ライフサイエンスコーパス: VE-cadherin

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

2 n-5), VWF (von Willebrand factor), and CDH5 (VE-cadherin).

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

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

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

6 ocytes to induce tyrosine phosphorylation of VE-cadherin.

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

8 ylation and reduced membrane localization of VE-cadherin.

9 tight junctions through dephosphorylation of VE-cadherin.

10 and VEGFR3 signal redundantly downstream of VE-cadherin.

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

12 e endothelial adherens junction (AJ) protein VE-cadherin.

13 rylation, internalization and degradation of VE-cadherin.

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

15 Levels of the salivary biomarkers MMP-3, VE-cadherin, 6Ckine, and PAI-1 were correlated to each o

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

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

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

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

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

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

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

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

24 n secondary to calpain-induced disruption of VE-cadherin adhesion.

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

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

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

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

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

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

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

32 ng endothelial cell membrane localization of VE-cadherin and beta-catenin complex and promoting their

33 ted confluent HUVEC monolayer by stabilizing VE-cadherin and beta-catenin on endothelial cell cytopla

34 P aeruginosa-induced dissociation between VE-cadherin and beta-catenin, but increased association

35 ession of the lipid raft-associated proteins VE-cadherin and caveolin-1.

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

37 he expression of the cell junction molecules VE-cadherin and claudin 5 in lymphatic vessels.

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

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

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

41 rter, ABCG2, was lower, while mRNAs encoding VE-cadherin and ICAM1 were higher in schizophrenia brain

42 n complex, which led to reduced cell surface VE-cadherin and increased vascular hyperpermeability; al

43 rmation, resulting in increased cell surface VE-cadherin and inhibition of vascular hyperpermeability

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

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

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

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

48 chymal transition (EndoMT) with decreases in VE-Cadherin and PECAM1 and increases in collagen, alpha-

49 reased the phosphorylation levels of Src and VE-cadherin and reduced the formation of the VEGFR2-Src-

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

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

52 In serum, VE-cadherin and VEGF were correlated with one another an

53 uorescent staining of established EC markers VE-cadherin and von Willebrand factor (vWF).

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

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

56 ility such as vascular endothelial cadherin (VE-Cadherin) and neuropilin (NRP)-1 and 2, but not with

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

58 nce of sterol homeostasis, downregulation of VE-cadherin, and a putative disturbance of Notch signali

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

60 2)) have altered expression of claudin 5 and VE-cadherin, and blocking miR-126 activity in HLECs phen

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

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

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

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

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

66 of the angiogenic peptide ephrinB2/CTF2, the VE-cadherin angiogenic complexes and EC sprouting and tu

67 Supporting this hypothesis, ischemia-induced VE-cadherin angiogenic complexes, levels of neoangiogene

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

69 t while S1PR-dependent vascular endothelial (VE)-cadherin assembly suppresses JunB expression in the

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

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

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

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

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

75 ermeability by inhibiting the disassembly of VE-cadherin at adherens junctions.

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

77 d brain secondary to reduced accumulation of VE-cadherin at AJs.

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

79 t activation of EC beta1-integrin stabilizes VE-cadherin at endothelial junctions and promotes endoth

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

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

82 bilization of vascular endothelial cadherin (VE-cadherin) at EC junctions.

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

84 osin light chain 2 and vascular endothelial (VE)-cadherin axis.

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 e calpain and degradation of the AJ proteins VE-cadherin, beta-catenin, and p120-catenin.

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

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

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

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

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

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

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

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

96 rom MEK/ERK, binds to the promoter region of VE-cadherin (chip assay) and is induced by VEGF in DPSCs

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

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

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

100 VE-cadherin clustering at adherens junctions promotes pr

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

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

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

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

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

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

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

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

109 and reduced the formation of the VEGFR2-Src-VE-cadherin complex, which led to reduced cell surface V

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

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

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

113 (EC)-specific deletion of Cept1 via induced VE-cadherin-CreERT2-mediated recombination (Cept1Lp/LpCr

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

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

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

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

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

119 sed the photoconvertible fluorescent protein VE-cadherin-Dendra2 to monitor VE-cadherin dynamics at a

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

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

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

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

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

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

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

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

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

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

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

131 scent protein VE-cadherin-Dendra2 to monitor VE-cadherin dynamics at adherens junctions (AJs) in conf

132 l cells reduced GEF-H1 activity and restored VE-cadherin dynamics at AJs.

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

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

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

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

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

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

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

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

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

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

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

144 erved that VEGF was no longer able to induce VE-cadherin expression and capillary sprout formation.

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

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

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

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

149 lar endothelial growth factor (VEGF) induces VE-cadherin expression in sprouting DPSCs undergoing ana

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

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

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

153 , but did show augmented early activation of VE-cadherin expression.

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

155 (+) EC progenitors expressing PECAM-1, CD34, VE-Cadherin, FLK1, and TIE2 lacked mature arterial, vena

156 Vascular endothelial (VE)-cadherin forms homotypic adherens junctions (AJs) in

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

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

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

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

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

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

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

164 Using VE-cadherin-GFP knockin reporter cells, female cells sho

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

166 VE-cadherin immunofluorescent staining at endothelial AJ

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

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

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

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

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

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

173 -cadherin in Serum and Angiogenin in Saliva, VE-cadherin in Saliva and Headaches, PA1 in Saliva and H

174 ctions of TGF-beta1 in Saliva and Headaches, VE-cadherin in Serum and Angiogenin in Saliva, VE-cadher

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

176 d on the role of VE-PTP in dephosphorylating VE-cadherin in the activated endothelium, little is know

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

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

179 ganization of vascular endothelial cadherin (VE-cadherin) in HUVECs in response to ATO were partially

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

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

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

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

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

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

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

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

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

189 E-cadherin junctions by reducing the rate of VE-cadherin internalization independently of its phospha

190 iting RhoA signaling at AJs and reducing the VE-cadherin internalization rate.

191 -silencing decreases ATP required for proper VE-cadherin internalization/traffic at endothelial cell-

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

193 VE-cadherin is essential for blood vessel lumen formatio

194 VE-cadherin is linked to the actin cytoskeleton through

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

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

197 ed CA4P-mediated actinomyosin contractility, VE-cadherin junction disruption and permeability rise.

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

199 Thus, VE-PTP stabilizes VE-cadherin junctions and restricts endothelial permeabi

200 orces Rac1 activation to promote assembly of VE-cadherin junctions and thereby establish the characte

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

202 We discovered that VE-PTP stabilizes VE-cadherin junctions by reducing the rate of VE-cadheri

203 acity, and disassembly of actin skeleton and VE-cadherin junctions, which were rescued using the MEK

204 cruitment to AJs and induces the assembly of VE-cadherin junctions.

205 1 modulates RhoA activity and tension across VE-cadherin junctions.

206 thelial-specific phosphatase that stabilizes VE-cadherin junctions.

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

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

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

210 t increased ER stress via O-GlcNAcylation of VE-Cadherin likely contribute to endothelial permeabilit

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

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

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

214 tion) but the role of integrin activation in VE-cadherin mediated endothelial barrier function is unk

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

216 VE-cadherin mediates adhesion through trans interactions

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

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

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

220 a subgroup had lower ABCG2 and higher ICAM1, VE-cadherin, occludin and interferon-induced transmembra

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

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

223 des Twist) or Snai1 (which encodes Snail) in VE-cadherin(+) or Tie1(+) endothelial cells inhibited th

224 integrin activating antibody normalized both VE-cadherin organization and EC barrier function.

225 Talin-deficient endothelium showed altered VE-cadherin organization at EC junctions in vivo.

226 In addition, VE-cadherin organization was normalized by reexpression

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

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

229 Strikingly, vascular endothelial (VE)-cadherin phosphorylation at the Y685, but not Y658,

230 Therapeutically, targeting VEGFR2-regulated VE-cadherin phosphorylation could suppress edema while l

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

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

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

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

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

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

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

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

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

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

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

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

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

244 1 (IRS1) was overexpressed in ECs using the VE-cadherin promoter to create ECIRS1 TG mice, which ele

245 cadherin functions by increasing the rate of VE-cadherin recruitment to AJs and induces the assembly

246 Interestingly, DPSC stably transduced with a VE-cadherin reporter demonstrated that vascular endothel

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

248 ed O-GlcNAcylation of proteins, particularly VE-Cadherin resulting in a defective complex partnering

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

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

251 cultures of brain ECs, EphB4 stimulates the VE-cadherin/Rok-alpha angiogenic complexes known to medi

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

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

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

255 Both VE-cadherin-silenced and mitogen-activated protein kinas

256 VE-cadherin-silenced primary human DPSCs seeded in tooth

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

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

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

260 Confluence was confirmed by VE-cadherin staining.

261 but increased association between N-WASP and VE-cadherin, suggesting a role for N-WASP in promoting P

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

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

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

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

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

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

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

269 d Rac1 activation induces the recruitment of VE-cadherin to AJs, whereas Trio GEF2-mediated RhoA acti

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

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

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

273 VE-cadherin trafficking to and from the plasma membrane

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

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

276 s leads to biomechanical signaling involving VE-cadherin, triggering nuclear localization of the Hipp

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

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

279 urther show an association of GRP78 with the VE-Cadherin under these conditions.

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

281 e tested the role of p120-catenin (p120) and VE-cadherin (VE-cad) endocytosis in vascular development

282 igration, inducing expression of EC markers (VE-cadherin, VEGFR2 [vascular endothelial growth factor

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

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

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

286 egin to understand the mechanisms regulating VE-cadherin, we stably silenced MEK1 and observed that V

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

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

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

290 ignificantly reduced, expression of CD31 and VE-Cadherin were unaffected, whereas SMAD1/5/8 signaling

291 on of Src and vascular endothelial cadherin (VE-cadherin), which increases VEGF receptor 2 (VEGFR2)-S

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

293 d activation of ERG leading to expression of VE-cadherin, which is required for anastomosis of DPSC-d

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

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

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

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

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

299 These findings support a mechanism whereby VE-cadherin Y685 phosphorylation is selectively associat

300 een integrin-mediated adhesion complexes and VE-cadherin yet the underlying molecular links are uncle