ライフサイエンスコーパス: E-cadherin

1 tion proteins, including ZO-1, occludin, and E-cadherin.

2 pment, associated with reduced expression of E-cadherin.

3 echanism that involves the adhesion molecule E-cadherin.

4 d Vimentin with relatively low expression of E-cadherin.

5 estoring expression of the epithelial marker E-cadherin.

6 d lasR genes, and (2) miR-9 and silencing of E-cadherin.

7 ut changes in EMT markers vimentin, slug and E-cadherin.

8 n and, in turn, the junctional expression of E-cadherin.

9 /Abl kinases and degradation of beta-catenin/E-cadherin.

10 ional loss of the cell-cell adhesion protein E-cadherin.

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

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

13 n machinery that binds the cytosolic tail of E-cadherin.

14 ing nuclear localization of beta-catenin and E-cadherin.

15 membrane in a complex with beta-catenin and E-cadherin.

16 expression of miR-34a, SIRT1, cyclin D1, and E-cadherin.

17 sively in co-immunoprecipitates of CAV1 with E-cadherin.

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

19 hibited by co-expression of the glycoprotein E-cadherin.

20 phospho-PRAS40, but increased expression of E-cadherin.

21 6F10 murine melanoma cells expressing or not E-cadherin.

22 helial barrier integrity through cleavage of E-cadherin.

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

24 f DCLK1 and active beta-catenin, and cleaved E-cadherin.

25 loss of the intercellular adhesion protein, E-cadherin(1,2), on the basis of inverse correlations be

26 metastasis via increasing the expression of E-cadherin, a tumor suppressor, and decreasing the expre

27 E-cadherin activation inhibits metastasis at multiple st

28 Our results reveal that E-cadherin acts as a survival factor in invasive ductal

29 It requires a Rho- and E-cadherin adhesion-dependent, substrate-parallel contra

30 Nonetheless, loss of E-cadherin alone does not predispose mice to mammary tum

31 We propose that the tension generated by the E-cadherin/AmotL2/actin filaments plays a crucial role i

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

33 maintains the robustness of polarisation of E-cadherin- an adherens junction component- in the perid

34 the apical surface of Tsc1-mutant cells with E-cadherin and alpha-catenin.

35 ncomitant decrement in the epithelial marker E-cadherin and altered the expression of the key EMT-med

36 on of S115 is characterized by a decrease in E-cadherin and an induction of the basal marker, K14, re

37 EMT, correlated with increased expression of E-cadherin and beta-catenin, and decreased expression of

38 ivity for beta-catenin/Tcf over beta-catenin/E-cadherin and beta-catenin/adenomatous polyposis coli (

39 n/Tcf PPI without affecting the beta-catenin/E-cadherin and beta-catenin/APC PPIs, suppressed transac

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

41 ntermolecular FRET measurements of wild-type E-cadherin and cis-interaction mutants combined with sim

42 tor for mutant beta-catenin-mediated loss of E-cadherin and Claudin-7 in HCT116-P and HCT116-MT cells

43 capacity and cortical contractility through E-cadherin and DDR1 proteins.

44 ls, and LGR4 knockdown resulted in increased E-cadherin and decreased expression of N-cadherin and sn

45 duced expression of claudin-1, occludin, and E-cadherin and decreased numbers of epithelial cells, wh

46 Immunofluorescent staining of E-cadherin and EdU revealed decreased epithelial cell pr

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

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

49 E-cadherin and its transcriptional regulators; Snail and

50 native bacterial strategy for InlA access to E-cadherin and its translocation.

51 E-cadherin and myosin colocalize at border cell-border c

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

53 ed dysregulation of tight junction proteins, E-cadherin and N-cadherin expression, and STAT3 phosphor

54 Paneth cells population and reinstating the E-cadherin and N-Cadherin expression.

55 Furthermore, E-cadherin and nectin-2 were found between adjoining mem

56 ssion of GFP-FIP2(S227E) induced the loss of E-cadherin and occludin, mutation of any of the NPF doma

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

58 Truncated ASPP2 cooperates with E-cadherin and PTEN loss to drive breast cancer initiati

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

60 educes Wnt signaling, but increases membrane E-cadherin and restores cell-cell adhesion.

61 G-PAC1 cells results in the up-regulation of E-cadherin and the down-regulation of CDC42.

62 FPR2 ligands resulted in down-regulation of E-cadherin and up-regulation of vimentin, which were rev

63 beta-catenin(+) cancer cells that coexpress E-cadherin and vimentin in core-needle biopsies from pat

64 Duplex immunofluorescence slides stained for E-cadherin and vimentin were digitally analyzed by mappi

65 tates migration primarily via crosstalk with E-cadherin and ZEB1.

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

67 However, many metastases continue to express E-cadherin, and a full EMT is not always necessary for m

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

69 were examined for alterations in claudin-1, E-cadherin, and N-cadherin.

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

71 ecipitate with PTPN14 even in the absence of E-cadherin, and overexpression of PTPN14 reduced CAV1 ph

72 or 1 (HIF-1), followed the downregulation of E-cadherin, and produced heterogeneous cell subsets whos

73 treatment that thins F-actin bands, depletes E-cadherin, and stimulates proliferation in long-quiesce

74 e, the downregulation of beta-defensin 1 and E-cadherin, and upregulation of hepatocyte growth factor

75 1c, CD3, CD4, tryptase, claudin-1, occludin, E-cadherin, and vascular endothelial growth factor A lev

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

77 dherin), whereas epithelial markers, such as E-cadherin, are down-regulated.

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

79 Further analysis identified E-cadherin as the top positive correlated gene, while he

80 from nephron progenitor cells and expressed E-cadherin as well as vimentin, a myofibroblastic marker

81 ctional localization of actin, spectrin, and E-cadherin assembly at the AJs.

82 oclonal antibodies that bind to and activate E-cadherin at the cell surface reduce lung metastasis fr

83 btypes where RAS/MAPK pathway activation and E-cadherin attenuation are common.

84 As such, the Snail1/E-cadherin axis described in the early mouse embryo corr

85 e and cellular fate mediated by differential E-cadherin based cell sorting.

86 For instance, changing levels of homophilic E-cadherin-based cell-cell adhesion induce cell sorting,

87 hanges in alphaE-catenin upon binding to the E-cadherin*beta-catenin complex, vinculin and F-actin.

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

89 the surrounding keratinocytes via homophilic E-cadherin binding.

90 We also demonstrated that E-cadherin binds to both WT and mutant beta-catenin, and

91 stitute acto-myosin connection of a tailless E-cadherin by two ways: direct recruitment of alpha-cate

92 lial cells with surface expression of PD-L1, E-cadherin, CD24, and VEGFR2 rapidly formed tumors outsi

93 ene expression and correlated with induction E-cadherin (CDH1) and mesenchymal-to-epithelial transiti

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

95 (2020) explore the potential role of E-cadherin (CDH1) as a marker for invasive behavior in m

96 The frequencies of rectal E-cadherin(+) cells remained stable despite multiple tis

97 E-cadherin(+) cells, CD4(+) cells and total mucosal cell

98 e that TMTC3 supports the O-mannosylation of E-cadherin, cellular adhesion, and embryonic gastrulatio

99 e junction proteins (e.g., zonula occludens, E-cadherin, claudins, and occludin).

100 ion remodeling also requires formin-mediated E-cadherin clustering and dynamin-dependent endocytosis.

101 NMIIB is involved in E-cadherin clustering, maintenance of a branched actin l

102 ntaining E-cadherin extend into gaps between E-cadherin clusters on neighboring cells, while reformat

103 Increased tension on the E-cadherin complex promoted the junctional recruitment o

104 tenance of a branched actin layer connecting E-cadherin complexes and perijunctional actin fibres lea

105 ylation compartmentalizes Daple/beta-catenin/E-cadherin complexes to cell-cell contact sites, enhance

106 or long-distance trafficking of beta-catenin/E-cadherin complexes to pericentriolar recycling endosom

107 nase-9 (MMP9), fibronectin (FN), and soluble E-cadherin, consistent with clinically reported elevated

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

109 defines a novel mechanism by which p190A and E-cadherin cooperate in modulating Hippo signaling to su

110 dherin-bound catenins, binds directly to the E-cadherin cytosolic tail and thereby localizes at cell-

111 e generated an extensive array of Drosophila E-Cadherin (DE-Cad) endogenous knock-in alleles that car

112 The presence of E-cadherin decreases cortical contractility during mitos

113 Intriguingly, E-cadherin-deficient LC displayed a dramatically changed

114 elaxation, enabling adhesion and survival of E-cadherin-deficient murine mammary epithelial cells on

115 tment of spectrin to the AJs and also reduce E-cadherin during the initial junctional formation of th

116 -regulated in HCT116-P vs. HCT116-WT without E-cadherin dysregulation.

117 ocalized expression of the epithelial marker E-cadherin (E) and the mesenchymal marker vimentin (V) a

118 tumor cells by autonomous downregulation of E-cadherin (E-cad) and consequent activity of p120-caten

119 In the pluripotent state, E-cadherin (E-CAD) transduces boundary forces to focus W

120 1 but not of the adherens junction component E-cadherin (Ecad) was dependent on the presence of serum

121 herin P-cadherin, all directly interact with E-cadherin ectodomains.

122 protein expression of the epithelial marker E-cadherin either remained unaltered or increased.

123 are characterized by the functional loss of E-cadherin (encoded by CDH1), inactivation of Cdh1 does

124 N3 drives breast tumorigenesis by increasing E-cadherin endocytosis, followed by the activation of a

125 tinocyte proliferation by downregulating the E-cadherin/epidermal growth factor receptor/mitogen-acti

126 d that changes in the functional activity of E-cadherin expressed on tumor cells in response to envir

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

128 adiol levels were positively correlated with E-cadherin expression and a more basal location for HIV

129 tenuates TNF-alpha/JNK pathway and increases E-cadherin expression and cell-cell junction in epitheli

130 e shortened neo-epithelia exhibited declined E-cadherin expression and diminished keratinocyte prolif

131 p1 signaling pathway, as shown by decreasing E-cadherin expression and increasing vimentin expression

132 ibition of DNA methylation not only restored E-cadherin expression in EMT memory, but also primed cel

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

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

135 xpression level of Snail but does not reduce E-cadherin expression level at the IC(50) (DPAGT1) conce

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

137 Mean E-cadherin expression per cell increased 5.6-fold in bot

138 We find that E-cadherin expression persists in metastatic lung nodule

139 and STAT3, which was accompanied by altered E-cadherin expression to induce a malignant morphology.

140 C)-like properties, including NANOG, CD133+, E-cadherin expression, and the CD44(+)/CD24(-/low) pheno

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

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

143 ion, and migration require a reduction in LC E-cadherin expression.

144 wth factor and fibronectin, and decreases in E-cadherin expression.

145 ve imaging shows that microspikes containing E-cadherin extend into gaps between E-cadherin clusters

146 ar, weak, lateral (cis) interactions between E-cadherin extracellular domains tethered to supported l

147 f anchoring the bacterium to F-actin through E-cadherin for bacterial invasion has not been tested di

148 ages of EMT, there was a gradual decrease in E-cadherin force and lumen pressure that correlated with

149 eases in CFTR activity resulted in increased E-cadherin forces, indicating that ionic gradients affec

150 ee-dimensional (3D) organotypic culture with E-cadherin fragment expression and steroid hormone pathw

151 , we present the first in vivo evidence that E-cadherin from tumor cells facilitate immune attack, us

152 tion of the exact mechanisms associated with E-cadherin function in mESCs is compounded by the diffic

153 ments in the proximal promoter region of the E-cadherin gene.

154 RNA-binding protein CUGBP1 with occludin and E-cadherin genes in DRA-KO mouse colon, suggesting that

155 oned in the endogenous niche: the C. elegans E-cadherin HMR-1, its intracellular associates alpha-cat

156 nd tumor coexpression of alpha6 integrin and E-cadherin in a cell-cell location and alpha6 integrin i

157 locytes impaired their capacity for cleaving E-cadherin in adherens junctions between acinar cells an

158 Selective disruption of trans engagement of E-cadherin in an otherwise cohesive cell monolayer, or l

159 AV1 co-inmunoprecipitated in the presence of E-cadherin in B16F10 melanoma and other cancer cells.

160 ed similar loss of membrane beta-catenin and E-cadherin in CK5+ but not intratumoral CK5- cells and s

161 egulation of vimentin, alpha-SMA and loss of E-cadherin in co-culture spheroids confirmed cellular cr

162 Blocking the expression of CaSR or E-cadherin in cultured keratinocytes markedly inhibited

163 trols transcription of the tumour suppressor E-cadherin in epithelial cancers.

164 is revealed down-regulation of Claudin-7 and E-cadherin in HCT116-MT vs. HCT116-WT.

165 tooth development through the suppression of E-cadherin in IEE cells.

166 pancy, we tested the genetic requirement for E-cadherin in metastasis using mouse and human models of

167 E-cadherin in one layer controls the localisation of E-c

168 s are invasive ductal carcinomas and express E-cadherin in primary tumours and metastases(4).

169 al cell-specific cell-cell adhesion molecule E-cadherin in the dental epithelium.

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

171 The findings suggest that high E-cadherin in those supporting cell junctions may be res

172 uced ROS-induced degradation of beta-catenin/E-cadherin in vitro and ameliorated skin damage in roden

173 While loss of E-cadherin increased invasion, it also reduced cancer ce

174 ssociated beta-catenin and nuclear localized E-cadherin, increases sequestration of these proteins in

175 periphery where it physically interacts with E-cadherin, indicating that it is important to maintain

176 ompanied by efficient clustering and loss of E-cadherin, indicating that this is an important adaptat

177 es, and ACTN4 down-regulation suppressed the E-cadherin-induced cell invasion increase via depolymeri

178 Our results show how E-cadherin instructs the assembly of the LGN/NuMA comple

179 We find that TBC1D2b suppresses E-cadherin internalization, thus hindering cancer cell i

180 The expression of E-cadherin is a key to this transition; yet precise unde

181 The cell adhesion molecule E-cadherin is a major component of adherens junctions an

182 E-cadherin is a tumor suppressor protein, and the loss o

183 Thus, the functional state of E-cadherin is an important determinant of metastatic pot

184 E-cadherin is critically required for skin barrier funct

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

186 erine cluster in the intracellular domain of E-Cadherin is essential for binding to beta-Catenin in v

187 using a B16F10 melanoma mouse model in which E-cadherin is exogenously expressed (B16.Ecad).

188 E-cadherin is retained on the cell surface during cell s

189 anscription of the adherens junction protein E-cadherin is upregulated, leading to accumulation of E-

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

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

192 Furthermore, expression of a mutant E-cadherin lacking the intracellular domain was sufficie

193 Decreased levels of E-cadherin, LaminB1 and increased levels of Cyc-D and p2

194 Moreover, NOX4 expression is associated with E-cadherin levels and inversely correlated with invasive

195 correlations between in vitro migration and E-cadherin levels(3).

196 reduced N-cadherin expression, but increased E-cadherin levels.

197 cked outer bud cells, which display stronger E-cadherin localization, reduced cell motility and decre

198 Wilms Tumor-1-YAP-mediated downregulation of E-cadherin, loosening cell-cell contacts, and YAP-TRIO-M

199 increased interleukin 6 (IL-6) that induced E-cadherin loss and N-cadherin gain and increased cell m

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

201 ding of the pathways involved in integrating E-cadherin loss to the gain of mesenchymal traits remain

202 eatures of mesenchymal transition, including E-cadherin loss.

203 talin assemble into a signaling complex upon E-cadherin loss.

204 beta-catenin at the cell membrane and total E-cadherin loss.

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

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

207 In the absence of E-cadherin-mediated cell adhesion, LC numbers remained s

208 t of reactive oxygen species induces loss of E-cadherin-mediated cell contact, followed by a regenera

209 defines the basal surface, setting in motion E-cadherin-mediated cell-cell contact, which establishes

210 adhesion to the host cell surface, and that E-cadherin-mediated coupling of the bacterium to F-actin

211 rrier function at tight junctions as well as E-cadherin-mediated formation of adherens junctions.

212 tion of intracellular Ca(2+) (Ca(2+)(i)) and E-cadherin-mediated signaling.

213 Identifying molecular strategies to inhibit E-cadherin-mediated survival in metastatic breast cancer

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

215 e essential for the export of neosynthesized E-cadherin, MMP14, and CFTR DeltaF508, three proteins wh

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

217 helial cell adhesion molecule [EpCAM](+)MPs, E-cadherin(+)MPs), platelet MPs (CD31(+)CD41(+)MPs), eos

218 changes in expression levels of EMT markers (E-cadherin, N-cadherin, fibronectin, vimentin, slug and

219 ining embryonic territories in the mouse, as E-cadherin needs to be downregulated in the primitive st

220 At the cellular level, disseminating E-cadherin-negative cells exhibited nuclear enrichment o

221 Colony formation of E-cadherin-negative cells was rescued by inhibition of T

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

223 ng LIF-dependent STAT3 phosphorylation, with E-cadherin null mESCs exhibiting over 3000 gene transcri

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

225 psoriatic skin inflammation, indicating that E-cadherin on LC does not influence their ability to orc

226 downregulate the cell-cell adhesion molecule E-cadherin on non-tumorigenic cells and promote tumor in

227 Duodenal E-cadherin (P = 0.03) and defensin alpha 5 (P = 0.03) in

228 ting increased junction turnover and reduced E-cadherin/p120-catenin binding and migrating as a faste

229 butes to junction turnover by modulating the E-cadherin/p120-catenin interaction and, in turn, the ju

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

231 fferent glycemic conditions, ZEB1 binding to E-cadherin promoter was investigated using chromatin imm

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

233 ic conditions, ZEB1 lost its ability to bind E-cadherin promoter.

234 K27, H3K9, and DNA methylation, in the CDH1 (E-cadherin) promoter following the chronic IL-1beta expo

235 Here we show that E-cadherin promotes metastasis in diverse models of inva

236 ed that the quintessential epithelial marker E-cadherin promotes metastasis of invasive ductal breast

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

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

239 calcium signaling, transformation, and novel E-cadherin-RalBP1 interaction.

240 total E-cadherin expression, and vimentin-to-E-cadherin ratio per cell (an average of 47,000 cells pe

241 ogenes transcytosis via interaction with the E-cadherin receptor, which is facilitated by epithelial

242 ly, loss of Ck1alpha also blocked junctional E-cadherin reduction around the wound.

243 Furthermore, E-cadherin regulated ACTN4 and beta-catenin colocalizati

244 s is known about how such phosphorylation of E-Cadherin regulates AJ formation and dynamics in vivo I

245 We have previously shown that E-cadherin regulates the naive pluripotent state of mous

246 both WT and mutant beta-catenin, and loss of E-cadherin releases beta-catenin from the cell membrane

247 lial-mesenchymal transition (EMT), including E-cadherin repression and fibronectin and N-cadherin ind

248 of Claudin-7, as well as both Claudin-7 and E-cadherin respectively caused tight junction (TJ) impai

249 Here, we demonstrate that E-cadherin responds to force by recruiting and activatin

250 kened circumferential F-actin bands at their E-cadherin-rich adherens junctions.

251 mmalian ears, where supporting cells develop E-cadherin-rich apical junctions reinforced by robust F-

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

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

254 at the same signaling molecules activated by E-cadherin rigidity sensing on PA gels contribute to act

255 E-cadherin showed a significant progressive decline of i

256 tions because loss of either beta-catenin or E-cadherin significantly rescued this WC defect.

257 E-cadherin silencing relies on the formation of a comple

258 nally, an immunohistochemical examination of E-cadherin, Snail, Slug, and Twist2 expression was perfo

259 elial-mesenchymal transition (EMT) including E-cadherin, Snail, Slug, and Twist2, in the Egyptian pop

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

261 ivities of HDAC6i involved regulation of the E-cadherin/STAT3 axis.

262 E-cadherin supplies a permissive haptotactic cue.

263 thelial cells, such interactions mediated by E-cadherin suppress ferroptosis by activating the intrac

264 epithelial cell line CLDE cells resulted in E-cadherin suppression.

265 and/or volume changes, both of which affect E-cadherin tension.

266 Keratinocyte E-cadherin, thus upregulated, resisted EMT required for

267 This results in E-cadherin titrating any available beta-catenin, the Wnt

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

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

270 resulting in clustering and accumulation of E-cadherin to the adherens junctions.

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

272 vidence that NCX1 interacts with and anchors E-cadherin to the cell surface independent of NCX1 ion t

273 gulators of Wnt signaling, beta-catenin, and E-cadherin, to the nucleus.

274 the Src tyrosine kinase to alter junctional E-cadherin trafficking.

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

276 eal that AmeloD functions as a suppressor of E-cadherin transcription in IEE cells.

277 PKIgamma and talin regulate the stability of E-cadherin transcriptional repressors, snail and slug, i

278 Loss of the E-cadherin tumor suppressor protein enhanced cell invasi

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

280 signaling was observed in stomachs only when E-cadherin was absent.

281 Transcriptionally, loss of E-cadherin was associated with upregulation of genes inv

282 eas the expression of negative regulators of E-cadherin was decreased.

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

284 In the present study, the expression of E-cadherin was downregulated, while the expression of al

285 NCs, claudin-1 redistributed to the nucleus; E-cadherin was lost and N-cadherin gained, with similar

286 less, maturation and migration of LC lacking E-cadherin was not altered, neither under steady-state n

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

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

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

290 CaSR and E-cadherin were co-expressed at the cell-cell membrane b

291 s force sensitive biosensors integrated into E-cadherin were used to resolve piconewton scale forces

292 ly decreased the expression of Zonulin-1 and E-cadherin, whereas Nlrp3 knockdown increased the permea

293 This cassette includes CDH1 encoding E-cadherin, which amplifies p190A-mediated LATS activati

294 ncreased levels of the cell adhesion protein E-CADHERIN, which lead to premature differentiation and

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

296 terocytes inhibit stem cell division through E-cadherin, which prevents secretion of mitogenic epider

297 tic enterocytes promote divisions by loss of E-cadherin, which releases cadherin-associated beta-cate

298 xpression of genes silenced by EZH2, such as E-cadherin, which suppresses epithelial-mesenchymal tran

299 unding resulted in loss of epithelial marker E-cadherin with concomitant gain of ZEB1.

300 ptide, as well as a neutralizing antibody to E-cadherin, works synergistically with ionizing radiatio