ライフサイエンスコーパス: cadherin

1 eased degradation, and/or mislocalization of cadherin.

2 10 murine melanoma cells expressing or not E-cadherin.

3 lial barrier integrity through cleavage of E-cadherin.

4 which is largely attributed to the loss of E-cadherin.

5 DCLK1 and active beta-catenin, and cleaved E-cadherin.

6 on proteins, including ZO-1, occludin, and E-cadherin.

7 ent, associated with reduced expression of E-cadherin.

8 details of adiponectin's interaction with T-cadherin.

9 SPRY motifs in the extracellular domain of N-cadherin.

10 alterations in claudin-1, E-cadherin, and N-cadherin.

11 nal loss of the cell-cell adhesion protein E-cadherin.

12 g nuclear localization of beta-catenin and E-cadherin.

13 vely in co-immunoprecipitates of CAV1 with E-cadherin.

14 neered to enhance its binding affinity for T-cadherin.

15 ILC in mice with mammary-specific loss of E-cadherin.

16 bited by co-expression of the glycoprotein E-cadherin.

17 hospho-PRAS40, but increased expression of E-cadherin.

18 s dispensable in the context of a stabilized cadherin.

19 (sub)nuclei differentially express classical cadherins.

20 different classes of cadherins (N-cadherin, cadherin 11, and protocadherin 19) results in homotypic

21 n cancer cells maintained in 3D (P < 0.001), cadherin-11 was downregulated (P < 0.001) and HER2 incre

22 escues the neural tube convergence defect of cadherin 2 mutants.

23 imbalance in the traffic of the model cargo Cadherin-2 also reduces neuronal migration.

24 f protocadherin 15 (PCDH15) joined to two of cadherin 23 (CDH23).

25 the MT complex, including protocadherin 15, cadherin 23, lipoma HMGIC fusion partner-like 5, transme

26 nal cadherins, protocadherin-15 (PCDH15) and cadherin-23 (CDH23), form the tip-links, whose tension g

27 les forming an antiparallel complex with two cadherin-23 EC1-2 molecules.

28 ay crystal structure of a protocadherin-15 + cadherin-23 heterotetrameric complex at 2.9- angstrom re

29 Protocadherin-15 and cadherin-23, two atypically large cadherins with 11 and

30 enotype, and lineage analysis tested whether Cadherin-6 (Cdh6)-expressing cells are PT progenitors.

31 ronment and interacted with tumor cells in a cadherin-6-dependent manner.

32 E-cadherin activation inhibits metastasis at multiple stag

33 econdary to calpain-induced disruption of VE-cadherin adhesion.

34 results in myosin II-dependent unzipping of cadherin adhesive bonds.

35 osin II-dependent contractility from tearing cadherin adhesive contacts apart.

36 We also find that disrupting cadherin adhesivity in dorsal oculomotor neurons impairs

37 gand ephrin-B1, and the classical cadherin P-cadherin, all directly interact with E-cadherin ectodoma

38 Nonetheless, loss of E-cadherin alone does not predispose mice to mammary tumor

39 g partners for the extracellular region of E-cadherin, an essential cell-cell adhesion protein.

40 aintains the robustness of polarisation of E-cadherin- an adherens junction component- in the perider

41 e apical surface of Tsc1-mutant cells with E-cadherin and alpha-catenin.

42 omitant decrement in the epithelial marker E-cadherin and altered the expression of the key EMT-media

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

44 ion of the lipid raft-associated proteins VE-cadherin and caveolin-1.

45 of TMTC3 rescued O-linked glycosylation of E-cadherin and cell adherence.

46 ermolecular FRET measurements of wild-type E-cadherin and cis-interaction mutants combined with simul

47 N-cadherin and connexin-43 in adherens junction and gap ju

48 ith small GTPase Rab11 in Golgi to transport cadherin and Crumbs components synergistically to the ap

49 Immunofluorescent staining of E-cadherin and EdU revealed decreased epithelial cell prol

50 eye development markers Lhx2, Pax6, Jag1, E-cadherin and gamma-crystallins.

51 r, ABCG2, was lower, while mRNAs encoding VE-cadherin and ICAM1 were higher in schizophrenia brain.

52 omplex, which led to reduced cell surface VE-cadherin and increased vascular hyperpermeability; all w

53 E-cadherin and its transcriptional regulators; Snail and S

54 NA and protein levels of metastasis marker N-cadherin and mesenchymal marker vimentin increased signi

55 dysregulation of tight junction proteins, E-cadherin and N-cadherin expression, and STAT3 phosphoryl

56 Furthermore, E-cadherin and nectin-2 were found between adjoining membr

57 of adherens junctions by downregulation of E-cadherin and p120-catenin resulted in a transition from

58 mal transition (EndoMT) with decreases in VE-Cadherin and PECAM1 and increases in collagen, alpha-smo

59 GLI2 transcriptional activation of atypical cadherin and planar cell polarity (PCP) genes.

60 Truncated ASPP2 cooperates with E-cadherin and PTEN loss to drive breast cancer initiation

61 sed the phosphorylation levels of Src and VE-cadherin and reduced the formation of the VEGFR2-Src-VE-

62 uces Wnt signaling, but increases membrane E-cadherin and restores cell-cell adhesion.

63 , disrupts collective networks, and both the cadherin and RhoA binding domains of p120-catenin are re

64 elial identity (with ectopic expression of N-cadherin and Sox2), actomyosin disorganisation, cell sha

65 e strength of the molecular clutch between N-cadherin and the actin cytoskeleton.

66 eta-catenin(+) cancer cells that coexpress E-cadherin and vimentin in core-needle biopsies from patie

67 plex immunofluorescence slides stained for E-cadherin and vimentin were digitally analyzed by mapping

68 Cadherin and Wnt signaling pathways were positive in ove

69 These results indicate that cadherins and extracellular matrix confinement cooperate

70 n expression of these proteins, particularly cadherins and integrins, are frequently associated with

71 s revealed that an adhesion complex based on cadherins and the motor protein myosin-7b (MYO7B) links

72 transition (EMT) with loss of epithelial (E-cadherin) and gain of mesenchymal (vimentin) markers.

73 wever, many metastases continue to express E-cadherin, and a full EMT is not always necessary for met

74 of sterol homeostasis, downregulation of VE-cadherin, and a putative disturbance of Notch signaling.

75 ed proteins such as vinculin, connexin 43, N-cadherin, and alpha-catenin showed no significant change

76 ll adhesion molecule 1, vascular endothelial-cadherin, and CD34) and an endothelial marker recognized

77 rmal organization of desmoplakin, plectin, N-cadherin, and connexin-43.

78 epithelial target genes (i.e., HNF4alpha, E-cadherin, and HNF1alpha) and cause their repression.

79 on, including members of the immunoglobulin, cadherin, and leucine-rich repeat superfamilies.

80 ere examined for alterations in claudin-1, E-cadherin, and N-cadherin.

81 or the interaction between adiponectin and T-cadherin, and our engineered globular domain variants ma

82 ipitate with PTPN14 even in the absence of E-cadherin, and overexpression of PTPN14 reduced CAV1 phos

83 eatment that thins F-actin bands, depletes E-cadherin, and stimulates proliferation in long-quiescent

84 tumour cells to be AE1/AE3, CK7, GCDFP-15, E-cadherin, androgen receptor stain and GATA3 positive.

85 the angiogenic peptide ephrinB2/CTF2, the VE-cadherin angiogenic complexes and EC sprouting and tube

86 porting this hypothesis, ischemia-induced VE-cadherin angiogenic complexes, levels of neoangiogenesis

87 Fat, Fat-like, and Dachsous family cadherins are giant proteins that regulate planar cell p

88 Cadherins are intercellular adhesion proteins that assem

89 Classical cadherins are well-known adhesion molecules responsible

90 We generate models of possible cadherin arrangements and perform an in silico screening

91 vitro cleavage experiments using casein or E-cadherin as substrates and in the FRET peptide assay.

92 ional localization of actin, spectrin, and E-cadherin assembly at the AJs.

93 ile S1PR-dependent vascular endothelial (VE)-cadherin assembly suppresses JunB expression in the nasc

94 eability by inhibiting the disassembly of VE-cadherin at adherens junctions.

95 lonal antibodies that bind to and activate E-cadherin at the cell surface reduce lung metastasis from

96 or instance, changing levels of homophilic E-cadherin-based cell-cell adhesion induce cell sorting, b

97 Cadherin-based cell-cell junctions help metazoans form p

98 Vertebrates also have a new type of cadherin-based intercellular junction called the desmoso

99 nents of the protein complexes that generate cadherin-based junctions have ancient origins, with cons

100 ike or filamentous junctions stabilized by N-cadherin, beta-catenin and p120-catenin, which undergo k

101 That treatment also caused decreases in E-cadherin, beta-catenin, and YAP in the striola, and stim

102 Using a cadherin binding peptide (ADTC5) to transiently open tig

103 gnetic enhanced convective diffusion and the cadherin binding peptide for transiently opening the BBB

104 e surrounding keratinocytes via homophilic E-cadherin binding.

105 cell-cell adhesion, suggesting that other N-cadherin-binding proteins may be involved.

106 finity purification proteomics to identify N-cadherin-binding proteins.

107 We found that T-cadherin binds to the globular domain of adiponectin, re

108 strates like amyloid precursor protein and N-cadherin, but not with its sheddases ADAM10 or BACE1 at

109 increased MMP-2 and MMP-9 levels, enhanced N-cadherin, but reduced E-cadherin expression.

110 itute acto-myosin connection of a tailless E-cadherin by two ways: direct recruitment of alpha-cateni

111 ression of different classes of cadherins (N-cadherin, cadherin 11, and protocadherin 19) results in

112 ar to that of adherens junctions, desmosomal cadherins - called desmogleins and desmocollins - link i

113 tron tomograms (cryo-ET) in which individual cadherins can be discerned; they appear variable in shap

114 y in which delta-catenin, a component of the cadherin-catenin cell adhesion complex, promotes coordin

115 The cadherin-catenin complex at adherens junctions (AJs) is

116 evidence that Pp1 promotes proper levels of cadherin-catenin complex proteins at cell-cell junctions

117 tioning, prevents FGFR degradation through N-Cadherin, causing Erk1/2 phosphorylation.

118 IHC confirmed the down-regulation of E-cadherin (CDH1) and up-regulation of CXCL12 in endometri

119 (2020) explore the potential role of E-cadherin (CDH1) as a marker for invasive behavior in mel

120 protrusive activity operates continuously at cadherin cell-cell junctions to keep them shut and to pr

121 that TMTC3 supports the O-mannosylation of E-cadherin, cellular adhesion, and embryonic gastrulation.

122 due to loss-of-function in the non-classical cadherin celsr1a.

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

124 n remodeling also requires formin-mediated E-cadherin clustering and dynamin-dependent endocytosis.

125 s on neighboring cells, while reformation of cadherin clusters across the cell-cell boundary correlat

126 aining E-cadherin extend into gaps between E-cadherin clusters on neighboring cells, while reformatio

127 Using optically manipulated N-cadherin-coated microspheres, we correlated this behavio

128 growth cone is selectively affected by an N-cadherin-coated substrate.

129 d reduced the formation of the VEGFR2-Src-VE-cadherin complex, which led to reduced cell surface VE-c

130 Tumor cells that have ever expressed N-cadherin constituted the majority of metastases in lungs

131 on of epithelial sheets depends on classical cadherin-containing adherens junctions, which link actin

132 Importantly, E-cadherin controls the localisation and levels of Lgl, a

133 fines a novel mechanism by which p190A and E-cadherin cooperate in modulating Hippo signaling to supp

134 C)-specific deletion of Cept1 via induced VE-cadherin-CreERT2-mediated recombination (Cept1Lp/LpCre (

135 Intriguingly, E-cadherin-deficient LC displayed a dramatically changed m

136 axation, enabling adhesion and survival of E-cadherin-deficient murine mammary epithelial cells on st

137 g the internal retrograde actin flow in an N-cadherin-dependent fashion.

138 he N-cadherin extracellular domain but not N-cadherin-dependent homophilic cell-cell adhesion, sugges

139 lls (IEC) exclusively express the desmosomal cadherins, Desmoglein-2 and Desmocollin-2 (Dsc2) that co

140 SPRY mutant N-cadherin does not support radial migration in vivo Radia

141 ent of spectrin to the AJs and also reduce E-cadherin during the initial junctional formation of the

142 alized expression of the epithelial marker E-cadherin (E) and the mesenchymal marker vimentin (V) at

143 umor cells by autonomous downregulation of E-cadherin (E-cad) and consequent activity of p120-catenin

144 large cadherins with 11 and 27 extracellular cadherin (EC) repeats, are involved in deafness and bala

145 rin P-cadherin, all directly interact with E-cadherin ectodomains.

146 rotein expression of the epithelial marker E-cadherin either remained unaltered or increased.

147 These results indicate that cadherin endocytosis coordinates cell polarity and migra

148 ctively, our results indicate that regulated cadherin endocytosis is essential for both dynamic cell

149 drives breast tumorigenesis by increasing E-cadherin endocytosis, followed by the activation of a be

150 ut might assemble cytoskeleton to facilitate cadherin exocytosis.

151 that changes in the functional activity of E-cadherin expressed on tumor cells in response to environ

152 In clinical samples, E-cadherin-expressing and -deficient tumours both invade c

153 iol levels were positively correlated with E-cadherin expression and a more basal location for HIV ta

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

155 ition of DNA methylation not only restored E-cadherin expression in EMT memory, but also primed cells

156 y for metastasis; also, positive roles for E-cadherin expression in metastasis have been reported.

157 endothelial growth factor (VEGF) induces VE-cadherin expression in sprouting DPSCs undergoing anasto

158 ression level of Snail but does not reduce E-cadherin expression level at the IC(50) (DPAGT1) concent

159 The increases in E-cadherin expression per cell from baseline to week 16 we

160 Mean E-cadherin expression per cell increased 5.6-fold in both

161 We find that E-cadherin expression persists in metastatic lung nodules

162 of tight junction proteins, E-cadherin and N-cadherin expression, and STAT3 phosphorylation in MLE-12

163 positive epithelial cells (primary), total E-cadherin expression, and vimentin-to-E-cadherin ratio pe

164 ed MMP-2 and MMP-9 expression, and reduced N-cadherin expression, but increased E-cadherin levels.

165 9 levels, enhanced N-cadherin, but reduced E-cadherin expression.

166 n, and migration require a reduction in LC E-cadherin expression.

167 h factor and fibronectin, and decreases in E-cadherin expression.

168 imaging shows that microspikes containing E-cadherin extend into gaps between E-cadherin clusters on

169 Remarkably, radial migration requires the N-cadherin extracellular domain but not N-cadherin-depende

170 , weak, lateral (cis) interactions between E-cadherin extracellular domains tethered to supported lip

171 Masatoshi Takeichi for the discovery of the cadherin family of Ca(2+)-dependent cell-cell adhesion p

172 poral gradients of two heterophilic atypical cadherins-Fat (Ft) and Dachsous (Ds)-and the levels of F

173 ression levels of EMT markers (E-cadherin, N-cadherin, fibronectin, vimentin, slug and snail) and ste

174 es of EMT, there was a gradual decrease in E-cadherin force and lumen pressure that correlated with l

175 ses in CFTR activity resulted in increased E-cadherin forces, indicating that ionic gradients affect

176 -dimensional (3D) organotypic culture with E-cadherin fragment expression and steroid hormone pathway

177 Perturbing cadherin function in these neurons results in distinct d

178 red that the r14 allele of the pink bollworm cadherin gene (PgCad1) has a 234-bp insertion in exon 12

179 A-binding protein CUGBP1 with occludin and E-cadherin genes in DRA-KO mouse colon, suggesting that po

180 including Notch, amyloid precursor protein, cadherins, growth factors, and chemokines.

181 planar polarization of Fat-like and Dachsous cadherins has ancient, prebilaterian origins, and Fat-li

182 ancient, prebilaterian origins, and Fat-like cadherins have ancient roles in cell adhesion, spindle o

183 1 co-inmunoprecipitated in the presence of E-cadherin in B16F10 melanoma and other cancer cells.

184 similar loss of membrane beta-catenin and E-cadherin in CK5+ but not intratumoral CK5- cells and sin

185 E-cadherin in one layer controls the localisation of E-cad

186 dherin in Serum and Angiogenin in Saliva, VE-cadherin in Saliva and Headaches, PA1 in Saliva and Head

187 ons of TGF-beta1 in Saliva and Headaches, VE-cadherin in Serum and Angiogenin in Saliva, VE-cadherin

188 primary tumor cells activated vimentin and N-cadherin in situ, but only N-cadherin was activated and

189 in one layer controls the localisation of E-cadherin in the second layer in a layer non-autonomous m

190 The findings suggest that high E-cadherin in those supporting cell junctions may be respo

191 lular domains of Cadherin3 (Cdh3; formerly C-cadherin in Xenopus) disrupts contact inhibition of loco

192 We identified Fat-like and Dachsous cadherins in Hydra, a member of phylum Cnidaria a sister

193 A highly ordered array of cadherins in the adhesive interface is hypothesized to d

194 pment of the mammalian neocortex depend on N-cadherin, including the radial migration of immature pro

195 In contrast, antibodies against desmosomal cadherins, including human and mouse pemphigus autoantib

196 ociated beta-catenin and nuclear localized E-cadherin, increases sequestration of these proteins in c

197 ules and are divided into four major groups: cadherins, integrins, selectins, and immunoglobulins.

198 The cell adhesion molecule E-cadherin is a major component of adherens junctions and

199 E-cadherin is a tumor suppressor protein, and the loss of

200 Thus, the functional state of E-cadherin is an important determinant of metastatic poten

201 In conclusion, our data demonstrate that E-cadherin is dispensable to maintain LC in the epidermis

202 E-cadherin is retained on the cell surface during cell sep

203 Although the structure of the desmosomal cadherins is known, the desmosome architecture-which is

204 onally attributed to binding Adipor1/2 and T-cadherin, its abundance in circulation, role in ceramide

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

206 and function, we generated CD11c-specific E-cadherin knockout mice (CD11c-Ecad(del)).

207 Decreased levels of E-cadherin, LaminB1 and increased levels of Cyc-D and p21

208 duced N-cadherin expression, but increased E-cadherin levels.

209 adherin-related protein 3 (CDHR3), a surface cadherin-like protein expressed primarily on the apical

210 Truncated ASPP2 collaborated with both E-cadherin loss and PI3K pathway activation via PTEN loss

211 eta-catenin at the cell membrane and total E-cadherin loss.

212 ls are Her2(+)Skp2(high)Tpl2(low)p-p38(low)E-cadherin(low) in the MMTV-Her2 breast cancer model.

213 human skin model, suggesting that desmosomal cadherins may have different roles during acquisition of

214 t TMTC3 regulates O-linked glycosylation and cadherin-mediated adherence, providing insight into its

215 Here we investigate the role of cadherin-mediated adhesion in the development of zebrafi

216 In the absence of E-cadherin-mediated cell adhesion, LC numbers remained sta

217 Cadherin-mediated cell-cell adhesion is actin-dependent,

218 and single-cell dissemination, controlled by cadherin-mediated cell-cell junctions.

219 In addition, we show that cadherin-mediated interactions between adjacent subnucle

220 HMR-1/cadherin mediates this process via inter-tissue attachme

221 ancing the epidermal Ca(2+)(i) signals and E-cadherin membrane expression.

222 he loss of Vangl2 decreased fast-diffusing N-cadherin membrane molecules and increased confined N-cad

223 essential for the export of neosynthesized E-cadherin, MMP14, and CFTR DeltaF508, three proteins whos

224 ply pico-Newton scale forces to lipids and E-cadherin molecules at the living cell surface.

225 inatorial expression of different classes of cadherins (N-cadherin, cadherin 11, and protocadherin 19

226 anges in expression levels of EMT markers (E-cadherin, N-cadherin, fibronectin, vimentin, slug and sn

227 Neuronal cadherin (NCAD) plays a pivotal role in the formation of

228 corresponded to an area with a non-intact E-cadherin net structure.

229 d novel signaling roles for "non-junctional" cadherins (NJCads); however, the function of cadherin si

230 ubgroup had lower ABCG2 and higher ICAM1, VE-cadherin, occludin and interferon-induced transmembrane

231 Contrarily, epithelial markers (E-cadherin, occludin) were suppressed in ST6Gal-I-high cel

232 oriatic skin inflammation, indicating that E-cadherin on LC does not influence their ability to orche

233 wnregulate the cell-cell adhesion molecule E-cadherin on non-tumorigenic cells and promote tumor inva

234 nerator, and indicate a non-canonical use of cadherin on the basal side of an epithelium that may app

235 Twist) or Snai1 (which encodes Snail) in VE-cadherin(+) or Tie1(+) endothelial cells inhibited the e

236 escence polarization microscopy to show that cadherin order is not required for hyperadhesion induced

237 e kinase ligand ephrin-B1, and the classical cadherin P-cadherin, all directly interact with E-cadher

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

239 erapeutically, targeting VEGFR2-regulated VE-cadherin phosphorylation could suppress edema while leav

240 the PKCalpha inhibitor Go6976 revealed that cadherins, plakoglobin, and desmoplakin have significant

241 To determine whether E-cadherin plays a role in regulating LC homeostasis and f

242 7, H3K9, and DNA methylation, in the CDH1 (E-cadherin) promoter following the chronic IL-1beta exposu

243 that the quintessential epithelial marker E-cadherin promotes metastasis of invasive ductal breast c

244 Two unconventional cadherins, protocadherin-15 (PCDH15) and cadherin-23 (CD

245 tal E-cadherin expression, and vimentin-to-E-cadherin ratio per cell (an average of 47,000 cells per

246 Our findings reveal that cadherins regulate distinct aspects of cranial motor neu

247 esulting in a Y529 versus C529 change in the cadherin related family member 3 (CDHR3) receptor which

248 d by the first extracellular domain (EC1) of cadherin-related protein 3 (CDHR3), a surface cadherin-l

249 PgCad1 protein that lacks 36 amino acids in cadherin repeat 5 (CR5).

250 erestingly, DPSC stably transduced with a VE-cadherin reporter demonstrated that vascular endothelial

251 ned circumferential F-actin bands at their E-cadherin-rich adherens junctions.

252 alian ears, where supporting cells develop E-cadherin-rich apical junctions reinforced by robust F-ac

253 develop unique, exceptionally reinforced, E-cadherin-rich intercellular junctions.

254 The findings suggest that E-cadherin-rich junctions, which are not present in the SC

255 nofluorescence was performed for vimentin, N-cadherin, ROCK1, RhoA, ZEB1, and Snail.

256 ltures of brain ECs, EphB4 stimulates the VE-cadherin/Rok-alpha angiogenic complexes known to mediate

257 E-cadherin showed a significant progressive decline of its

258 cadherins (NJCads); however, the function of cadherin signaling independent of cell-cell contacts rem

259 Both VE-cadherin-silenced and mitogen-activated protein kinase k

260 VE-cadherin-silenced primary human DPSCs seeded in tooth sl

261 splayed enrichment in mesenchymal markers (N-cadherin, slug, snail, fibronectin) and cell invasivenes

262 lly, an immunohistochemical examination of E-cadherin, Snail, Slug, and Twist2 expression was perform

263 ial-mesenchymal transition (EMT) including E-cadherin, Snail, Slug, and Twist2, in the Egyptian popul

264 Fbxo45 binding requires N-cadherin SPRY motifs that are not involved in cell-cell

265 cells, and signs of metaplasia (attenuated E-cadherin staining).

266 Confluence was confirmed by VE-cadherin staining.

267 ities of HDAC6i involved regulation of the E-cadherin/STAT3 axis.

268 xia-inducible factor-1), reduces endothelial cadherin, stimulates vascular hypertrophy, increases vas

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

270 Conservation of these atypical cadherins suggests a wider prevalence of heterophilic ce

271 The cadherin superfamily of adhesion molecules carry O-linke

272 We demonstrate that members of the cadherin superfamily, the clustered gamma-Protocadherins

273 E-cadherin supplies a permissive haptotactic cue.

274 nd/or volume changes, both of which affect E-cadherin tension.

275 We find a truss-like arrangement of cadherins that resembles the characteristic footprint se

276 sduction on cell-cell contacts mediated by C-cadherin, the mechanism by which keratin filament reorga

277 we establish that p190A is obligatory for E-cadherin to activate LATS kinases and induce CIP.

278 PKC, is transduced in a stepwise manner by E-cadherin to the basal layer.

279 operty, specific contributions of desmosomal cadherins to intestinal mucosal repair after injury rema

280 lators of Wnt signaling, beta-catenin, and E-cadherin, to the nucleus.

281 membrane molecules and increased confined N-cadherin trajectories.

282 MT markers assessed were Snail-1, Snail-2, N-cadherin, Twist and vimentin.

283 ested the role of p120-catenin (p120) and VE-cadherin (VE-cad) endocytosis in vascular development us

284 thelial markers such as vascular endothelial cadherin(VECAD) and occludin but low expression of Tek r

285 vimentin and N-cadherin in situ, but only N-cadherin was activated and functionally required during

286 s the expression of negative regulators of E-cadherin was decreased.

287 ss, maturation and migration of LC lacking E-cadherin was not altered, neither under steady-state nor

288 similar expression pattern of occludin and E-cadherin was observed in colonoids derived from DRA-KO m

289 Using FRET-force biosensors for E-cadherin, we observed significant increases in the avera

290 n to understand the mechanisms regulating VE-cadherin, we stably silenced MEK1 and observed that VEGF

291 ificantly reduced, expression of CD31 and VE-Cadherin were unaffected, whereas SMAD1/5/8 signaling an

292 This cassette includes CDH1 encoding E-cadherin, which amplifies p190A-mediated LATS activation

293 oR1 and AdipoR2, as well as to the protein T-cadherin, which is highly expressed in the cardiovascula

294 ctivation of ERG leading to expression of VE-cadherin, which is required for anastomosis of DPSC-deri

295 reased levels of the cell adhesion protein E-CADHERIN, which lead to premature differentiation and ce

296 ression of genes silenced by EZH2, such as E-cadherin, which suppresses epithelial-mesenchymal transi

297 avior to a stronger mechanical coupling of N-cadherin with the actin cytoskeleton.

298 rin-15 and cadherin-23, two atypically large cadherins with 11 and 27 extracellular cadherin (EC) rep

299 hese findings support a mechanism whereby VE-cadherin Y685 phosphorylation is selectively associated

300 ix via integrins or to neighboring cells via cadherins, yet little is known regarding its mechanical

301 and positive for alpha-SMA, vimentin, CK7, N-cadherin, ZEB1, Snail, ROCK1, and RhoA.