ライフサイエンスコーパス: VEGFR2

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

2 angiogenic effects through VEGF receptor 2 (VEGFR2).

3 EM1 does not bind with any great affinity to VEGFR2.

4 pathways in endothelial cells by binding to VEGFR2.

5 rvival are triggered by VEGF-A activation of VEGFR2.

6 ffinities for monomeric and dimeric forms of VEGFR2.

7 as a result of shear stress is dependent on VEGFR2.

8 of EC markers such as CD144, eNOS, CD31, and VEGFR2.

9 n 50 (IC(50)) of <0.003 muM for both RET and VEGFR2.

10 ng activation of p38MAPK/STAT1 signaling via VEGFR2.

11 n and increased expression of both Nanog and VEGFR2.

12 their surface membrane, including VEGFR1 and VEGFR2.

13 reases dramatically the cleavage/shedding of VEGFR2.

14 to UIM recognition of ubiquitin moieties on VEGFR2.

15 ohistochemical staining was used to localize VEGFR2.

16 UIM were found to interact with residues in VEGFR2.

17 l drug candidate Pz-1, which targets RET and VEGFR2.

18 angiogenic variant would preferentially bind VEGFR2.

19 hypomethylation and expression/activation of VEGFR2.

20 between VEGF-A(165a):VEGFR1 and VEGF-A(165a):VEGFR2, 1.0 pM and 10 pM respectively, and validated the

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

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

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

24 GREM1 does not interfere with VEGF-mediated VEGFR2 activation, suggesting that GREM1 does not bind w

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

26 pped with sialic acid oppose ligand-mediated VEGFR2 activation, whereas the uncapped asialo-glycans f

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

28 dc2-VEGFA(165)-VEGFR2 complex which enhances VEGFR2 activation.

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

30 Inhibition of VEGFR2 activity by cediranib rescues vascular abnormalit

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

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

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

34 ion of angiogenic signaling pathways such as VEGFR2, Akt, mTOR, eNOS, and Notch, and reduces EC migra

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

36 Remarkably, inactivation of VEGFR2 also results in increased axon branching in vitro

37 Here we show that VEGF and its receptor VEGFR2 (also known as KDR or FLK1) are expressed in mous

38 , we show that in the developing hippocampus VEGFR2 (also known as KDR or FLK1) is expressed specific

39 We posit that the VEGFR2/AMPK/PEG3 axis integrates the anti-angiogenic and

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

41 Furthermore, cotargeting VEGFR2 and APLNR synergistically improved survival of mi

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

43 altered F-actin morphology, and reduces both VEGFR2 and cholesterol in buoyant raft membranes.

44 ults demonstrate the functional crosstalk of VEGFR2 and ephrinB2 in vivo to control dendritic arboriz

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

46 nic factors VEGFA, FGF2, and their receptors VEGFR2 and FGFR1, respectively, by directly binding to t

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

48 metalloproteinases, and reduced activity of VEGFR2 and its downstream signaling.

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

50 rns and functional blockade of the receptors VEGFR2 and NRP1 demonstrated that VEGF mediates its plei

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

52 ce that supports dual inhibition of the VEGF-VEGFR2 and PD-1-PD-L1 pathways.

53 on of all tested RET oncoproteins as well as VEGFR2 and proliferation of cells transformed by RET.

54 unction through the activation of VEGFR1 and VEGFR2 and the suppression of the G6PD/PPP and the antio

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

56 In contrast, FAK-Y861F ECs showed decreased Vegfr2 and Tie2 expression with an enhancement in beta1

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

58 scular endothelial growth factor receptor 2 (VEGFR2) and promote hyaloid vessel regression.

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

60 ular proteins in response to VEGF, including VEGFR2, and gene expression profiles, such as that of ne

61 ckdown predominantly inhibited activation of VEGFR2, and phosphorylation of p38MAPK and STAT1, as wel

62 atinib is a multikinase inhibitor of VEGFR1, VEGFR2, and VEGFR3, and other receptor tyrosine kinases.

63 dard of care, plus ramucirumab, a human IgG1 VEGFR2 antagonist, or placebo in patients with untreated

64 APLNR and its cognate ligand apelin in VEGFA/VEGFR2 antiangiogenic therapy against distinct subtypes

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

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

67 and validated the known affinity VEGF-A(121):VEGFR2 as K(D) = 0.66 nM.

68 scular Endothelial Growth Factor Receptor 2 (VEGFR2), as a novel PAH candidate gene.

69 anced synchronous inhibition of both RET and VEGFR2, as well the resistance to demethylation, renders

70 Furthermore, we report that VEGFR2 Asn-247-linked glycans capped with sialic acid op

71 VEGFR2 assessment with BR55 demonstrated significant dif

72 further facilitates Sema3E-induced PlexinD1-VEGFR2 association, VEGFR2 transphosphorylation at Y1214

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

74 We show that ORP2 regulates the integrity of VEGFR2 at the PM in a cholesterol-dependent manner, the

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

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

77 ic variant, VEGF-A(165b) selectively prefers VEGFR2 binding at an affinity = 0.67 pM while binding VE

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

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

80 VEGF receptor (VEGFR)1 or VEGFR2 blockade prevented the inhibitory effect of PlGF

81 apelin levels were downregulated by VEGFA or VEGFR2 blockade.

82 ause increased expression of plasma membrane VEGFR2, but in a manner associated with low signaling st

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

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

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

88 A recent finding that VEGFR2 can dimerize in the absence of ligand raises the

89 ased plasma membrane localization of phospho-VEGFR2 compared with normal ECs.

90 f its HS chains and promotes Sdc2-VEGFA(165)-VEGFR2 complex formation.

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

92 s and formation of a ternary Sdc2-VEGFA(165)-VEGFR2 complex which enhances VEGFR2 activation.

93 ulation of VEGFR1 and ~30% downregulation of VEGFR2 concentration via 24 h VEGF-A(165) treatment.

94 We observe no change in VEGFR1 or VEGFR2 concentration with 24 h VEGF-B(167) treatment.

95 scular endothelial growth factor receptor 2 (VEGFR2) controls angiogenesis and is critically importan

96 Overexpression of VEGFR2 correlated with resistance to cisplatin and combi

97 ion could suppress edema while leaving other VEGFR2-dependent functions intact.

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

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

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

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

102 rovide evidence that cell surface-associated VEGFR2 displays sialylated N-glycans at Asn-247 and, in

103 ke (DLL) 3, and Notch2 but reduced levels of VEGFR2, DLL1, DLL4, Notch1, Notch3, and Notch4.The regul

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

105 Although VEGF-VEGFR2 effective binding constants have been measured, t

106 we examined the effect of EMCN depletion on VEGFR2 endocytosis and activation.

107 These results indicate that EMCN modulates VEGFR2 endocytosis and activity and point to EMCN as a p

108 othelial cells (ECs), loss of EMCN prevented VEGFR2 endocytosis.

109 scular endothelial growth factor receptor 2 (VEGFR2), EPHA2-VEGFR2, EPHA2-fibroblast growth factor re

110 ial growth factor receptor 2 (VEGFR2), EPHA2-VEGFR2, EPHA2-fibroblast growth factor receptor 1 (FGFR1

111 VEGFR2-ephrinB2 compound mice (Nes-cre Kdr(lox/+) Efnb2(

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

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

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

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

116 VEGFR2 expression and percentage area of blood vessels w

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

118 VEGFR2 expression in vessel endothelial cells was upregu

119 ndo-T) cells in 3D cultures exhibited higher VEGFR2 expression levels, accelerated migration, invasio

120 VEGFR2 expression was determined 8 minutes after BR55 in

121 s exhibit increased Tie2 expression, reduced Vegfr2 expression, decreased beta1 integrin activation,

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

123 ve STAT3 mutant, but not of STAT1, abrogated VEGFR2 expression.

124 esses Dll4-Notch signaling thereby promoting VEGFR2 expression.

125 eceptor 1 (FGFR1), EPHA2-FGFR2, EPHA2-FGFR3, VEGFR2-FGFR1, VEGFR2-FGFR2, and VEGFR2-FGFR3, using a FR

126 R1), EPHA2-FGFR2, EPHA2-FGFR3, VEGFR2-FGFR1, VEGFR2-FGFR2, and VEGFR2-FGFR3, using a FRET-based metho

127 EPHA2-FGFR3, VEGFR2-FGFR1, VEGFR2-FGFR2, and VEGFR2-FGFR3, using a FRET-based method.

128 Cell surface analysis revealed a decrease in VEGFR2 following VEGF stimulation in control but not siR

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

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

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

132 -A(165) treatment induces a ~15% decrease in VEGFR2 heterogeneity, but little to no change in VEGFR1

133 uces little to no change in either VEGFR1 or VEGFR2 heterogeneity.

134 that N-linked glycans at the Asn-247 site in VEGFR2 hinder VEGF ligand-mediated receptor activation a

135 mpts, we did not observe GREM1 activation of VEGFR2 in any of the cell lines reported by the above-me

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

137 id show expression of CD31, CD144, TIE-2 and VEGFR2 in atherosclerotic ApoE(-/-) aortas.

138 s DNMT1 stability, induces the expression of VEGFR2 in endothelial cells via a promoter methylation-d

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

140 ligand-dependent activation and signaling of VEGFR2 in endothelial cells.

141 ), significantly reduced perinuclear (Golgi) VEGFR2 in human ECs with a concomitant increase in phosp

142 tor 2) and decreases blood levels of soluble VEGFR2 in Lztr1 haploinsufficient mice.

143 the potential interaction between GREM1 and VEGFR2 in mammalian cells.

144 Mice lacking VEGFR2 in neurons (Nes-cre Kdr(lox/-)) show decreased de

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

146 onstitutively colocalized and complexed with VEGFR2 in TECs.

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

148 ELISA screening of soluble VEGFR2 in the blood of LZTR1-mutated patients with NS ma

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

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

151 cells and promote angiogenesis via elevating VEGFR2 in vessel endothelial cells.

152 gration in vitro and increased expression of VEGFR2 in vivo in the vasculature of TRPV4 KO tumors com

153 The knockdown also increased phospho-VEGFR2 in whole cell lysates and membrane fractions comp

154 scular endothelial growth factor receptor-2 (VEGFR2) in endothelial cells, human kidney epithelial ce

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

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

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

158 ity of cabozantinib, an inhibitor of MET and VEGFR2, in patients with advanced Ewing sarcoma and oste

159 Simultaneous VEGFR2 inactivation fully rescues these defects.

160 thout affecting filopodia formation, loss of VEGFR2 increases the number of filopodia and enhances th

161 ng different steps in VEGFA/VEGF receptor 2 (VEGFR2)-induced vascular permeability, we show that targ

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

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

164 bolism and chemosensitization in response to VEGFR2 inhibition.

165 In addition, SU5416, a VEGFR2 inhibitor, was used to induce emphysema.

166 Using a Vegf-receptor 2 (VegfR2) inhibitor (cabozantinib; CBZ) via oral gavage in

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

168 mentally validated mechanisms by which VEGFA-VEGFR2 inhibitors contribute to nephrotoxicity, as well

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

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

171 y genes in endothelial cells disrupts VEGF-A/VEGFR2 internalization and downstream signaling.

172 ENDOA2 deficiency reduces VEGFR2 internalization and inhibits downstream activatio

173 owed that although VEGF stimulation promoted VEGFR2 internalization in control endothelial cells (ECs

174 logy to endothelial cells, ephrinB2 controls VEGFR2 internalization in neurons.

175 Mechanistically, VEGFR2 internalization is required for VEGF-induced spin

176 VEGFR2 is a highly N-glycosylated receptor tyrosine kina

177 Mechanistically, VEGFR2 is directed towards ENDOA2-mediated endocytosis b

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

179 VEGF signaling via VEGF receptor-2 (VEGFR2) is a major regulator of endothelial cell (EC) fu

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

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

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

183 compensate for this limitation by increasing VEGFR2 levels at the plasma membrane via microRNA-mediat

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

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

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

187 hippocampal neurons during development, with VEGFR2 locally expressed in the CA3 region.

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

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

190 ic endocytic pathway controlling a subset of VEGFR2 mediated responses that could be targeted to prev

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

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

193 es the question whether VEGF binds to either VEGFR2 monomers or dimers or to both.

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

195 ) to optimize and dually quantify VEGFR1 and VEGFR2 on human umbilical vein endothelial cells (HUVECs

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

197 yclin D1, VEGF and its receptors, VEGFR1 and VEGFR2 (p < 0.001) in xenograft tumors.

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

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

200 nonical program that controls the cell cycle/VEGFR2 pathway in the developing vasculature.

201 oliferation and by anomalous function of the VEGFR2 pathway.

202 al growth factor-A (VEGF-A)/VEGF receptor 2 (VEGFR2) pathway.

203 ly relies on overactivated PI3K/Akt/mTOR and VEGFR2 pathways in endothelial cells (ECs).

204 rrection of endothelial Smad1/5/8, mTOR, and VEGFR2 pathways opposes HHT pathogenesis.

205 strate measurement of 1 100 VEGFR1 and 6 900 VEGFR2 per HUVEC.

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

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

208 In contrast, no VEGFR2 phosphorylation was detected when cells were incu

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

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

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

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

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

214 ation of the holoreceptor complex comprising VEGFR2, PlexinD1, and neuropilin-1, thereby preventing d

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

216 VEGFR2+) progenitor cells in cardiac mesoderm, distinct

217 ereby preventing degradation of internalized VEGFR2, prolonging downstream signal transductions via P

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

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

220 g VEGF stimulation with an increase in total VEGFR2 protein.

221 show that targeting signaling downstream of VEGFR2 pY949 limits vascular permeability in retinopathy

222 Y685, but not Y658, residue is reduced when VEGFR2 pY949 signaling is impaired.

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

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

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

226 Therapeutically, targeting VEGFR2-regulated VE-cadherin phosphorylation could suppr

227 danib blocked the overactivation of mTOR and VEGFR2, respectively.

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

229 Blocking VEGFR2, RNase application, or VWF deficiency interfered

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

231 d on pSer-473 AKT, and was in complexes with VEGFR2, serving as co-factor of ER-alpha to regulate act

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

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

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

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

236 ovel noncanonical regulation of soluble VEGF/VEGFR2 signaling by mechanosensitive ion channel TRPV4.

237 These reports suggest that the GREM1 -> VEGFR2 signaling can drive angiogenesis both in vitro an

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

239 Activation of VEGF/VEGFR2 signaling in isolated hippocampal neurons results

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

241 Thus, a controlled VEGF/VEGFR2 signaling is required for proper CA3 hippocampal

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

243 and vascular barrier function via the VEGF-A/VEGFR2 signaling pathway.

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

245 egradation of VEGFR2 and thereby attenuating VEGFR2 signaling.

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

247 scular endothelial growth factor receptor 2 (VEGFR2) signaling is a common therapeutic strategy in on

248 scular endothelial growth factor receptor 2 (VEGFR2) signaling pathways in myoepithelial (CD10(+)) an

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

250 scular endothelial growth factor receptor 2 (VegfR2) signaling; and (3) Vegf secretion from macrophag

251 lexinD1 to VEGFR2, which then terminates the VEGFR2 signals.

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

253 ist of vascular endothelial growth factor 2 (VEGFR2), soluble decorin signals via the energy sensing

254 -cadherin), which increases VEGF receptor 2 (VEGFR2)-Src-VE-cadherin complex formation, resulting in

255 VE-cadherin and reduced the formation of the VEGFR2-Src-VE-cadherin complex, which led to reduced cel

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

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

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

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

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

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

262 forms a mechanocomplex with neuropilin-1 and VEGFR2 that is necessary and sufficient for conferring m

263 inding to five receptors: VEGFRs (VEGFR1 and VEGFR2), their coreceptor neuropilin1 (NRP1), and platel

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

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

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

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

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

272 sults thus show that TRPV4 channels regulate VEGFR2 trafficking and activation to identify novel cros

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

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

275 odulates expression of MYO1C, a regulator of VEGFR2 trafficking to the cell surface.

276 via rho kinase, which were shown to increase VEGFR2 trafficking to the plasma membrane.

277 on of the miR-15a/16-1 cluster, which limits VEGFR2 transcript stability and negatively modulates exp

278 Sema3E-induced PlexinD1-VEGFR2 association, VEGFR2 transphosphorylation at Y1214, and p38 MAPK activ

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

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

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

282 yr202/Tyr185) as well as VEGFR1(Tyr1213) and VEGFR2(Tyr1175) were also detected in HG-treated hRECs.

283 ombinant VEGF triggered a robust increase in VEGFR2 tyrosine phosphorylation.

284 IL-6-induced VEGFR2 up-regulation was inhibited by overexpression of

285 oblast growth factor 2), and their receptors VEGFR2 (vascular endothelial growth factor receptor 2) a

286 al accumulation and subsequent activation of VEGFR2 (vascular endothelial growth factor receptor 2) a

287 ial hyaluronan receptor 1), neuropilin-1 and VEGFR2 (vascular endothelial growth factor receptor 2),

288 ucing expression of EC markers (VE-cadherin, VEGFR2 [vascular endothelial growth factor receptor 2],

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

290 ted by targeting VEGF signaling with an anti-VEGFR2 (VEGF receptor 2) antibody.

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

292 scular endothelial growth factor receptor 2 (VEGFR2) was established, which was upregulated by SAHA.

293 in specifically interacts with and regulates VEGFR2 were unknown.

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

295 scular endothelial growth factor receptor 2 (VEGFR2), which was confirmed by intravital microscopic s

296 DP-bound state, RhoJ shifts from PlexinD1 to VEGFR2, which then terminates the VEGFR2 signals.

297 endorepellin evoked transient activation of VEGFR2, which, in turn, phosphorylated PERK at Thr(980)

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

299 scular endothelial growth factor receptor 2 (VEGFR2) with sialic acid-capped N-glycans.

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