ライフサイエンスコーパス: cadherin

1 markers ZEB1, ZEB2 and CDH2 (which encodes N-cadherin).

2 Slug, Zeb1 and N-cadherin, and upregulated E-cadherin.

3 bl kinases and degradation of beta-catenin/E-cadherin.

4 P-7 promotes VSMC apoptosis by cleavage of N-cadherin.

5 machinery that binds the cytosolic tail of E-cadherin.

6 embrane in a complex with beta-catenin and E-cadherin.

7 pression of miR-34a, SIRT1, cyclin D1, and E-cadherin.

8 ng its interaction with vascular endothelial-cadherin.

9 ation, internalization and degradation of VE-cadherin.

10 the tight-junction proteins Pals1/PATJ and E-cadherin.

11 acyl-CoA oxidase 1 (ACOX1) and FAT atypical cadherin 1 (FAT1)], whereas the PUFA diet did not signif

12 Furthermore, cadherin-10 exhibits differential participation in compl

13 Cadherin-10 localizes to both excitatory and inhibitory

14 Knockdown of cadherin-10 reduces excitatory but increases inhibitory

15 Cadherin-11 (Cad-11, also known as OB cadherin or CDH11)

16 ipose tissue inflammation and thus highlight cadherin-11 as a potential therapeutic target for the ma

17 Here, we show that mesenchymal cadherin-11 modulates stromal fibroblast function.

18 Cleavage of cadherin-11 produces an extracellular fragment that prom

19 suggest that stromal fibroblasts expressing cadherin-11 regulate adipose tissue inflammation and thu

20 ates including itself, fibronectin, ephrinB, cadherin-11, pcdh8 and pcdh8l (this work).

21 Higher expression levels of IL-33 in cadherin-11-deficient mice mediated ILC2 activation, res

22 nt with reduced adipose tissue inflammation, cadherin-11-deficient mice were protected from obesity-i

23 CDH2 encodes cadherin 2 (also known as N-cadherin), a protein that pl

24 quencing was used to screen for mutations in cadherin 2 (CDH2) gene in unrelated genotype-negative pa

25 ses, which changes a conserved amino acid of cadherin 2 protein and is supported as the causal mutati

26 o observed upon knockdown of Cdh23, encoding cadherin-23 (USH1D protein).

27 st presynaptic cadherin-9 binds postsynaptic cadherins-6 and -10 to regulate mushroom spine density a

28 observed in the SR layer, demonstrating that cadherins-6, -9, and -10 are gatekeepers for high-magnit

29 ences require the Type II classic cadherins, cadherins-6, -9, and -10.

30 nteractions, our results suggest presynaptic cadherin-9 binds postsynaptic cadherins-6 and -10 to reg

31 CDH2 encodes cadherin 2 (also known as N-cadherin), a protein that plays a vital role in cell adh

32 e we address these issues with a focus on VE-cadherin, a major endothelial cell-specific junctional p

33 etastasis via increasing the expression of E-cadherin, a tumor suppressor, and decreasing the express

34 wed limited effects on the decrease in the E-cadherin abundance and stress fiber formation by TGF-bet

35 AM-1-VE-cadherin association and promoted VE-cadherin-actin association.

36 lasmic domains has been reported to regulate cadherin adhesion and signaling.

37 amine the mechano-responsive properties of N-cadherin adhesion sites in isolated VSMCs.

38 It requires a Rho- and E-cadherin adhesion-dependent, substrate-parallel contract

39 c event that regulates the trafficking of VE-cadherin after endocytosis.

40 0(-5) m) induced a significant increase of N-cadherin AJ density at 50 mmHg, whereas vasodilatation i

41 ervations provide compelling evidence that N-cadherin AJs are sensitive to pressure and vasomotor ago

42 The formation of N-cadherin AJs in the vessel wall depends on the intralumi

43 in VSMCs and support a functional role of N-cadherin AJs in vasomotor regulation.

44 , both the density and the average size of N-cadherin AJs increased significantly.

45 ignificant decrease in density and size of N-cadherin AJs.

46 ted the expression of EndMT markers (Slug, N-cadherin, alpha-SMA) in EC exposed to low shear stress.

47 propose that the tension generated by the E-cadherin/AmotL2/actin filaments plays a crucial role in

48 ut cell lines exhibited down-regulation of E-cadherin and a reduction in alpha/beta-catenin at cell-c

49 T, correlated with increased expression of E-cadherin and beta-catenin, and decreased expression of v

50 apacity and cortical contractility through E-cadherin and DDR1 proteins.

51 , and LGR4 knockdown resulted in increased E-cadherin and decreased expression of N-cadherin and snai

52 the structural and signalling functions of E-cadherin and demonstrate that complete absence of E-cadh

53 NT mice also expressed increased levels of E-cadherin and fibroblast growth factor 21 (FGF21), target

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

55 that is necessary for phosphorylation of VE-cadherin and for breakdown of the endothelial barrier.

56 tal xenografts by sustaining expression of E-cadherin and inhibitor of differentiation 2 (ID2).

57 with altered expression of Scribble, ZO1, E-cadherin and N-cadherin and their mislocalization.

58 aneth cells population and reinstating the E-cadherin and N-Cadherin expression.

59 ion of GFP-FIP2(S227E) induced the loss of E-cadherin and occludin, mutation of any of the NPF domain

60 -migration and anti-invasion by activating E-cadherin and repressing Vimentin.

61 sed E-cadherin and decreased expression of N-cadherin and snail transcription factor -2 ( SNAI2) (als

62 to cellular junctions to associate with VE/E-cadherin and subsequently the organization of radial act

63 is effect was mediated by up-regulation of P-cadherin and the beta-catenin downstream target fascin1.

64 -positive basal epithelial cells expressed E-cadherin and the undifferentiated epithelial cell marker

65 xpression of Scribble, ZO1, E-cadherin and N-cadherin and their mislocalization.

66 PR2 ligands resulted in down-regulation of E-cadherin and up-regulation of vimentin, which were rever

67 ented the association of presenilin 1 with N-cadherin and VE-cadherin, thereby compromising pericyte-

68 tes migration primarily via crosstalk with E-cadherin and ZEB1.

69 GFRalpha blocks NC migration by inhibiting N-cadherin and, consequently, impairing CIL.

70 Surprisingly, O-mannosylation of cadherins and protocadherins does not require POMT1 and/

71 sisting of vascular endothelial cadherin (VE-cadherin) and beta-catenin.

72 Expression of epithelial (E-cadherin) and mesenchymal markers (vimentin, fibronectin

73 dothelial cells could be identified among VE-Cadherin+ and CD45- cells.

74 cell adhesion molecule-1 (PECAM-1), CD144/VE-cadherin, and CD106/Endoglin, from vascular endothelial

75 ylation of paxillin, its association with VE-cadherin, and internalization of the latter.

76 y binds to and promotes internalization of N-cadherin, and N-cadherin/LLGL1 interaction is inhibited

77 hanical regulation of the T-cell receptor, E-cadherin, and Notch pathways, suggesting a common featur

78 (27) trimethylation (H3K27me3), decreased E-cadherin, and other protein features indicating a more m

79 ssociated with displacement of p120 from the cadherin, and p120 protects VE-cadherin from K5.

80 1 (HIF-1), followed the downregulation of E-cadherin, and produced heterogeneous cell subsets whose

81 onectin accumulates in the vasculature via T-cadherin, and the adiponectin-T-cadherin association pla

82 cated by the decrease in epithelial marker E-cadherin, and the increase in mesenchymal markers alpha-

83 ion of beta-catenin, Snail, Slug, Zeb1 and N-cadherin, and upregulated E-cadherin.

84 the downregulation of beta-defensin 1 and E-cadherin, and upregulation of hepatocyte growth factor-r

85 A complex consisting of PECAM-1, VE-cadherin, and vascular endothelial growth factor recepto

86 aortic adiponectin protein disappeared in T-cadherin/ApoE double-knockout (Tcad/ApoE-DKO) mice with

87 nt when levels of PI3-kinase activity and DE-cadherin are elevated in NBs.

88 When levels of PI3-kinase activity and/or DE-Cadherin are reduced in NBs, NBs lose niche position and

89 Cadherins are a superfamily of calcium-dependent cell ad

90 roglycan, and moreover, the O-Man glycans on cadherins are not elongated.

91 erin), whereas epithelial markers, such as E-cadherin, are down-regulated.

92 Further analysis identified E-cadherin as the top positive correlated gene, while hepa

93 rom nephron progenitor cells and expressed E-cadherin as well as vimentin, a myofibroblastic marker n

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

95 isions by loss of E-cadherin, which releases cadherin-associated beta-catenin (Armadillo in Drosophil

96 n, SHP-2 down-regulation prevented ICAM-1-VE-cadherin association and promoted VE-cadherin-actin asso

97 lature via T-cadherin, and the adiponectin-T-cadherin association plays a protective role against neo

98 erotic plaque lesions, and the adiponectin-T-cadherin association protected against vascular injury.

99 VE-cadherin dissociation from ICAM-1 and VE-cadherin association with actin, SHP-2 down-regulation p

100 Src inhibition increased VE-cadherin at adherens junctions and increased endothelial

101 120 binding masks the motif, stabilizing the cadherin at cell junctions.

102 VE-cadherin at endothelial cell-cell junctions links the co

103 minished levels of vascular endothelial (VE)-cadherin at the cell surface in these blood vessels.

104 ypes where RAS/MAPK pathway activation and E-cadherin attenuation are common.

105 As such, the Snail1/E-cadherin axis described in the early mouse embryo corres

106 plays a key role in this process by coupling cadherin-based cell-cell adhesion together with actomyos

107 immunoprecipitated with vascular endothelial cadherin-based complexes, including beta- and gamma-cate

108 eage of over a period of 14 days based on VE-cadherin biomarker.

109 pts a three-dimensional structure similar to cadherin-bound catenins, binds directly to the E-cadheri

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

111 hese differences require the Type II classic cadherins, cadherins-6, -9, and -10.

112 ur results suggest that rapid disordering of cadherins can communicate a change in extracellular Ca(2

113 Studies in zebrafish revealed that both cadherins can interact with each other in cell adhesion.

114 al cells with surface expression of PD-L1, E-cadherin, CD24, and VEGFR2 rapidly formed tumors outside

115 The cadherin (cdh) superfamily of adhesion molecules carry O

116 e expression and correlated with induction E-cadherin (CDH1) and mesenchymal-to-epithelial transition

117 Kras(G12D) expression plus inactivation of E-cadherin (Cdh1) and p53 in the gastric parietal cell lin

118 hibits a striking complementary pattern to N-cadherin (CDH2), marking the interface of the future som

119 he collagen receptor tyrosine kinase DDR1, N-Cadherin, CLCP1/DCBLD2, KIRREL, BCAM and others.

120 Disruption of VE-cadherin clustering at AJs (function-blocking antibody,

121 pulling force ( approximately 1 nN) to the N-cadherin-coated beads via an atomic force microscope ind

122 pulling force ( approximately 1 nN) to the N-cadherin-coated-beads with the AFM induced a localized m

123 E-knockout (ApoE-KO) mice, adiponectin and T-cadherin colocalized on endothelial cells and synthetic

124 Increased tension on the E-cadherin complex promoted the junctional recruitment of

125 st from focal adhesions and recruited by the cadherin complex to intercellular junctions.

126 Challenging cadherin complexes mechanical coupling with magnetic twe

127 nin is an identified force transducer within cadherin complexes that is autoinhibited under low tensi

128 erin expression and stabilized junctional VE-cadherin complexes through associated phosphatases.

129 ation compartmentalizes Daple/beta-catenin/E-cadherin complexes to cell-cell contact sites, enhances

130 long-distance trafficking of beta-catenin/E-cadherin complexes to pericentriolar recycling endosomes

131 Cadherin complexes transduce force fluctuations at junct

132 er cells and MCAs are influenced by cellular cadherin composition.

133 ated by N-cadherin ligation and involves the cadherin coreceptor Cdo with its downstream effector, Cd

134 -catenin and p120-binding domains within the cadherin cytoplasmic tail.

135 erin-bound catenins, binds directly to the E-cadherin cytosolic tail and thereby localizes at cell-ce

136 generated an extensive array of Drosophila E-Cadherin (DE-Cad) endogenous knock-in alleles that carry

137 pressors and down-regulation of Drosophila E-cadherin (DEcad) transcription.

138 The presence of E-cadherin decreases cortical contractility during mitosis

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

140 uced KC Par3 function fosters a permissive P-cadherin-dependent niche for MC transformation, invasion

141 mics of order and disorder of the desmosomal cadherin desmoglein 3 (Dsg3) in living cells.

142 unction elongation, which results in local E-cadherin dilution at the ingressing adherens junction.

143 is essential for morphogenesis as loss of N-cadherin disrupts cell rearrangements.

144 whereas the activation of ICAM-1 leads to VE-cadherin dissociation from ICAM-1 and VE-cadherin associ

145 includes the membrane-proximal extracellular cadherin domains EC5 and EC6.

146 conserved residues in specific extracellular cadherin domains, and it was suggested that the function

147 s been well studied, but rigidity sensing by cadherins during cell adhesion is largely unexplored.

148 a consequence of the switch between E- and N-cadherins during epithelial-to-mesenchymal transition (E

149 Epithelial cadherin (Ecadherin) is responsible for the intercellula

150 WC1 (WW and C2 domain containing 1), CELSR3 (Cadherin EGF LAG seven-pass G-type receptor 3), NIPBL (N

151 a significant increase or decrease of the N-cadherin-EGFP clustering, respectively.

152 re characterized by the functional loss of E-cadherin (encoded by CDH1), inactivation of Cdh1 does no

153 identify an additional motif that drives VE-cadherin endocytosis and pathological junction disassemb

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

155 multiple context-dependent signals drive VE-cadherin endocytosis, but p120 binding to the cadherin j

156 nuates TNF-alpha/JNK pathway and increases E-cadherin expression and cell-cell junction in epithelial

157 f TRAF2/JNK pathway increases E (epithelial)-cadherin expression and enhances epithelial barrier inte

158 ling pathway and relevant phosphatases in VE-cadherin expression and function, vascular tone in aorti

159 ovel interplay between spontaneous activity, cadherin expression and gap junction communication.

160 signaling pathway, as shown by decreasing E-cadherin expression and increasing vimentin expression.

161 gulate inflammation by maintaining normal VE-cadherin expression and promoting T lymphocyte transmigr

162 d Akt/WNT/beta-catenin signaling to drive VE-cadherin expression and stabilized junctional VE-cadheri

163 ce, were the only TspanC8s that regulated VE-cadherin expression and were required for lymphocyte tra

164 In agreement, low epidermal PAR3 and high P-cadherin expression correlate with human melanoma progre

165 Decreased claudin-4, caudin-7, and E-cadherin expression in Lpa1(-/-) mice further suggested

166 We further showed that N-cadherin expression in mural cells plays a key role in b

167 A decrease in VE-cadherin expression is associated with tumor pathology.

168 This indicates that E- and P-cadherin expression patterns evolved differently between

169 y among EOC metastatic units with respect to cadherin expression profiles and invasive behavior; howe

170 del of germ-layer formation in which, upon N-cadherin expression, endodermal cells actively migrate a

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

172 ulation and reinstating the E-cadherin and N-Cadherin expression.

173 ll-cell adhesion by negative regulation of E-cadherin expression.

174 In addition, proteolytic processing of cadherin extracellular and cytoplasmic domains has been

175 The atypical cadherins Fat and Dachsous (Ds) have been found to under

176 at the contact zone of T lymphocytes with rE-cadherin-Fc-coated beads.

177 anchoring the bacterium to F-actin through E-cadherin for bacterial invasion has not been tested dire

178 KEY POINTS: N-cadherin formed punctate adherens junctions (AJ) along t

179 incubating Cry1Ac toxin with a Manduca sexta cadherin fragment, with BBMV from both strains.

180 In vitro, knockdown of T-cadherin from human aortic smooth muscle cells (HASMCs)

181 p120 from the cadherin, and p120 protects VE-cadherin from K5.

182 on of the exact mechanisms associated with E-cadherin function in mESCs is compounded by the difficul

183 mainly caused by germline mutations in the E-cadherin gene (CDH1), renders a lifetime risk of gastric

184 and mouse in directly repressing ectodermal cadherin genes to contribute to the delamination of mese

185 However, N-cadherin has an indirect control on cell shape.

186 Loss of these cadherins has no effect on the lower-magnitude LTP typic

187 olecules, including integrin alpha3beta1, VE-cadherin, ICAM-2, junctional adhesion molecule-B (JAM-B)

188 elective disruption of trans engagement of E-cadherin in an otherwise cohesive cell monolayer, or los

189 of barrier function, and overexpression of N-cadherin in CHO cells promoted barrier function.

190 ols transcription of the tumour suppressor E-cadherin in epithelial cancers.

191 e early mouse embryo corresponds to Snail2/P-cadherin in the chick, but both Snail factors and Zeb2 f

192 r function, as CRISPR-mediated knockout of N-cadherin in the mural cells led to loss of barrier funct

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

194 ed ROS-induced degradation of beta-catenin/E-cadherin in vitro and ameliorated skin damage in rodent

195 hat the arrangement, or order, of desmosomal cadherins in the intercellular space is critical for adh

196 ss PECAM-1 but decreases the force across VE-cadherin, in close association with downstream signaling

197 panied by efficient clustering and loss of E-cadherin, indicating that this is an important adaptatio

198 Our results show how E-cadherin instructs the assembly of the LGN/NuMA complex

199 ral progenitors lacking Lgl1 had decreased N-cadherin internalization and abnormal cell junctions, ge

200 thermore, p120-catenin overexpression blocks cadherin internalization and cleavage, coupling entry in

201 The expression of E-cadherin is a key to this transition; yet precise unders

202 Here we provide evidence that VE-cadherin is cleaved by calpain upon entry into clathrin-

203 ine cluster in the intracellular domain of E-Cadherin is essential for binding to beta-Catenin in vit

204 We tested the hypothesis that N-cadherin is part of a novel mechanosensory mechanism in

205 scription of the adherens junction protein E-cadherin is upregulated, leading to accumulation of E-ca

206 Here, we show that in the chick embryo, E-cadherin is weakly expressed in the epiblast at pre-prim

207 adherin endocytosis, but p120 binding to the cadherin juxtamembrane domain acts as a master regulator

208 Furthermore, expression of a mutant E-cadherin lacking the intracellular domain was sufficient

209 reover, NOX4 expression is associated with E-cadherin levels and inversely correlated with invasive f

210 man melanoma progression, whereas elevated P-cadherin levels are associated with reduced survival of

211 One pathway of activation is initiated by N-cadherin ligation and involves the cadherin coreceptor C

212 Disruption of the N-cadherin-LLGL1 interaction during cortical development i

213 romotes internalization of N-cadherin, and N-cadherin/LLGL1 interaction is inhibited by atypical prot

214 ed outer bud cells, which display stronger E-cadherin localization, reduced cell motility and decreas

215 ng of the pathways involved in integrating E-cadherin loss to the gain of mesenchymal traits remains

216 lin assemble into a signaling complex upon E-cadherin loss.

217 Thus, Type II cadherins may uniquely contribute to the specificity and

218 enzyme USP48 stabilizes TRAF2 and reduces E-cadherin-mediated adherens junctions.

219 mbly of motor neurons into nuclei depends on cadherin-mediated adhesion.

220 hrough PI3-kinase-dependent regulation of DE-Cadherin-mediated cell adhesion between NBs and neighbor

221 of reactive oxygen species induces loss of E-cadherin-mediated cell contact, followed by a regenerati

222 fines the basal surface, setting in motion E-cadherin-mediated cell-cell contact, which establishes a

223 dhesion to the host cell surface, and that E-cadherin-mediated coupling of the bacterium to F-actin i

224 Cadherin-mediated homophilic adhesion is necessary for t

225 IY domain has a separate role in Rho1- and E-cadherin-mediated polarization at the initiation stage i

226 lial cell adhesion molecule [EpCAM](+)MPs, E-cadherin(+)MPs), platelet MPs (CD31(+)CD41(+)MPs), eosin

227 The neuronal cadherin (N-cadherin; Ncdh) is known for its important r

228 The neuronal cadherin (N-cadherin; Ncdh) is known for its important role in neuru

229 ing embryonic territories in the mouse, as E-cadherin needs to be downregulated in the primitive stre

230 LIF-dependent STAT3 phosphorylation, with E-cadherin null mESCs exhibiting over 3000 gene transcript

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

232 ragment of desmoglein 2 (Dsg2), a desmosomal cadherin often overexpressed in malignancies.

233 tility and reveal an unprecedented role of N-cadherin on cell shapes and cell arrangements.

234 Cadherin-11 (Cad-11, also known as OB cadherin or CDH11) is a cell-to-cell adhesion molecule i

235 ivity patterns are disrupted by manipulating cadherin or gap junction expression.

236 that over-expression of EC4-Fc (truncated N-cadherin), or deletion of matrix-metalloproteinase-7 (Mm

237 rapidly (lambda = 5.5 min), indicating that cadherin order is not required for adhesion.

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

239 y to TRPM2-activated Ca(2+) signaling and VE-cadherin phosphorylation resulting in the disassembly of

240 ve behavior; however, the impact of distinct cadherin profiles on peritoneal anchoring of metastatic

241 decreased binding of CUX1 to Snail and the E-cadherin promoter, reversed EMT, and decreased cell migr

242 is upregulated, leading to accumulation of E-cadherin protein at the cell-cell boundary.

243 mRNA levels are inversely correlated with E-cadherin protein expression in different cancers.

244 n and demonstrate that complete absence of E-cadherin protein is likely required for hierarchical sig

245 with increased MMP-7 activity and reduced N-cadherin protein levels in HAAA sections compared to HA.

246 lcium signaling, transformation, and novel E-cadherin-RalBP1 interaction.

247 is known about how such phosphorylation of E-Cadherin regulates AJ formation and dynamics in vivo In

248 We have previously shown that E-cadherin regulates the naive pluripotent state of mouse

249 se data demonstrate the role of a paRNA in E-cadherin regulation and the impact of a noncoding geneti

250 issense mutation c.4136G>T (p.Arg1379Leu) in cadherin-related 23 (CDH23).

251 The use of cadherin-related family member 3 (CDHR3) by RV-C as its

252 Most expression patterns of both cadherins remain constant with a few exceptions particul

253 echanism that controls the upregulation of N-cadherin remains unknown.

254 e postendocytic trafficking itinerary of the cadherin, resulting in a higher turnover rate due to dec

255 the same signaling molecules activated by E-cadherin rigidity sensing on PA gels contribute to actin

256 E-cadherin silencing relies on the formation of a complex

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

258 plexes (e.g., occludin-ZO-1, CAR-ZO-1, and N-cadherin-ss-catenin), through a down-regulation of p-Akt

259 e domain acts as a master regulator guarding cadherin stability.

260 malian cells is predicted to serve the large cadherin superfamily and other proteins.

261 We recently discovered that the cadherin superfamily carries O-linked mannose (O-Man) gl

262 erged as a critical mechanism for regulating cadherin surface levels and adhesion strength.

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

264 Of importance, the cleavage of the VE-cadherin tail alters the postendocytic trafficking itine

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

266 o reveal biologically relevant changes in VE-cadherin tension that occur as the dorsal aorta matures

267 KC-specific Par3 loss up-regulates surface P-cadherin that is essential to promote MC proliferation a

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

269 This migration depends on N-cadherin that, when imposed in ectodermal cells, is suff

270 at is required for pericyte cell survival; N-cadherin, the key adherens junction protein between endo

271 ation of presenilin 1 with N-cadherin and VE-cadherin, thereby compromising pericyte-endothelial cell

272 sed from the nucleus and competes LGN from E-cadherin to locally form the LGN/NuMA complex.

273 dence that NCX1 interacts with and anchors E-cadherin to the cell surface independent of NCX1 ion tra

274 VE-cadherin trafficking to and from the plasma membrane has

275 The repression of E-cadherin transcription by the EMT inducers Snail1 and Ze

276 We also show that Snail2 and Zeb2 repress P-cadherin transcription in the primitive streak and the n

277 Igamma and talin regulate the stability of E-cadherin transcriptional repressors, snail and slug, ind

278 Though cadherins typically function via trans-cellular homophil

279 Btbd7 can enhance E-cadherin ubiquitination, internalization, and degradatio

280 Vascular endothelial (VE)-cadherin undergoes constitutive internalization driven b

281 autonomous regulator of CIL by controlling N-cadherin upregulation during EMT.

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

283 herens junction protein vascular endothelial cadherin (VEC).

284 gnaling was observed in stomachs only when E-cadherin was absent.

285 and it was suggested that the function of E-cadherin was dependent on the O-Man glycans.

286 In the present study, the expression of E-cadherin was downregulated, while the expression of alph

287 In this study, T-cadherin was essential for accumulation of adiponectin i

288 uced in Nlrp3(-/-) mice, and expression of E-cadherin was reestablished.

289 reak stages where it is substituted for by P-cadherin We also show that Snail2 and Zeb2 repress P-cad

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

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

292 force sensitive biosensors integrated into E-cadherin were used to resolve piconewton scale forces al

293 gain of mesenchymal markers (vimentin and N-cadherin), whereas epithelial markers, such as E-cadheri

294 decreased the expression of Zonulin-1 and E-cadherin, whereas Nlrp3 knockdown increased the permeabi

295 binds to the epithelial host cell receptor E-cadherin, which mediates a physical link between the bac

296 rocytes inhibit stem cell division through E-cadherin, which prevents secretion of mitogenic epiderma

297 c enterocytes promote divisions by loss of E-cadherin, which releases cadherin-associated beta-cateni

298 articipation of the cell adhesion molecule N-cadherin, which starts to be expressed by NC cells as a

299 D5-2), which disrupted the interaction of VE-cadherin with its regulator miR-27a, resulting in increa

300 ide, as well as a neutralizing antibody to E-cadherin, works synergistically with ionizing radiation