ライフサイエンスコーパス: VEGFR

1 VEGFR-1 blockade and genetic deletion of the tyrosine ki

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 increases caspase-1 activation in HAE

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

7 VEGFR-2 knockdown or inhibition abrogated VEGF-mediated

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

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

10 VEGFR-3 neutralization for 2 weeks before mating blocked

11 VEGFR-3-mediated lymphangiogenesis thus appears to modul

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

31 scular endothelial growth factor receptor 3 (VEGFR-3), with its cognate ligand vascular endothelial g

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

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

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

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

36 Targeting VEGF-A/VEGFR axis seems sufficient to affect Treg percentages,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

52 Further, we show that VEGFR-2 and VEGFR-1 blocking antibodies displayed opposing effects o

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

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

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

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

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

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

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

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

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

62 blots and immunostaining revealed VEGF-C and VEGFR-3 expression in CNV lesions, mainly in macrophages

63 VEGF-C and VEGFR-3 expressions were examined with immunohistochemis

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

85 20 genes that encode proteins acting around VEGFR-3 signaling but also downstream of other tyrosine

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

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

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

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

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

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

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

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

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

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

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

97 A structural model of the VEGF-C/VEGFR-3 D1-7 complex derived from small-angle X-ray scat

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

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

100 Conversely, VEGFR-1-specific blockade produced virtually no obvious

101 erine blood or lymphatic vascular densities, VEGFR-3 neutralization reduced serum and ovarian estradi

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

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

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

105 lular adhesion molecule-2), but not all (eg, VEGFR-1 and VEGFR-2), EC-enriched genes.

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

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

108 ermal macrophages themselves did not express VEGFR-3.

109 In vitro, Treg expressing VEGFR from tumor-bearing mice directly proliferated in r

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

111 interactions in D5 and D7 are essential for VEGFR activation, opening promising possibilities for th

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

113 g interface in D2 and a unique mechanism for VEGFR dimerization and activation, with homotypic intera

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

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

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

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

118 4, the receptor tyrosine kinases EGFR, HGFR, VEGFR, PDGFR, NGFR and IGF1R, as well as interleukin-2 r

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

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

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

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

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

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

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

126 The same trend was found in VEGFR 1 and 2 which were significantly reduced in WT gro

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

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

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

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

131 phosphorylation of key tyrosine residues in VEGFR-2.

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

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

134 eraction (Arg737) compromised VEGF-C induced VEGFR-3 activation.

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

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

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

144 VEGFR-2- but not VEGFR-1-specific blockade led to the same results.

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

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

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

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

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

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

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

152 A thermodynamic analysis of VEGFR-3 deletion mutants showed that D3, D4-5, and D6-7

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

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

155 Blockade of VEGFR-2 signaling suppressed these vascular abnormalitie

156 ng promising possibilities for the design of VEGFR-specific drugs.

157 ic deletion of the tyrosine kinase domain of VEGFR-1 resulted in enhanced tumor angiogenesis.

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

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

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

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

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

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

164 ar remodeling in NOD mice, and inhibition of VEGFR activity with RTKIs abrogated the increase in isle

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

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

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

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

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

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

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

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

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

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

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

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

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

178 lymphangiogenesis, showing its dependence on VEGFR-3 ligands.

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

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

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

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

183 l, we tested inhibitors of human EGFR and/or VEGFR as possible anti-trypanosome compounds.

184 genome of T. brucei does not encode EGFR or VEGFR, indicating that the drugs recognize alternate pro

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

208 y neutralizing antibodies for VEGF receptor (VEGFR) 1 and 2 or neuropilin receptor 1 or by VEGFR2 inh

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

227 ascular endothelial growth factor receptors (VEGFRs).

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

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

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

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

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

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

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

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

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

237 156S, a mutant form of VEGF-C with selective VEGFR-3 binding, alleviates an established rejection res

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

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

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

241 eno-associated viral vector-mediated soluble VEGFR-3 (VEGF-C/D Trap) completely blocked lymphangiogen

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

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

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

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

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

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

248 uced Treg but masitinib, a TKI not targeting VEGFR, did not.

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

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

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

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

260 complex with VEGFR-3 domains D1-2 and of the VEGFR-3 D4-5 homodimer.

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

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

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

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

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

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

267 er association rate and affinity compared to VEGFR.

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

269 MET is implicated in resistance to VEGFR inhibitors.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

285 (CT26) treated with drugs targeting the VEGF/VEGFR axis.

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

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

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

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

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

291 Herein, we examined whether VEGFR participated in the pathogenesis of type 1 diabete

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

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

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

295 crystal structures of VEGF-C in complex with VEGFR-3 domains D1-2 and of the VEGFR-3 D4-5 homodimer.

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

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

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