ライフサイエンスコーパス: VE-cadherin

1 e dynamics of vascular endothelial cadherin (VE-cadherin).

2 expression of vascular endothelial cadherin (VE-cadherin).

3 rylation, internalization and degradation of VE-cadherin.

4 -proximal motif in the cytoplasmic domain of VE-cadherin.

5 ocytes to induce tyrosine phosphorylation of VE-cadherin.

6 s of the fenestrated endothelium and loss of VE-cadherin.

7 ylation and reduced membrane localization of VE-cadherin.

8 tight junctions through dephosphorylation of VE-cadherin.

9 and VEGFR3 signal redundantly downstream of VE-cadherin.

10 genesis markers including PECAM1, VEGFR, and VE-cadherin.

11 rs, induced the interaction of Galpha13 with VE-cadherin.

12 enuated TGF-beta1-induced down-regulation of VE-cadherin.

13 f claudin-5 is governed by the expression of VE-cadherin.

14 ion of Snail and Slug and down-regulation of VE-cadherin.

15 tyrosine phosphatases PTP1B and TC-PTP, and VE-cadherin.

16 n of miR-101, which led to downregulation of VE-cadherin.

17 of miR-101 resulted into the suppression of VE-cadherin.

18 e junctional, endothelial-specific cadherin, VE-cadherin.

19 e miRNA inhibitor enhanced the expression of VE-cadherin.

20 tors that bind to the miR-27 binding site in VE-cadherin.

21 inuous EC layer, and increased expression of VE-cadherin.

22 ndothelial-specific markers TIE2, PECAM, and VE-CADHERIN.

23 ar leakage via loss of vascular endothelial (VE)-cadherin.

24 se reporter assay, which showed that mutated VE-cadherin 3'UTR and miR-101 cotransfection did not cha

25 horylation of vascular endothelial cadherin (VE-cadherin), a constituent of adherens junctions, leads

26 These include VE-cadherin, a homotypic adhesion molecule that regulate

27 Here we address these issues with a focus on VE-cadherin, a major endothelial cell-specific junctiona

28 e derived from the Galpha13 binding motif on VE-cadherin abrogated the disruption of AJs in response

29 Mutating the Pals1-binding motif in VE-cadherin abrogates the ability of VE-cadherin to regu

30 ICAM-1-VE-cadherin association and promoted VE-cadherin-actin association.

31 n-driven, ARP2/3-controlled formation of new VE-cadherin adhesion sites via intermittently appearing

32 ma membranes and facilitate formation of new VE-cadherin adhesion sites, which quickly move into the

33 ction in actomyosin-dependent tension across VE-cadherin adhesion sites.

34 ularly and phenotypically distinct subset of VE-cadherin adhesions, defined here as focal adherens ju

35 on at AJs, resulting in the stabilization of VE-cadherin adhesions.

36 The results suggest a new model of VE-cadherin adhesive interaction mediated by Rac1-induce

37 ytic event that regulates the trafficking of VE-cadherin after endocytosis.

38 of its endothelial cell-specific substrate, VE-cadherin, after systemic injection of VEGF.

39 audins and ZO proteins), adherens junctions (VE-cadherin, alpha-Actinin), and the basement membrane (

40 -2 exhibited significantly reduced levels of VE-cadherin (also known as CDH5), which is essential for

41 o the barrier effector vascular endothelial (VE)-cadherin and induced vascular leakage.

42 robial abundance, intestinal barrier protein VE-cadherin and anti-inflammatory molecule IL-10 express

43 released bone morphogenetic proteins through VE-cadherin and bone morphogenetic protein receptor-II/S

44 altered NPY signaling in ECs caused reduced VE-cadherin and CD31 expression along EC junctions, resu

45 ranscription factor ERG drives expression of VE-cadherin and controls junctional integrity.

46 a gene expression time course revealed that VE-cadherin and FLK1 were upregulated in a dynamically s

47 lls that is necessary for phosphorylation of VE-cadherin and for breakdown of the endothelial barrier

48 Blockmir CD5-2 demonstrated specificity for VE-cadherin and inhibited vascular leak in vitro and in

49 spectrin-actin cytoskeleton, associates with VE-cadherin and inhibits its endocytosis.

50 lating actin dynamics, is a novel partner of VE-cadherin and is able to modulate YAP activity.

51 nctions to stress fibers, reduced tension on VE-cadherin and loss of junctional mechanotransducers su

52 ell movements by inhibiting stabilization of VE-cadherin and maturation of adherens junctions.

53 BRC to this site likely precedes movement of VE-cadherin and may play a role in clearing VE-cadherin

54 tion between adherens junction (AJ) proteins VE-cadherin and p120-catenin and stimulated AJ reanneali

55 and validated FRET-based tension sensors for VE-cadherin and PECAM-1 using our previously developed F

56 The Pi-induced MPs expressed VE-cadherin and superficial phosphatidylserine, and in a

57 yrosine phosphatase (VE-PTP) associates with VE-cadherin and supports endothelial cell contact integr

58 tenin stability, through signals mediated by VE-cadherin and the Wnt receptor Frizzled-4.

59 consisting of vascular endothelial cadherin (VE-cadherin) and beta-catenin.

60 co-expressing vascular endothelial-cadherin (VE-cadherin) and cytokeratins consistent with vasculogen

61 cifically demarcate acquisition of vascular (VE-cadherin) and hematopoietic (CD41a) cell fate and use

62 tight junction-associated proteins (ZO-1 and VE-cadherin) and PVM/M stabilizing neural cell adhesion

63 endothelial cells could be identified among VE-Cadherin+ and CD45- cells.

64 n, a lack of proper cell contacts, a loss of VE-cadherin, and aberrant actin stress fiber formation.

65 al cell adhesion molecule-1 (PECAM-1), CD144/VE-cadherin, and CD106/Endoglin, from vascular endotheli

66 cell genes including von Willebrand factor, VE-cadherin, and eNOS were observed when compared to CD3

67 scular endothelial cells, phosphorylation of VE-cadherin, and increased vascular permeability.

68 most (eg, CD31, von Willebrand factor [vWF], VE-cadherin, and intercellular adhesion molecule-2), but

69 horylation of paxillin, its association with VE-cadherin, and internalization of the latter.

70 horylation of beta-catenin, p120-catenin and VE-cadherin, and reduction in the barrier properties of

71 A complex consisting of PECAM-1, VE-cadherin, and vascular endothelial growth factor rece

72 ssays for endothelial nitric oxide synthase, VE-cadherin, and vWF indicated functional promoter activ

73 Previous work identified VE-cadherin as an essential component, along with PECAM-

74 We also found that VE-cadherin associated with the ICAM-1-SHP-2 complex.

75 ctin, SHP-2 down-regulation prevented ICAM-1-VE-cadherin association and promoted VE-cadherin-actin a

76 to VE-cadherin dissociation from ICAM-1 and VE-cadherin association with actin, SHP-2 down-regulatio

77 ate that local lack of vascular endothelial (VE)-cadherin at established cell junctions causes actin-

78 y diminished levels of vascular endothelial (VE)-cadherin at the cell surface in these blood vessels.

79 Src inhibition increased VE-cadherin at adherens junctions and increased endothel

80 issociation, leading to increased density of VE-cadherin at AJs.

81 VE-cadherin at endothelial cell-cell junctions links the

82 and altered the organization of F-actin and VE-cadherin at junctions.

83 EGFR2) signaling by dissociating VEGFR2 from VE-cadherin at the cell junctions.

84 Endocytosis of VE-cadherin, away from the interendothelial junction (IE

85 ion protein ZO-1 regulates tension acting on VE-cadherin-based adherens junctions, cell migration, an

86 the F-BAR protein pacsin2 in the control of VE-cadherin-based endothelial adhesion.

87 ession of the adherens junctional molecules, VE-cadherin, beta-catenin, and plakoglobin, and reduced

88 Apo(a) caused the disruption of VE-cadherin/beta-catenin complexes in a Src-dependent ma

89 lineage of over a period of 14 days based on VE-cadherin biomarker.

90 rway-hyperreactivity were also attenuated by VE-cadherin blockade, via mechanisms that blunted endoth

91 ocytes was dependent on ADAM10 regulation of VE-cadherin, but not CX3CL1 and CXCL16.

92 duced the ICAM-1-mediated phosphorylation of VE-cadherin by immunofluorescence and confocal analysis

93 lial cell junctions critically depend on the VE-cadherin/catenin complex and its interaction with the

94 increased permeability due to modulation of VE-cadherin/catenin complex.

95 re they mature through vascular endothelial (VE)-cadherin(+)CD45(-)CD41(low) (type 1 pre-HSCs) and VE

96 rin(+)CD45(-)CD41(low) (type 1 pre-HSCs) and VE-cadherin(+)CD45(+) (type 2 pre-HSCs) intermediates.

97 y increased the numbers of HSCs derived from VE-cadherin(+)CD45(+) AGM hematopoietic cells, consisten

98 a 2.2-fold increase in vascular endothelial (VE)-cadherin cell-surface expression above wild-type (WT

99 he PKA-CREB and BMP pathways in isolated AGM VE-cadherin(+) cells from mid-gestation embryos, we demo

100 cell sorting showing a 48% yield of CD31(+)/VE-cadherin(+) cells on CHL, compared to 27% on matrigel

101 LT-HSCs (Hoxb5(+)) are directly attached to VE-cadherin(+) cells, implicating the perivascular space

102 ociates with and inhibits the endocytosis of VE-cadherin cis dimers.

103 ting of the LBRC to the site of TEM precedes VE-cadherin clearance.

104 Inhibition of VE-cadherin clustering at adherens junctions (function-b

105 VE-cadherin clustering at adherens junctions promotes pr

106 Disruption of VE-cadherin clustering at AJs (function-blocking antibod

107 VE-cadherin clusters Pals1 at cell-cell junctions.

108 novel molecular mechanism through which the VE-cadherin complex controls YAP transcriptional activit

109 recruitment inhibits internalization of the VE-cadherin complex from FAJ trailing ends and is import

110 we demonstrate that EPS8 associates with the VE-cadherin complex of remodeling junctions promoting YA

111 erved adherens junction integrity and VEGFR2.VE-cadherin complex, and suppressed CS-induced EC permea

112 ed junctions, 14-3-3-YAP associates with the VE-cadherin complex, whereas Eps8 is excluded.

113 vinculin dissociation from the alpha-catenin-VE-cadherin complex.

114 adherin expression and stabilized junctional VE-cadherin complexes through associated phosphatases.

115 e(+)), endothelial cells (Adora2b(loxP/loxP) VE-cadherin Cre(+)), or alveolar epithelial cells (Adora

116 Lineage tracing of endothelial cells using VE-cadherin(Cre) driver failed to reveal a significant c

117 from the embryonic endothelium stage (using VE-cadherin-Cre recombinase), but not from embryonic hem

118 Interestingly, VE-cadherin cytoplasmic tyrosine Y658 can be phosphoryla

119 ns prompted us to address the involvement of VE-cadherin cytoplasmic tyrosines in flow sensing.

120 Furthermore, expression of VE-Cadherin decreased, whereas expression of Notch1 and

121 A (siRNA) transfection elicited induction of VE-cadherin, decreased Ajuba expression, increased Hippo

122 ic mesoderm can be matured into >90% CD31(+)/VE-cadherin(+) definitive ECs.

123 lloproteinase-14 (MMP-14) axis that controls VE-cadherin degradation, Endo-MT, and vascular abnormali

124 ZO-1 is thus a central regulator of VE-cadherin-dependent endothelial junctions that orchest

125 Thr41-phosphorylated beta-catenin attenuates VE-cadherin-dependent junction structures to increase EC

126 through VE-PTP expression and the resultant VE-cadherin dephosphorylation-mediated assembly of AJs.

127 rrupting IL-8-mediated vascular endothelial (VE)-cadherin disassembly.

128 We show that Src mediates VE-cadherin disassembly in response to metastatic melano

129 R2-mediated Src-dependent phosphorylation of VE-cadherin, disassembly of adherens junctions, and EC b

130 r, whereas the activation of ICAM-1 leads to VE-cadherin dissociation from ICAM-1 and VE-cadherin ass

131 ted that Rac1 activation reduced the rate of VE-cadherin dissociation, leading to increased density o

132 ho kinase inhibitor also reduced the rate of VE-cadherin dissociation.

133 A VE-cadherin double mutant (Y658F, Y731F) expressed in en

134 ARP2/3 inhibitors, CK-548 and CK-666, blocks VE-cadherin dynamics and causes intercellular gaps.

135 This coordinated mechanism controls VE-cadherin dynamics and cell motility and maintains mon

136 ich quickly move into the junctions, driving VE-cadherin dynamics and remodeling.

137 er substrates, which may relate to increased VE-cadherin endocytosis and degradation.

138 we identify an additional motif that drives VE-cadherin endocytosis and pathological junction disass

139 This mechanism allows constitutive VE-cadherin endocytosis and recycling to contribute to a

140 hosphorylation of VE-cadherin, which reduced VE-cadherin endocytosis and thereby augmented AJ integri

141 K5-induced VE-cadherin endocytosis does not require the constitutiv

142 n tightened the vascular barrier by reducing VE-cadherin endocytosis in ECs, and rendering pericytes

143 Ankyrin-G inhibits VE-cadherin endocytosis independent of p120 binding.

144 However, K5-induced VE-cadherin endocytosis is associated with displacement

145 20 stabilizes cadherins and demonstrate that VE-cadherin endocytosis is crucial for endothelial cell

146 support a novel mechanism for regulation of VE-cadherin endocytosis through ankyrin association with

147 hus multiple context-dependent signals drive VE-cadherin endocytosis, but p120 binding to the cadheri

148 grafting embryonic precursors, including the VE-cadherin-expressing population that lacks hematopoiet

149 gnaling pathway and relevant phosphatases in VE-cadherin expression and function, vascular tone in ao

150 regulate inflammation by maintaining normal VE-cadherin expression and promoting T lymphocyte transm

151 ered Akt/WNT/beta-catenin signaling to drive VE-cadherin expression and stabilized junctional VE-cadh

152 thelial cells via its modulation of CD31 and VE-cadherin expression and the Hippo pathway.

153 uence, were the only TspanC8s that regulated VE-cadherin expression and were required for lymphocyte

154 d CD31KO endothelial cells exhibit a reduced VE-cadherin expression correlating with increased surviv

155 A decrease in VE-cadherin expression is associated with tumor patholog

156 increased with the increase of the amount of VE-cadherin expression on the cell surface during cell d

157 ts regulator miR-27a, resulting in increased VE-cadherin expression.

158 at CD31 deficiency results in a reduction in VE-cadherin expression.

159 am effector of TGFbeta-2, strongly decreased VE-cadherin expression.

160 thermore, overexpression of Snail suppressed VE-cadherin expression.

161 reduced adherens junction molecule (CD31 and VE-cadherin) expression, increased survivin and Ajuba ex

162 dilatation in old arteries treated with the VE-cadherin FBA.

163 Lamellipodia overlap the VE-cadherin-free adjacent plasma membranes and facilitat

164 of p120 from the cadherin, and p120 protects VE-cadherin from K5.

165 VE-cadherin and may play a role in clearing VE-cadherin from the site of TEM.

166 ment of the LBRC may play a role in clearing VE-cadherin from the site of TEM.

167 By contrast, VE-cadherin functions as an adaptor that interacts with

168 s acted as a dominant negative and inhibited VE-cadherin gap formation and TEM, yet targeting of the

169 ection of an antibody that inhibits kinesin, VE-cadherin gaps do not form around the blocked leukocyt

170 , the association between LBRC recycling and VE-cadherin gaps remains unknown.

171 These results identify a pivotal function of VE-cadherin homophilic interaction in modulating endothe

172 l molecules, including integrin alpha3beta1, VE-cadherin, ICAM-2, junctional adhesion molecule-B (JAM

173 VE-cadherin immunofluorescent staining at endothelial AJ

174 the Par3-binding motif at the C-terminus of VE-cadherin impairs apicobasal polarity and vascular lum

175 measurements showed that in static culture, VE-cadherin in cell-cell junctions bears significant myo

176 endothelial growth factor (VEGF), Flk1, and VE-cadherin in ECs and granulation tissues (GTs) of full

177 n phosphorylation, increases plasma membrane VE-cadherin in ECs and in mice, blocks vascular permeabi

178 iR-101 via posttranscriptional regulation of VE-cadherin in human BMVECs exposed to the HIV-1 Tat C p

179 To explore tensile changes across VE-cadherin in live zebrafish, we tailored an optical bi

180 dentify a unique role of Galpha13 binding to VE-cadherin in mediating VE-cadherin internalization and

181 ngs indicate that the biological activity of VE-cadherin in regulating endothelial polarity and vascu

182 Our work establishes a role for VE-cadherin in T-cell infiltration in tumors and offers

183 ibition (saracatinib) increased: (i) 140 kDa VE-cadherin in the TTX-insoluble fraction, (ii) VE-cadhe

184 in tumor-bearing mice enhanced expression of VE-cadherin in tumor endothelium, activating TIE-2 and t

185 Galpha13 binding to VE-cadherin in turn induced Src activation and VE-cadher

186 cross PECAM-1 but decreases the force across VE-cadherin, in close association with downstream signal

187 iated with stemness of cell columns, myc and VE-cadherin, in Notch1(-) fusogenic precursors, and boun

188 re, expression of carboxy-terminal-truncated VE-cadherin increases the number of ARP2/3-controlled la

189 e we report that induced cis dimerization of VE-cadherin inhibits endocytosis independent of both p12

190 cadherin in the TTX-insoluble fraction, (ii) VE-cadherin intensity at AJs, (iii) AJ width, and (iv) a

191 Inhibition of Galpha13-VE-cadherin interaction using an interfering peptide der

192 promotes transmigration by enhancing ICAM-1-VE-cadherin interaction.

193 l cell elongation and proper organization of VE-cadherin intercellular junctions.

194 Galpha13 binding to VE-cadherin in mediating VE-cadherin internalization and endothelial barrier disr

195 rosine phosphorylates p18 concomitantly with VE-cadherin internalization and pulmonary edema formatio

196 n binding site thought to be responsible for VE-cadherin internalization.

197 docytosis, downstream kinase activation, and VE-cadherin internalization.

198 Vascular endothelial (VE)-cadherin is a constitutively expressed endothelial c

199 We have demonstrated that VE-cadherin is a direct target of miR-101 using a lucife

200 Here we provide evidence that VE-cadherin is cleaved by calpain upon entry into clathr

201 VE-cadherin is essential for blood vessel lumen formatio

202 Similar to SOX7, VE-cadherin is expressed in haemogenic endothelium and i

203 VE-cadherin is linked to the actin cytoskeleton through

204 VE-cadherin is required for VM in NCI-H446 SCLC xenograf

205 Vascular endothelial cadherin (VE-cadherin) is an adhesive protein found in adherens ju

206 of alpha-pv, blood vessels display impaired VE-cadherin junction morphology.

207 permeability by inducing the dissociation of VE-cadherin junctions between LECs via the activation of

208 ed continuous vascular endothelial-cadherin (VE-cadherin) junctions and basement membrane, similar to

209 nd, mutating Y731 in the cytoplasmic tail of VE-cadherin, known to selectively affect leukocyte diape

210 s, whereas NLGN1 deletion causes an aberrant VE-cadherin, laminin and alpha6 integrin distribution in

211 lipodia, whereas overexpression of wild-type VE-cadherin largely blocks it and decreases cell motilit

212 gulate lumen formation through modulation of VE-cadherin localization.

213 report that K5 targets two membrane-proximal VE-cadherin lysine residues for ubiquitination, driving

214 identified HIV-1 Tat C-induced disruption of VE-cadherin mediated by miRNA-101 in human brain microva

215 tudy identifies a novel adapter function for VE-cadherin mediated by transmembrane domain association

216 trate a functional interrelationship between VE-cadherin-mediated cell adhesion and actin-driven, ARP

217 VE-cadherin mediates adhesion through trans interactions

218 We now show that the transmembrane domain of VE-cadherin mediates an essential adapter function by bi

219 In this study, VE-cadherin monomer Ab reduced angiogenesis in the lungs

220 Abs targeted to VE-cadherin monomers inhibit angiogenesis by blocking th

221 flammation, a vascular endothelial cadherin (VE-cadherin) mutant defective in endocytosis assembled n

222 Of interest, VE-cadherin mutants that are resistant to endocytosis ar

223 Changes in tension across VE-cadherin observed using ratio-metric or lifetime FRET

224 he membrane protein expression in the ileum, VE-cadherin, occludin, and claudin-3, Western blot analy

225 from platelets, which promoted expression of VE-cadherin on HEVs ex vivo.

226 ound that phosphorylation of a small pool of VE-cadherin on Y658 is essential for flow sensing throug

227 , whereas there was no detectable tension on VE-cadherin outside of junctions.

228 (p < 0.05) and the adherens junction protein VE-cadherin (p < 0.05).

229 targets at cell adhesions and cytoskeleton: VE-cadherin, p120-catenin, ZO-1, cortactin, and VASP.

230 ce of macrophage activation on expression of VE-cadherin/p120-catenin/beta-catenin complex in co-cult

231 ophages to produce NO provoked a decrease in VE-cadherin/p120-catenin/beta-catenin expression in H5V

232 risingly, Tiam1 functions as an adaptor in a VE-cadherin-p67phox-Par3 polarity complex that directs l

233 ctional mechanosensory complex consisting of VE-cadherin, PECAM-1, and VEGFR2.

234 -cadherin in turn induced Src activation and VE-cadherin phosphorylation at Tyr 658, the p120-catenin

235 inhibition of the Rho pathway, and decreased VE-cadherin phosphorylation at Tyr658.

236 ANG2 inhibition blocked VE-cadherin phosphorylation at tyrosine residue 685 and

237 dary to TRPM2-activated Ca(2+) signaling and VE-cadherin phosphorylation resulting in the disassembly

238 AGGF1 inhibits VE-cadherin phosphorylation, increases plasma membrane V

239 endothelium attenuated CS-induced VEGFR2 and VE-cadherin phosphorylation, preserved adherens junction

240 ation increased VE-PTP expression, decreased VE-cadherin phosphorylation, promoted AJ integrity, and

241 ed decreased VE-PTP expression and increased VE-cadherin phosphorylation, resulting in defective AJs.

242 osphosite Y949, regulating dynamic c-Src and VE-cadherin phosphorylation.

243 mphocyte TEM and converged functionally with VE-cadherin phosphorylation.

244 Vascular endothelial (VE)-cadherin plays a critical role in endothelial cell-c

245 characteristic SCLC genomic changes in both VE-cadherin-positive and -negative CTCs.

246 X), where molecular analysis of fractionated VE-cadherin-positive cells uncovered copy-number alterat

247 o and in vivo, through enhanced recycling of VE-cadherin-positive early endosomes to the IEJ.

248 However, the fate of the VE-cadherin-positive endosome has yet to be elucidated.

249 vitro and in vivo, by enhancing recycling of VE-cadherin-positive endosomes to the IEJ.

250 1 (IRS1) was overexpressed in ECs using the VE-cadherin promoter to create ECIRS1 TG mice, which ele

251 es showed the direct binding of Snail to the VE-cadherin promoter.

252 Signaling through VE-cadherin requires association and activity of differe

253 lial junction protein, vascular endothelial (VE)-cadherin, resulting in the disruption of endothelial

254 increased internalization and degradation of VE-cadherin, resulting in impaired activity of adherens

255 However, VE-cadherin's precise role is poorly understood.

256 d firm adhesion of neutrophils that regulate VE-cadherin's role as a negative regulator of leukocyte

257 Interestingly, VE-cadherin shifted toward a smaller molecular weight in

258 A 140 kDa VE-cadherin species was present on the cell surface and

259 sed, whereas levels of a TTX-soluble 115 kDa VE-cadherin species were increased in old compared to yo

260 manifested as gaps in vascular endothelial (VE)-cadherin staining at the site of TEM and targeted tr

261 ICAM-1-induced Src activation and modulates VE-cadherin switching association with ICAM-1 or actin,

262 Of importance, the cleavage of the VE-cadherin tail alters the postendocytic trafficking it

263 We validate localization and function of a VE-cadherin tension sensor (TS) in vivo.

264 S to reveal biologically relevant changes in VE-cadherin tension that occur as the dorsal aorta matur

265 Our results demonstrate that the domain of VE-cadherin that binds to beta-catenin is required for t

266 al complex is mediated by a specific pool of VE-cadherin that is phosphorylated on Y658 and bound to

267 Vascular endothelial (VE)-cadherin, the major adherens junction adhesion molec

268 ociation of presenilin 1 with N-cadherin and VE-cadherin, thereby compromising pericyte-endothelial c

269 a VE-PTP substrate to dissociate VE-PTP from VE-cadherin, thereby facilitating efficient transmigrati

270 Pals1 directly interacts with VE-cadherin through a membrane-proximal motif in the cyt

271 he site at which TEM will take place and for VE-cadherin to move away.

272 Instead, the binding of VE-cadherin to p120 regulates adhesive contact area in a

273 otif in VE-cadherin abrogates the ability of VE-cadherin to regulate apicobasal polarity and vascular

274 We sought to elucidate a role for p18 in VE-cadherin trafficking and thus endothelial barrier fun

275 VE-cadherin trafficking to and from the plasma membrane

276 Thus, Rac1 functions by stabilizing VE-cadherin trans-dimers in mature AJs by counteracting

277 Vascular endothelial (VE)-cadherin transfers intracellular signals contributin

278 n at endothelial cell boundaries of ZO-1 and VE-Cadherin, two components of tight and adherens juncti

279 results in VEGFR2 activation, Src-dependent VE-cadherin tyrosine phosphorylation, and internalizatio

280 Vascular endothelial (VE)-cadherin undergoes constitutive internalization driv

281 Moreover, knockdown of VE-cadherin using siRNA decreased the invasiveness of HT

282 ptor and signaling mechanism that stimulates VE-cadherin/VE-PTP dissociation are unknown.

283 sitive tyrosine kinase Pyk2 as essential for VE-cadherin/VE-PTP dissociation.

284 is mechanism, CS induces dissociation of the VE-cadherin.VEGFR2 complex localized at the adherens juc

285 Increased phosphorylation of VE-cadherin was also accompanied by a reduction of Src h

286 ition, the inhibitory effect of TGF-beta1 on VE-cadherin was confirmed in primary cultures of human t

287 To determine that VE-cadherin was the dominant target of miR-27a function,

288 gged Notch or vascular endothelial cadherin (VE-cadherin), we provide stepwise instructions for mecha

289 Levels of the 140 kDa VE-cadherin were decreased, whereas levels of a TTX-solu

290 ase activity and tyrosine phosphorylation of VE-cadherin were increased in old arteries.

291 Src activity and tyrosine phosphorylation of VE-cadherin were increased in old compared to young arte

292 ted peptide of Tie-2 dissociates VE-PTP from VE-cadherin when introduced with the help of a Tat pepti

293 Sow fed piglets showed significantly more VE-Cadherin, which associated with levels of calcium, an

294 d a rapid (<30 s) decrease in tension across VE-cadherin, which paralleled a decrease in total cell-c

295 PTP expression enhanced dephosphorylation of VE-cadherin, which reduced VE-cadherin endocytosis and t

296 ediates TGF-beta1-induced down-regulation of VE-cadherin, which subsequently contributed to TGF-beta1

297 ve mechanism during polarized trafficking of VE-cadherin, which supports barrier maintenance within d

298 Antagonizing VE-cadherin widened cell-cell junctions and reduced the

299 (CD5-2), which disrupted the interaction of VE-cadherin with its regulator miR-27a, resulting in inc

300 Here we describe a functional interaction of VE-cadherin with the cell polarity protein Pals1.