ライフサイエンスコーパス: VEGFR2

1 s required signaling by the VEGF receptor 2 (VEGFR2).

2 scular endothelial growth factor receptor 2 (VEGFR2).

3 argets vascular endothelial growth factor 2 (VEGFR2).

4 erentiation are mediated by Vegf receptor 2 (Vegfr2).

5 reases dramatically the cleavage/shedding of VEGFR2.

6 to UIM recognition of ubiquitin moieties on VEGFR2.

7 ohistochemical staining was used to localize VEGFR2.

8 UIM were found to interact with residues in VEGFR2.

9 nducer of autophagy via its interaction with VEGFR2.

10 xhibit single-digit nanomolar potency toward VEGFR2.

11 these events, as these cells lack VEGFR1 and VEGFR2.

12 cted by early binding of the microbubbles to VEGFR2.

13 the VEGF-binding domain at the N terminus of VEGFR2.

14 hown to be required for the interaction with VEGFR2.

15 appreciated ubiquitin-binding surface within VEGFR2.

16 -binding domain from the membrane remnant of VEGFR2.

17 r endothelium to induce vasopermeability via VEGFR2.

18 , p-ERK1/2, p-NFkappabeta, p-PLCgamma1 and p-VEGFR2.

19 al epsins by competitively binding activated VEGFR2.

20 n lacteals requires activation of VEGFR3 and VEGFR2.

21 regulating VEGF secretion and expression of VEGFR2.

22 of vascular endothelial cell marker CD31 and VEGFR2.

23 s in the surface-to-internal distribution of VEGFR2.

24 n and increased expression of both Nanog and VEGFR2.

25 their surface membrane, including VEGFR1 and VEGFR2.

26 scular endothelial growth factor receptor 2 (VEGFR2), a protein that is not associated to amyloidosis

27 ISPR/Cas9 gene editing technology to silence VEGFR2, a major regulator of angiogenesis, in retinal en

28 VEGF binding to its cognate receptor, VEGFR2, activates a number of signaling pathways includi

29 sion of miR-497 showed inhibitory effects on VEGFR2 activation and downstream Raf/MEK/ERK signal path

30 shows for the first time a mechanism whereby VEGFR2 activation mediates EC permeability induced by pa

31 early show that differences in site-specific VEGFR2 activation when stimulated with immobilized VEGF

32 This results in VEGFR2 activation, Src-dependent VE-cadherin tyrosine ph

33 After VEGFR2 activation, the mast cell-derived vasodilatory an

34 Calpain inhibitor ALLN induced VEGFR2 activation, which can be completely blocked by PT

35 ated the effect of R-Ras on VEGF receptor 2 (VEGFR2) activation by VEGF, the key mechanism for angiog

36 levels correlated with decreased VEGFR1, not VEGFR2, activation.

37 levels correlated with decreased VEGFR1, not VEGFR2, activation.

38 hat both express VEGFR2 and are dependent on VEGFR2 activity for survival.

39 Consistent with elevated VEGFR2 activity, vascular endothelial cadherin showed re

40 ited VEGF signaling through VEGF receptor 2 (VEGFR2), Akt, and ERK pathways in lungs and primary endo

41 The VEGF/VEGFR2/Akt/eNOS/NO pathway is essential to VEGF-induced

42 The major signaling receptor for VEGF, i.e VEGFR2, also appears to be under a direct and positive r

43 Inhibitors of VEGFR2 and AKT induced senescence in HCT116 cells.

44 erexpression of PTP1B inhibited VEGF-induced VEGFR2 and Akt phosphorylation in bovine aortic endothel

45 is observed only in cells that both express VEGFR2 and are dependent on VEGFR2 activity for survival

46 tively induced HUVECs apoptosis by targeting VEGFR2 and downstream PI3K/AKT signaling pathway.

47 stigated the interactions between doppel and VEGFR2 and evaluated whether blocking the doppel/VEGFR2

48 HCC angiogenesis through directly binding to VEGFR2 and has broad applications in treating VEGF-media

49 VEGF receptors VEGFR1, VEGFR2 and Neuropilin-1 (NRP1) are mostly in 'Free State

50 GF165-induced vascular leakage requires both VEGFR2 and NRP1, including the VEGF164-binding site of N

51 Simulations also show that ligated VEGFR2 and phosphorylated VEGFR2 levels diverge over tim

52 In addition, inhibitors of both VEGFR2 and PKCbeta1 blocked the angiogenic response.

53 viously implicated in autophosphorylation of VEGFR2 and reported in angiosarcomas alongside other dri

54 ucing the internalization and degradation of VEGFR2 and thereby attenuating VEGFR2 signaling.

55 pulmonary endothelium attenuated CS-induced VEGFR2 and VE-cadherin phosphorylation, preserved adhere

56 VEGFR2 and VEGFR3 signal redundantly downstream of VE-ca

57 1(+) , CD14(+) /CD31(+) , CD31(+) , CD34(+) /VEGFR2(+) and CD62E(+) peripheral blood mononuclear cell

58 e a distinct endothelial phenotype (Cx40(+), VEGFR2(+), and endoglin(-)) to the surrounding endocardi

59 -)) to the surrounding endocardium (Cx40(-), VEGFR2(-), and endoglin(+)).

60 nd expressed high levels of VEGF receptor 2 (VEGFR2) and its phosphorylated forms as compared with tM

61 r endothelial growth factor receptor type 2 (VEGFR2), and vascular endothelial growth factor receptor

62 bound higher (versus VEGF165a) to VEGFR1 not VEGFR2, and (3) levels correlated with decreased VEGFR1,

63 bound higher (versus VEGF165a) to VEGFR1 not VEGFR2, and (3) levels correlated with decreased VEGFR1,

64 F, 55% stained with VEGFR1, 98% stained with VEGFR2, and 96% stained with VEGFR3.

65 ression increased, GIV was phosphorylated by VEGFR2, and p-GIV bound and activated Galphai3 and enhan

66 ar endothelial growth factor (VEGF), phospho-VEGFR2, and phospho-Akt mesenteric protein expression.

67 tor 2 (VEGFR2), the endosomal trafficking of VEGFR2, and site-specific VEGFR2 tyrosine phosphorylatio

68 herapeutic intervention by targeting VEGF-A, VEGFR2, and VEGFR3 inhibited tumor growth, consistent wi

69 The VEGFR2 antagonist ZM323881 [5-((7-benzyloxyquinazolin-4-

70 vely target VEGFR2 phosphorylation, VEGF, or VEGFR2 are ineffective in shutting down signaling to ERK

71 The VEGF-C receptors VEGFR3 and VEGFR2 are required for embryonic blood vessel formation

72 ise that mutant p53 impacts transcription of VEGFR2 as well as myriad other genes by promoter remodel

73 ding directly to the transmembrane domain of VEGFR2, as well as VEGFR3, which we now identify as anot

74 VEGFR2 assessment with BR55 demonstrated significant dif

75 lial cells and decreased the availability of VEGFR2 at the cell surface.

76 R2 and evaluated whether blocking the doppel/VEGFR2 axis suppresses the process of angiogenesis.

77 angiogenic-endogenic-associated gene (VEGF, VEGFR2, BFGF, PGF, HGF, Ang-1, VWF, PECAM-1 and ENOS) ex

78 ties lead to distinct profiles of VEGFR1 and VEGFR2 binding and VEGFR2 site-specific phosphorylation

79 ain of KIF13B that compete specifically with VEGFR2 binding of KIF13B and thereby potently inhibit an

80 bioactive peptides based on deep analysis of VEGFR2-binding domain of KIF13B that compete specificall

81 Transcriptional regulation of VEGFR2 by ADAM17 was confirmed in cocultured cardiomyocy

82 to identify possible feedback regulation of VEGFR2 by calpain via its substrate protein phosphotyros

83 sed both, implicating negative regulation of VEGFR2 by PTP1B.

84 EGF receptor 1 (VEGFR1) and VEGF receptor 2 (VEGFR2) by translocating to the nuclei of ECs.

85 mputational model of signaling downstream of VEGFR2, by including SphK1 and calcium positive feedback

86 Inhibition of constitutive endocytosis of VEGFR2, by interference with the function of clathrin, d

87 in CD14(+) /CD31(+) , CD62E(+) and CD34(+) /VEGFR2(+) CACs, respectively, and reduced CD3(+) /CD31(-

88 ion to the primary signaling pathway of VEGF/VEGFR2/calpain/PI3K/AMPK/Akt/eNOS.

89 /VEGFR2(+) generation and suppresses CD34(+)/VEGFR2(+) cell mobilization and homing to the injured ve

90 HHcy reduced bone marrow (BM) CD34(+)/VEGFR2(+) cells and suppressed replenishment of postinju

91 ppressed replenishment of postinjury CD34(+)/VEGFR2(+) cells in peripheral blood (PB).

92 CD34(+)/VEGFR2(+) cells were examined by flow cytometry.

93 , CS induces dissociation of the VE-cadherin.VEGFR2 complex localized at the adherens juctions, causi

94 Overexpression of VEGFR2 correlated with resistance to cisplatin and combi

95 CD34+ and CD34+/VEGFR2+ counts significantly improved risk prediction me

96 Low CD34+/VEGFR2+ counts were associated with a 1.40-fold (95% con

97 scular endothelial growth factor receptor-2 (VEGFR2+) counts was associated with a 31% (P=0.032) and

98 After colitis induction, VEGFR2(DeltaIEC) mice developed significantly fewer tumo

99 reater number of intestinal tumor cells from VEGFR2(DeltaIEC) mice were in senescence than tumor cell

100 CAC was induced in VEGFR2(DeltaIEC) mice, which do not express VEGFR2 in th

101 2) VEGF increased glioma MIF production in a VEGFR2-dependent manner, suggesting that bevacizumab-ind

102 embryonic organ explants, we determined that VEGFR2-dependent signaling is required for salivary glan

103 were not mimicked by selective inhibition of VEGFR2 despite equivalent vascular pruning, but were acc

104 GF can bind to and activate VEGF receptor 2 (VEGFR2) directly, with a different pattern of site-speci

105 results in altered cellular distribution of VEGFR2 due to trafficking defects from the Golgi apparat

106 Mutational analysis revealed that the VEGFR2-epsin interaction is supported by VEGFR2 interact

107 Furthermore, we found that the VEGF-induced VEGFR2-epsin interaction promoted casitas B-lineage lymp

108 giogenic therapeutic interventions targeting VEGFR2-ERK1/2 axis.

109 This also acts on VEGF receptor 2 (VEGFR2) expressed in PD prolactin-producing cells known

110 ose in the control group; similarly, ex vivo VEGFR2 expression (P = .03) and percentage area of blood

111 arly targeted US signal correlated well with VEGFR2 expression (r = 0.86, P = .001), and rBV (r = 0.7

112 exhibit angiogenic features, including early VEGFR2 expression and active proliferation of adjacent e

113 VEGFR2 expression and percentage area of blood vessels w

114 VEGFR3 limits VEGFR2 expression and VEGF/VEGFR2 pathway activity in qu

115 ical analysis showed significantly increased VEGFR2 expression in the mast cells along the venules in

116 cardium, which could underlie the suppressed VEGFR2 expression in these hearts.

117 cardiomyocyte-fibroblast as ischemia-induced VEGFR2 expression was blocked by ADAM17-siRNA.

118 ase were blocked pharmacologically, S1P3 and VEGFR2 expression was decreased.

119 VEGFR2 expression was determined 8 minutes after BR55 in

120 VEGFR2 immunofluorescence demonstrated that VEGFR2 expression was significantly higher in pancreatic

121 angiogenesis and diminishing lactotroph (LT) VEGFR2 expression, lifting reproductive axis repression

122 l suppressed angiogenesis through inhibiting VEGFR2 expression, which can be enhanced by FGF inhibiti

123 onconducting TRPC1 mutant decreased S1P3 and VEGFR2 expression.

124 ess VEGFR2 in the intestinal epithelium, and VEGFR2(fl/fl) mice (controls) by administration of azoxy

125 Moreover, LHbisD4 eliminated VEGFR2 from the cell membrane, prevented VEGF binding in

126 Doppel inhibition depleted VEGFR2 from the cell membrane, subsequently inducing the

127 eceptor 2 (VEGFR2) signaling by dissociating VEGFR2 from VE-cadherin at the cell junctions.

128 pacity to repress the activity of vehgr1 and vegfr2 gene promoters.

129 fy uPA-dependent de-repression of vegfr1 and vegfr2 gene transcription through binding to HHEX/PRH as

130 for the SNPs rs4576072 and rs6828477 in the VEGFR2 gene.

131 In conclusion, HHcy reduces BM CD34(+)/VEGFR2(+) generation and suppresses CD34(+)/VEGFR2(+) ce

132 vival by triggering assembly of an activated VEGFR2/GIV/Galphai3 signaling complex and enhancing down

133 nhibitors (TKI) that target VEGF receptor-2 (VEGFR2) have not been effective as adjuvant treatments f

134 and decrease activation of VEGF receptor-2 (VEGFR2), hereunto considered the dominant receptor in po

135 Ex vivo quantitative VEGFR2 immunofluorescence demonstrated that VEGFR2 expre

136 progression, reduce levels of phosphorylated VEGFR2 in articular chondrocytes and synovial cells and

137 by retaining expression of TNFR1 and -2 and VEGFR2 in endothelial cells.

138 e factor in this process because deletion of Vegfr2 in osteoblastic lineage cells enhanced osteoblast

139 onstitutively colocalized and complexed with VEGFR2 in TECs.

140 lpha and proangiogenic factors NF-kappaB and VEGFR2 in the 7-d first generation and second generation

141 VEGFR2(DeltaIEC) mice, which do not express VEGFR2 in the intestinal epithelium, and VEGFR2(fl/fl) m

142 f VEGFR2 with KIF13B but also trafficking of VEGFR2 in the plus-end direction to the EC plasmalemma.

143 blocked the phosphorylation of both RET and VEGFR2 in tumor tissue.

144 ococcus pyogenes (SpCas9) is used to deplete VEGFR2 in vascular endothelial cells (ECs), whereby the

145 r endothelial growth factor receptor type 2 (VEGFR2) in the regulation of gingival venules in a rat m

146 insert domain receptor (KDR), also known as VEGFR2, in a myeloid cell sublineage is necessary for ma

147 alpain/PTP1B negative feedback regulation of VEGFR2, in addition to the primary signaling pathway of

148 iate specific interactions between epsin and VEGFR2, in addition to UIM recognition of ubiquitin moie

149 Simultaneous VEGFR2 inactivation fully rescues these defects.

150 tumor angiogenesis and growth via targeting VEGFR2, indicating miR-497 can be explored as a potentia

151 (low) monocytes or neutrophils improved anti-VEGFR2-induced SL4 tumor growth delay similar to the CXC

152 VEGFR2 therapy, CXCR4 blockade enhanced anti-VEGFR2-induced tumor growth delay but specific depletion

153 bolism and chemosensitization in response to VEGFR2 inhibition.

154 thelial barrier disruption was attenuated by VEGFR2 inhibition.

155 resistance to cisplatin and combination with VEGFR2-inhibitor apatinib synergistically increased cisp

156 the VEGFR2-epsin interaction is supported by VEGFR2 interacting specifically with the UIM and with ub

157 that drive the specificity of the epsin and VEGFR2 interaction and (2) to ascertain whether such det

158 We discovered new PDGF:VEGFR2 interactions with PDGF-AA:R2 KD = 530 nM, PDGF-AB

159 VEGFR2 interacts with phosphatidylinositol-4,5-bisphosph

160 Thus, the expression of S1P3 and VEGFR2 is mediated by a calcium-dependent mechanism.

161 We show that tyrosine phosphorylation of VEGFR2 is significantly elevated in the tumor vasculatur

162 the function of constitutive endocytosis of VEGFR2 is to protect the receptor against plasma membran

163 ron, whereas expression of its receptor (Kdr/Vegfr2) is largely restricted to adjacent peritubular ca

164 n therapeutic inhibition of VEGF receptor 2 (VEGFR2) is utilized in combination with hornerin knockdo

165 scular endothelial growth factor receptor 2 (VEGFR2), its mRNA, and total protein levels were reduced

166 in ubiquitin-interacting motif (UIM) and the VEGFR2 kinase domain.

167 response modifier raloxifene with the c-Met/VEGFR2 kinase inhibitor cabozantinib, dramatically poten

168 Finally, oral administration of the VEGFR2 kinase inhibitor Vandetanib attenuates OA progres

169 We find that genetic deletion of endothelial VEGFR2, knockout of the Pdgf-c gene or pharmacological b

170 show that ligated VEGFR2 and phosphorylated VEGFR2 levels diverge over time following stimulation.

171 y PDGF binding could contribute up to 96% of VEGFR2 ligation in healthy conditions and in cancer.

172 validated cell-level computational model of VEGFR2 ligation, intracellular trafficking, and site-spe

173 scular endothelial growth factor receptor 2 (VEGFR2) localized on the surface of endothelial cells (E

174 hologic vessels, and that editing of genomic VEGFR2 locus using rAAV1-mediated CRISPR/Cas9 abrogates

175 otein-specific and conditional-determined by VEGFR2 loss of function in a biological context in which

176 i-angiogenesis and anti-tumor effects in the VEGFR2-luc breast tumor model proven by BLI, WB and immu

177 isclose the role of miR-497 on angiogenesis, VEGFR2-luc transgenic mice were treated with miR-497 mim

178 Distinct residues in the epsin UIM and VEGFR2 mediate specific interactions between epsin and V

179 rens juctions, causing activation of VEGFR2, VEGFR2-mediated Src-dependent phosphorylation of VE-cadh

180 lomerular microvasculature, not only through VEGFR2-mediated vasculotrophism, but also through modula

181 Up-regulation of VEGFR2 mediates the role of mutant p53 in increasing cel

182 r the first time demonstrate a calpain/PTP1B/VEGFR2 negative feedback loop in the regulation of VEGF-

183 tor receptor alpha (PDGFRalpha)-positive and VEGFR2-negative cells by enabling indirect activation of

184 sociated receptors (GP130, GMRA, GMRB, CCR5, VEGFR2, NRP1, VEGFR3, NRP2) in the basal, HER2 (human ep

185 essential component, along with PECAM-1 and VEGFR2, of a complex that mediates flow signaling.

186 Mechanistically, inhibiting VEGFR2 or AMP-activated protein kinase (AMPK), a major d

187 We also examined angiogenesis (VEGFR2, p-ERK, p-PLCr1/2), hedgehog (Gli1, Ptch1, SMO),

188 VEGFR3 limits VEGFR2 expression and VEGF/VEGFR2 pathway activity in quiescent and angiogenic bloo

189 ies, specifically those targeting the VEGF-A/VEGFR2 pathway, have been approved for subsets of solid

190 PAD is associated with low CD34+ and CD34+/VEGFR2+ PC counts.

191 d signaling as measured by decreased phospho-VEGFR2, phospho-ERK1/2 and phospho-p38-MAPK levels.

192 lations demonstrate distinct localization of VEGFR2 phosphorylated on Y1175 and Y1214.

193 ted in minimal PSC, high ITSC, and sustained VEGFR2 phosphorylation inhibition until day 14.

194 hough PlGF is predicted to slightly increase VEGFR2 phosphorylation when over-expressed by 10-fold.

195 e that monotherapies that exclusively target VEGFR2 phosphorylation, VEGF, or VEGFR2 are ineffective

196 r, calpain activation inhibited VEGF-induced VEGFR2 phosphorylation, which can be restored by PTP1B s

197 ly, silencing of R-Ras resulted in increased VEGFR2 phosphorylation.

198 eltaCD counteract Vegfr2-Y949 (Y951 in human VEGFR2) phosphorylation by signalling through the endoth

199 r endothelial growth factor receptor type 2 (VEGFR2) phosphorylation, tumor volume, and histopatholog

200 kage depends on signalling initiated via the VEGFR2 phosphosite Y949, regulating dynamic c-Src and VE

201 lators in the eye and kidney through reduced VEGFR2/PKC-alpha/CREB signaling.

202 VEGFR2 plays a fundamental role in blood vessel formatio

203 We report here that both VEGF receptor 2 (VEGFR2)-positive and -negative cells depended on VEGF to

204 confirmed the lower microvessel density and VEGFR2-positive area fraction in tumors treated with ant

205 ed a single somatic mutation in KDR (encodes VEGFR2), possibly in response to ramucirumab.

206 Furthermore, concurrent deletion of Vegfr2 prevented VEGF-induced excessive vascular leakage

207 Shedding of VEGFR2 produces an N-terminal soluble fragment (100 kDa,

208 Mutant p53 binds near the VEGFR2 promoter transcriptional start site and plays a r

209 omplex, which is required for remodeling the VEGFR2 promoter.

210 suggest that constitutive internalization of VEGFR2 protects the receptor against shedding and provid

211 Furthermore, western blot indicated that the VEGFR2 protein level was reduced after CHIP overexpressi

212 VEGFR3 gene silencing upregulated VEGFR2 protein levels and phosphorylation in cultured en

213 ith antibodies against VEGF (bevacizumab) or VEGFR2 (ramucirumab) has been proven efficacious in colo

214 e expression of PD-L1, E-cadherin, CD24, and VEGFR2 rapidly formed tumors outside the primary tumor m

215 Genetic deletion of the signal-transducing Vegfr2 receptor prevents excessive angiogenesis but does

216 ation, which in turn is required to activate VEGFR2-recruited SRC family kinases (SFKs).

217 th factor (VEGF) signaling via its receptor, VEGFR2, regulates senescence and proliferation of tumor

218 ificance of these futile transport cycles of VEGFR2 remains unclear.

219 anib is a novel tyrosine kinase inhibitor of VEGFR2, RET, and EGFR, all of which are in involved in t

220 chemotherapy-driven cell death; blocking of VEGFR2 sensitized chemoAML to chemotherapy (re-)treatmen

221 In capturing essential features of VEGFR2 signaling and trafficking, our model suggests tha

222 on in mice and show that a DLL4/NOTCH1/VEGFA/VEGFR2 signaling axis is key for coronary artery develop

223 Regulated by a DLL4/NOTCH1/VEGFA/VEGFR2 signaling axis, these angiogenic cells generate m

224 etic or pharmacological inhibition of Vegfab/Vegfr2 signaling blocks the formation of the VTAs and su

225 evere PAD (Balb/c strain) without activating VEGFR2 signaling but with increased VEGFR1 activation.

226 s crucial signal transducers to mediate VEGF-VEGFR2 signaling during angiogenesis.

227 letion of endothelial cells or inhibition of VEGFR2 signaling in organ explants caused an aberrant in

228 Inhibition of VEGFR2 signaling leads to senescence of human and mouse

229 othelial cords were removed by blocking VEGF-VEGFR2 signaling or using a vascular deficient zebrafish

230 These changes were linked to increased VEGFR2 signaling that counteracted chemotherapy-driven c

231 VEGF/VEGFR2 signaling through Erk1/2 and Stat3 leads to upreg

232 tumor progression by shifting the balance of VEGFR2 signaling toward uncontrolled tumor angiogenesis,

233 egradation of VEGFR2 and thereby attenuating VEGFR2 signaling.

234 dial glia control these processes via Vegfab/Vegfr2 signaling: vegfab is expressed by radial glia, an

235 otein (GIV)/girdin mediates VEGF receptor 2 (VEGFR2) signaling and compensates for nephrin loss.

236 d to significantly impaired VEGF receptor 2 (VEGFR2) signaling and decreased levels of matrix metallo

237 (18% CS) rapidly activates VEGF receptor 2 (VEGFR2) signaling by dissociating VEGFR2 from VE-cadheri

238 hagic program downstream of VEGF receptor 2 (VEGFR2) signaling that requires paternally expressed gen

239 we demonstrate that abolishment of the VEGF-VEGFR2 signalling pathway as well as ablation of sprouti

240 c association between the minor alleles of 2 VEGFR2 single nucleotide polymorphisms (SNPs) and greate

241 ct profiles of VEGFR1 and VEGFR2 binding and VEGFR2 site-specific phosphorylation in vivo, mediated b

242 a pharmacogenetic association between the 2 VEGFR2 SNPs, rs4576072 and rs6828477, and change in VA i

243 Most (94%) of the VEGFR2 staining was diffuse.

244 rs 1 and 3 (S1P1/S1P3), and VEGF receptor 2 (VEGFR2) stimulates migration.

245 scular endothelial growth factor receptor 2 (VEGFR2)-targeted microbubbles and (b) 3D dynamic contras

246 venous injection of 5 x 10(7) clinical-grade VEGFR2-targeted microbubble contrast material.

247 (BR1, BR38; Bracco, Geneva, Switzerland) and VEGFR2-targeted microbubbles (BR55, Bracco) before and 4

248 US with clinical-grade VEGFR2-targeted microbubbles allows detection of small f

249 techniques: (a) molecularly targeted US with VEGFR2-targeted microbubbles, (b) bolus DCE US with nont

250 Results Molecularly targeted US signal with VEGFR2-targeted microbubbles, peak enhancement, and rBV

251 VEGFR2-targeted US of PDAC showed significantly higher s

252 The highest VEGFR2-targeted US signal intensities were observed in s

253 VEGFR2-targeted US signal, peak enhancement, area under

254 re detected earlier and more distinctly with VEGFR2-targeted US than with functional US.

255 ng2-specific CovX-body) can be combined with VEGFR2-targeting TKIs (sunitinib or regorafenib) to succ

256 ion mechanism involving NCK1/2, ROBO1/2, and VEGFR2 that controls endothelial cell front-rear polarit

257 from the site of interaction of KIF13B with VEGFR2 that inhibit VEGFR2 trafficking and thereby starv

258 ng uncovered 2 novel binding surfaces within VEGFR2 that mediate specific interactions with epsin UIM

259 and immobilized ligands to VEGF receptor 2 (VEGFR2), the endosomal trafficking of VEGFR2, and site-s

260 scular endothelial growth factor receptor 2 (VEGFR2), the primary functional VEGF receptor that media

261 yte recruitment and improved outcome of anti-VEGFR2 therapy in mouse CRCs.

262 Here we found that anti-VEGFR2 therapy up-regulates both C-X-C chemokine ligand

263 In CT26 CRCs, highly resistant to anti-VEGFR2 therapy, CXCR4 blockade enhanced anti-VEGFR2-indu

264 nhanced inhibition of tumor growth with anti-VEGFR2 therapy.

265 ptide specifically targets tumor endothelial VEGFR2 through an unconventional binding mechanism that

266 netrates cells, and seeds the aggregation of VEGFR2 through direct interaction.

267 s, including VEGF, VEGF receptor 1 (VEGFR1), VEGFR2, Tie2, erythropoietin, transforming growth factor

268 kidney cancer; and as single agents or with VEGFR2 TKIs in resected colorectal cancer.

269 resected breast cancer; in combination with VEGFR2 TKIs in resected kidney cancer; and as single age

270 in combination with VEGF-A blockers (but not VEGFR2 TKIs) in resected breast cancer; in combination w

271 We found VEGFR2 to activate phosphatidylinositol-4,5-bisphosphate

272 esin family plus-end motor KIF13B transports VEGFR2 to the EC surface, and as such, specific inhibiti

273 teraction of KIF13B with VEGFR2 that inhibit VEGFR2 trafficking and thereby starve cancer of blood su

274 ing and trafficking, our model suggests that VEGFR2 trafficking parameters are largely consistent acr

275 nd as such, specific inhibition of polarized VEGFR2 trafficking prevents angiogenesis.

276 yte ADAM17 in post-MI recovery by regulating VEGFR2 transcription and angiogenesis, thereby limiting

277 ficantly enhanced treatment efficacy of anti-VEGFR2 treatment in both CRC models.

278 cells, which are recruited to CRCs upon anti-VEGFR2 treatment.

279 o monocytes that mediates resistance to anti-VEGFR2 treatment.

280 mal trafficking of VEGFR2, and site-specific VEGFR2 tyrosine phosphorylation to study differences in

281 scular endothelial growth factor receptor 2 (VEGFR2) tyrosine kinase inhibitors.

282 are mainly localized at the plasma membrane, VEGFR2 undergoes constitutive endocytosis (in the absenc

283 n, preserved adherens junction integrity and VEGFR2.VE-cadherin complex, and suppressed CS-induced EC

284 the adherens juctions, causing activation of VEGFR2, VEGFR2-mediated Src-dependent phosphorylation of

285 Increased shedding of VEGFR2 (via inhibition of constitutive endocytosis) resu

286 Phosphorylation of VEGFR2 was inhibited until day 14 after TACE with both s

287 Furthermore, the expression of S1P3 and VEGFR2 was significantly down-regulated.

288 This effect of R-Ras on VEGFR2 was, at least in part, dependent on vascular endo

289 PSC, ITSC, and phosphorylation of VEGFR2 were assessed on days 1 and 14.

290 in specifically interacts with and regulates VEGFR2 were unknown.

291 d vascular permeability via VEGF receptor 2 (VEGFR2), whereas lymphangiogenesis signals are transduce

292 y standpoint, Pz-1 was shown to be active on VEGFR2, which can block the blood supply required for RE

293 lls, R-Ras suppressed the internalization of VEGFR2, which is required for full activation of the rec

294 bitor (KAI) not only prevents interaction of VEGFR2 with KIF13B but also trafficking of VEGFR2 in the

295 n be accounted for by altered trafficking of VEGFR2 without an intrinsic difference in receptor activ

296 lling, but Robo4 and Robo4DeltaCD counteract Vegfr2-Y949 (Y951 in human VEGFR2) phosphorylation by si

297 bolished Y949 signalling in the mouse mutant Vegfr2(Y949F/Y949F) leads to VEGFA-resistant endothelial

298 Tumour-bearing Vegfr2(Y949F/Y949F) mice display reduced vascular leakag

299 Vessels in Vegfr2(Y949F/Y949F) mice remain sensitive to inflammator

300 of its cytoplasmic domain, while activating VEGFR2-Y951 via ROBO4 inhibition might accelerate tissue