive 60 mg caboza

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

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

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

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

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

150 Furthermore, administration of VEGFR blocking antibody selectively improved survival of

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

152 Blockade of VEGFR-2 signaling suppressed these vascular abnormalitie

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

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

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

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

157 tracers that enable the selective imaging of VEGFR-1 and VEGFR-2.

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

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

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

161 Here we tested whether dual inhibition of VEGFR/Ang-2 could improve survival in two orthotopic mod

162 Thus, dual inhibition of VEGFR/Ang-2 prolongs survival in preclinical GBM models

163 small interfering RNA-mediated knockdown of VEGFR-1 expression in brain ECs was able to prevent up-r

164 Interestingly, knockdown of VEGFR-3 does not affect galectin-8-mediated lymphatic en

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

166 Overexpression of VEGFR-1 in brain ECs readily induced senescence, suggest

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

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

169 inhibited VEGF-C-induced phosphorylation of VEGFR-3, ERK1/2, and AKT.

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

171 established TRIM28 as a crucial regulator of VEGFR-Notch signaling circuit through HIF-1alpha and RBP

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

173 uced senescence, suggesting a direct role of VEGFR-1 signaling events in this paradigm.

174 h specific blockade of different isoforms of VEGFRs that may be involved.

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

176 ished, and we find that drugs targeting only VEGFRs (Apatinib and Vandetanib) are not effective, wher

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

178 d not influence binding to either VEGFR-2 or VEGFR-3, indicating distinct determinants of receptor bi

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

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

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

182 initial decrease following cediranib (a pan-VEGFR tyrosine kinase inhibitor) administration.

183 on of angiogenesis markers including PECAM1, VEGFR, and VE-cadherin.

184 cell carcinoma who progressed after previous VEGFR tyrosine-kinase inhibitor treatment.

185 disease and evidence of progression on prior VEGFR-targeted therapy were enrolled in this single-arm

186 nty-one patients had received only one prior VEGFR-targeted therapy (sorafenib, pazopanib, or cediran

187 enced disease progression while taking prior VEGFR-targeted therapy.

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

189 respective cytoplasmic domains and promotes VEGFR activation in flow [6].

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

191 ing domain (HBD) with the signaling receptor VEGFR-2 up to atomic detail.

192 vascular endothelial growth factor receptor (VEGFR) 2 plays an essential role, is associated with a v

193 vascular endothelial growth factor receptor (VEGFR) 3-Ig in the skin, scavenging VEGF-C and VEGF-D, t

194 vascular endothelial growth factor receptor (VEGFR) and approved for radioiodine (RAI)-refractory dif

195 vascular endothelial growth factor receptor (VEGFR) and VEGF to bevacizumab.

196 vascular endothelial growth factor receptor (VEGFR) expression in the Abeta1-42 oligomer-treated ECs,

197 vascular endothelial growth factor receptor (VEGFR) signaling pathways.

198 vascular endothelial growth factor receptor (VEGFR) stands out for its multiple effects on immunity,

199 vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitor sunitinib have shown po

200 vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitors (TKIs).

201 vascular endothelial growth factor receptor (VEGFR), vascular endothelial growth factor receptor type

202 vascular endothelial growth factor receptor (VEGFR)-2 and is associated with significant changes in t

203 vascular endothelial growth factor receptor (VEGFR)-2, and TSP1 inhibits VEGFR2 phosphorylation and s

204 vascular endothelial growth factor receptor (VEGFR)-2/VEGFR-3 signaling of lung lymphatics in sustain

205 vascular endothelial growth factor receptor (VEGFR)-Notch signaling.

206 c agent with activity against VEGF receptor (VEGFR) 1, VEGFR2, and VEGFR3.

207 rated increased expression of VEGF receptor (VEGFR) 2 as well as VEGF signaling molecules VEGF-A, VEG

208 othelial growth factor (VEGF)/VEGF receptor (VEGFR) 2 pathways, despite similar Vegfa expression leve

209 The role of CD34(+)/VEGF receptor (VEGFR) 2(+) progenitor cells (PCs) in vascular repair in

210 Anti-VEGF/VEGF receptor (VEGFR) drugs treat cancer, but the underlying mechanisms

211 er, EPAC activation inhibited VEGF receptor (VEGFR) signaling through the Ras/MEK/ERK pathway.

212 promises the benefits of anti-VEGF receptor (VEGFR) treatment in murine GBM models and that circulati

213 ggested that treatment with a VEGF receptor (VEGFR) tyrosine kinase inhibitor might be effective in p

214 meter and mRNA expression for VEGF receptor (VEGFR)-1 (P = 0.04 and P < 0.001) and VEGFR-2 (P < 0.001

215 heparin/HS interactions with VEGF receptor (VEGFR)-1, NRP-1, and VEGF165 in complex with VEGFR-2 and

216 GF3 and its cognate receptor, VEGF receptor (VEGFR)-10-Ig, is also essential for the deployment of th

217 by decreased transcription of VEGF receptor (VEGFR)-2 and neuropilin (NRP)-1, the primary receptors r

218 genesis through signaling via VEGF receptor (VEGFR)-2 and VEGFR-3, respectively.

219 ry of an anti-VEGF or an anti-VEGF receptor (VEGFR)-2 neutralizing antibody caused global vascular re

220 cal significance of the VEGFC/VEGF receptor (VEGFR)-3 pathway in ovarian cancer growth and disseminat

221 VEGF receptor (VEGFR)1 or VEGFR2 blockade prevented the inhibitory effe

222 nals: neuropilin-2 (Nrp2) and VEGF-receptor (VEGFR)-2/3.

223 d exclusively by the corresponding receptor, VEGFR-1 or VEGFR-2, respectively.

224 genic growth factor VEGF-C and its receptor, VEGFR-3, are essential for SC development.

225 ascular endothelial growth factor receptors (VEGFR) in live cells, and use this to assess the geometr

226 ms (SNPs) in VEGF genes and their receptors (VEGFR) with the response rate to ranibizumab in 366 pati

227 ascular endothelial growth factor receptors (VEGFRs) and G protein-coupled receptors, which classical

228 ascular endothelial growth factor receptors (VEGFRs) provided important insights into endothelial cel

229 ascular endothelial growth factor receptors (VEGFRs) that resides at endothelial cell-cell junctions

230 growth factors (VEGFs) and their receptors (VEGFRs) are key drivers of blood and lymph vessel format

231 tor (VEGF) that can activate VEGF receptors (VEGFRs) on or within tumor cells to promote growth in an

232 ntains the binding sites for VEGF receptors (VEGFRs), but their biological functions were unclear.

233 ascular endothelial growth factor receptors, VEGFR-1 and VEGFR-2, that play important and distinct ro

234 njugated antibody binding to five receptors: VEGFRs (VEGFR1 and VEGFR2), their coreceptor neuropilin1

235 hanistic studies revealed that VEGF recptor (VEGFR)-3 alone drove lymphatic growth in adult mice, but

236 with a NRP1 antagonist significantly reduced VEGFR signaling and PDA tumor growth in vivo.

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

238 VR2 with enhanced affinity to, respectively, VEGFR-1 and VEGFR-2, were constructed.

239 safety of tivozanib (a potent and selective VEGFR inhibitor) with those of sorafenib as third-line o

240 156S, a mutant form of VEGF-C with selective VEGFR-3 binding, alleviates an established rejection res

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

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

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

244 truncated isoform of this molecule, soluble VEGFR-3 (sVEGFR-3), which is critical for corneal alymph

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

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

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

248 are not effective, whereas drugs that target VEGFRs, PDGFR and Tie2 (Linifanib and Cabozantinib) do r

249 r received a multikinase inhibitor targeting VEGFR (cohort 1) or had been treated previously with a V

250 tically, blocking experiments indicated that VEGFR-mediated tumor uptake of scVR1/Zr and scVR2/Zr was

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

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

253 Altogether, these findings suggest that VEGFR blockade by tivozanib has potential anti-glioma ef

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

255 ic and pro-fibrotic pathways mediated by the VEGFR family, the fibroblast growth factor receptor (FGF

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

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

258 vo with structural analysis to establish the VEGFR tyrosine kinase inhibitor axitinib as a selective

259 e associated increase of tumor uptake in the VEGFR-targeting positron emission tomography (PET) imagi

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

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

262 ts ability to transcriptionally regulate the VEGFR pathway.

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

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

265 s VEGF-C, thereby blocking signaling through VEGFR-3 and suppressing lymphangiogenesis induced by VEG

266 VEGF-C signaling through VEGFR-3 promotes lymphangiogenesis, which is a clinicall

267 inase inhibitor targeting MET in addition to VEGFR and is approved for medullary thyroid cancer.

268 -fold improvement in the binding affinity to VEGFR with IC(50) value of 25 pm.

269 l form, which showed preferential binding to VEGFR-3.

270 er association rate and affinity compared to VEGFR.

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

272 MET is implicated in resistance to VEGFR inhibitors.

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

274 growth factor A (VEGF-A) and its binding to VEGFRs is an important angiogenesis regulator, especiall

275 on resonance to identify and measure PDGF-to-VEGFR binding rates, establishing cut-offs for binding a

276 SFKs), which phosphorylate and transactivate VEGFRs [3-5].

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

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

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

280 demonstrated a significant blockage of VEGF-VEGFR binding by bevacizumab.

281 nts of bevacizumab drug efficacy to the VEGF-VEGFR angiogenic switch in living SKOV-3 cells.

282 d to mimic the in vivo condition of the VEGF-VEGFR angiogenic switch.

283 tions of these angiogenic cues with the VEGF-VEGFR-Delta-like ligand 4 (Dll4)-Jagged-Notch pathway.

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

285 Together, anti-VEGF/VEGFR drugs act in part by inhibiting eNOS, causing vaso

286 Patients and mice receiving anti-VEGF/VEGFR drugs develop hypertension, reflecting systemic ar

287 o-l-arginine methyl ester mimicked anti-VEGF/VEGFR drugs, rapidly collapsing MV to GMP.

288 that vary in their sensitivity to anti-VEGF/VEGFR inhibition, with VEGFA-targeted therapy suppressin

289 factor VEGFA and consequently reducing VEGF/VEGFR downstream signaling in the endothelial cells.

290 tumor cells, which in turn upregulated VEGF/VEGFR signaling in surrounding tumor cells to support tu

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

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

293 acological blockade of lymphangiogenesis via VEGFR-3 inhibition results in increased corneal thicknes

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

295 n the context of Abeta was commensurate with VEGFR-dependent changes in multiple signaling pathways t

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

297 CLEC14A formed a complex with VEGFR-3 in endothelial cells (ECs), and CLEC14A KO resul

298 p and the number of previous treatments with VEGFR tyrosine-kinase inhibitors.

299 ted by transmembrane domain association with VEGFRs.

300 functions as an adaptor that interacts with VEGFRs through their respective cytoplasmic domains and