ライフサイエンスコーパス: E-cadherin

1 expression ratio of the EMT markers Vimentin/E-cadherin.

2 ells was inversely related to membrane-bound E-cadherin.

3 , Slug, Snail and Zeb1), and upregulation of E-cadherin.

4 cer cells that expressed Vimentin and lacked E-cadherin.

5 expression of the adherens junction protein E-cadherin.

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

7 ctivation of two mechanoreceptors: Notch and E-cadherin.

8 and skin tumors, UVB radiation downregulates E-cadherin.

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

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

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

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

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

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

15 howed limited effects on the decrease in the E-cadherin abundance and stress fiber formation by TGF-b

16 Loss of E-cadherin activates the E2F4 and p130/107 transcription

17 pressing Snail) cancer cells expressed lower E-cadherin activity, higher Snail, vimentin, and Cat L a

18 ronin 1B, which is recruited to junctions by E-cadherin adhesion and is necessary to establish contra

19 ated nucleation and micron-scale assembly of E-cadherin adhesion complexes by confining the movement

20 surface regulation without inhibiting basic E-cadherin adhesion function.

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

22 ctional hierarchy and pathways that modulate E-cadherin adhesion.

23 ecent screens uncovering novel components of E-cadherin adhesions.

24 mammary gland to the lung depends on reduced E-cadherin adhesive function.

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

26 kout cell lines exhibited down-regulation of E-cadherin and a reduction in alpha/beta-catenin at cell

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

28 -CADHERIN while show a lack of expression of E-CADHERIN and CLAUDIN, being this profile characteristi

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

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

31 tiation, based on significantly higher total E-cadherin and decreased keratin 5 staining than epithel

32 g the structural and signalling functions of E-cadherin and demonstrate that complete absence of E-ca

33 itiation of contractile pulses, lower apical E-cadherin and F-actin levels, and aberrantly mobile Rho

34 V-NT mice also expressed increased levels of E-cadherin and fibroblast growth factor 21 (FGF21), targ

35 nchymal transition as a result of decreasing E-Cadherin and increasing N-Cadherin and vimentin expres

36 gy and characteristics by destabilization of E-cadherin and induction of beta-catenin signaling.

37 Mang-NPs also inhibited EMT by up-regulating E-cadherin and inhibiting N-cadherin and transcription f

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

39 rated that Foxf2 transcriptionally represses E-cadherin and miR-200, independent of Zeb1, to form a d

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

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

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

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

44 ls' microtubule-organizing centres, and that E-cadherin and retrograde recycling endosomes are prefer

45 2 to cellular junctions to associate with VE/E-cadherin and subsequently the organization of radial a

46 on of the tight junction components ZO-1 and E-cadherin and the formation of ZO-1 containing tight ju

47 33-positive basal epithelial cells expressed E-cadherin and the undifferentiated epithelial cell mark

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

49 by downregulating epithelial markers such as E-cadherin and upregulating mesenchymal markers such as

50 In contrast to DP cells, TS cells lost E-cadherin and were all vimentin-positive as shown by im

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

52 e found that HMGB1 induced downregulation of E-cadherin and ZO-1, and upregulation of vimentin mRNA t

53 Expression of epithelial (E-cadherin) and mesenchymal markers (vimentin, fibronect

54 enes included OCLN, TJP1 (ZO-1), FZD7, CDH1 (E-cadherin), and LAMA5.

55 The biomarker pairs CD44/CD24, N-cadherin/E-cadherin, and CD74/CD59 stratified DCIS samples.

56 d for comparison of diffuse alveolar damage, E-cadherin, and molecular biology variables.

57 echanical regulation of the T-cell receptor, E-cadherin, and Notch pathways, suggesting a common feat

58 nd protein expression concentrations of VDR, E-cadherin, and occludin as well as decreased protein ex

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

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

61 dicated by the decrease in epithelial marker E-cadherin, and the increase in mesenchymal markers alph

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

63 coated with purified extracellular domain of E-cadherin, and was designed for collision with the heal

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

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

66 tted in part through the actin connection to E-cadherin as well as other components in the adherens j

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

68 ownregulate the epithelial markers including E-cadherin, as well as estrogen receptor.

69 the four potential N-glycosylation sites of E-cadherin, Asn-554 is the key site that is selectively

70 hancing actin polymerization and stabilizing E-cadherin at epithelial junctions.

71 epletion leads to a reduction in F-actin and E-cadherin at junctions and a weakening of cell-cell adh

72 leads to aberrantly enhanced localization of E-cadherin at oocyte-oocyte contact sites.

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

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

75 ortical F-actin elevation increased membrane E-cadherin, beta-catenin, and Na(+)K(+) ATPase.

76 ology and the expression of Twist1-regulated E-cadherin, beta-catenin, vimentin and Slug, but it part

77 MMP7 disrupted E-cadherin/beta-catenin complex to upregulate EMT transc

78 adherin neutralising antibody DECMA-1 or the E-cadherin binding peptide H-SWELYYPLRANL-NH2 (Epep) exh

79 echanistically, Src-driven ubiquitination of E-cadherin by Cbl-like ubiquitin ligase releases P120-ca

80 and repression of the cell adhesion protein E-cadherin by the 5AR inhibitor dutasteride requires bot

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

82 f-renewal capacity and reduced expression of E-cadherin (CDH1) and CD24.

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

84 n Kras(G12D) expression plus inactivation of E-cadherin (Cdh1) and p53 in the gastric parietal cell l

85 t tumor models revealed that FIP1C regulated E-cadherin (CDH1) trafficking and ZONAB (YBX3) function

86 ntin (VIM), and MMP2 and the reexpression of E-cadherin (CDH1).

87 epression or up-regulation, respectively, of E-cadherin (cdh1).

88 EMT-regulator ZEB1-known to directly repress E-cadherin/CDH1-as a downstream target of FOXC2, critica

89 ntation required mechanotransduction through E-cadherin cell-cell adhesions.

90 l-type-related inhibitor (LEKTI), filaggrin, E-cadherin, claudin, occludin, desmoglein-1 was found, i

91 ated nucleation and micron-scale assembly of E-cadherin clusters, which could be distinguished as eit

92 that adhesions formed between cells, and the E-cadherin-coated MTM resembled the morphology and dynam

93 n healthy human eSCs in situ by antagonizing E-cadherin, combined with transforming growth factor-bet

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

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

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

97 In turn, the reduction in E-cadherin concentration and the contractility of the ne

98 When we blocked apoptosis, E-cadherin-controlled feedback suppressed divisions, and

99 roscopy, we find that ubiquitously localized E-cadherin coordinates tissue polarization of tension-be

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

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

102 repressors and down-regulation of Drosophila E-cadherin (DEcad) transcription.

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

104 main of E-cadherin (Ecad-Fc), we showed that E-cadherin-dependent epithelial cell adhesion was sensit

105 phages undergo reprograming events involving E-cadherin-dependent formation of epithelial-like cell-c

106 In conclusion, our data identify an E-cadherin-dependent mechanical circuit that integrates

107 acrophage reprogramming events that parallel E-cadherin-dependent mesenchymal-epithelial transitions.

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

109 droplets, functionalized with extracellular E-cadherin domains, reveals a hierarchy of homophilic in

110 Depletion of E-cadherin drastically diminished the cell-surface distr

111 ctionalized with the extracellular domain of E-cadherin (Ecad-Fc), we showed that E-cadherin-dependen

112 wnregulating the cell-cell adhesion protein, E-cadherin, enables MCF-10A cells to slide on narrower m

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

114 , well-known regulators of Rho-type GTPases, E-cadherin endocytosis, and epithelial junctional remode

115 ns of membrane protein organization, such as E-cadherin enrichment in epithelial junctional complexes

116 s and MCAs invade much more efficiently than E-cadherin-expressing (Ecad+) cells.

117 First, we find that the metastasis of an E-cadherin-expressing mammary cell line from the mammary

118 Herein, we report that membrane surface E-cadherin-expressing prostate cancer cells were resista

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

120 Further, down-regulation of USP48 increases E-cadherin expression and epithelial barrier integrity t

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

122 e, arsenic suppressed the downstream protein E-cadherin expression and induced beta-catenin/TCF-depen

123 1(-/-) mice demonstrated increased pulmonary E-cadherin expression and soluble E-cadherin shedding co

124 Mir-194 mimics increased E-cadherin expression and suppressed cancer cell migrati

125 The loss of E-cadherin expression in association with the epithelial

126 Furthermore, loss of E-cadherin expression in hepatocytes is associated with

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

128 E-cadherin expression in lung tissue was reduced in volu

129 1, which serves as an additional blocker for E-cadherin expression in metastatic tumor cells.

130 We showed that C3-induced reduction in E-cadherin expression in ovarian cancer cells was mediat

131 glycosylation causes an abnormal pattern of E-cadherin expression in the gastric mucosa.

132 ect of C3 on EMT and found that C3 decreased E-cadherin expression on cancer cells and promoted EMT.

133 yst breakdown and is accompanied by abnormal E-cadherin expression patterns.

134 lmonary acute respiratory distress syndrome, E-cadherin expression was similar in volume-controlled v

135 However, metastases often retain E-cadherin expression, an EMT is not required for metast

136 ing disrupted cell-cell contacts and reduced E-cadherin expression, and promotes sliding on the narro

137 R-675 processing from H19, promoted ZO-1 and E-cadherin expression, and restored the epithelial barri

138 MDA-MB-231 cells grew slower, had increased E-cadherin expression, and yielded fewer lung metastases

139 howed cytoskeletal abnormalities and reduced E-cadherin expression, indicating epithelial-mesenchymal

140 BC cells, kinase-active PTK6 also suppressed E-cadherin expression, promoted cell migration, and incr

141 nail1, a transcription factor that represses E-cadherin expression.

142 ease in N-cadherin and Zeb1, and decrease in E-cadherin expression.

143 a significant correlation between Notch4 and E-cadherin expression.

144 cription factors and significantly increased E-cadherin expression.

145 motes breast cancer progression via reducing E-cadherin expression.

146 epithelial phenotype with increased membrane E-cadherin expression.

147 nstream pathway resulting in upregulation of E-cadherin expression.

148 cell-cell adhesion by negative regulation of E-cadherin expression.

149 sured rates of trans binding between soluble E-cadherin extracellular domains, we conducted simulatio

150 We report the crystal structure of an E-cadherin extracellular fragment in complex with a pept

151 Binding to immobilized recombinant (r)E-cadherin-Fc of CD103 integrin expressed on tumor-speci

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

153 havior establish that Btbd7 promotes loss of E-cadherin from cell-cell adhesions with enhanced migrat

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

155 onstrate that the cell-cell adhesion protein E-cadherin functions as an instructive cue for cell divi

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

157 ir ability to transcriptionally activate the E-cadherin gene CDH1 in a promoter reporter assay as a m

158 ssociated germline missense mutations in the E-cadherin gene in patients with hereditary diffuse gast

159 the role that site-specific glycosylation of E-cadherin has in its defective function in gastric canc

160 acterized by an oncogenic transition from an E-cadherin-high nonmigratory state toward a ZEB1-high in

161 hesize that a transition in the stiffness of E-cadherin homotypic interactions regulates actin and me

162 Knockdown of E-cadherin, however, had no effect on HCV RNA replicatio

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

164 s sufficient to restore endogenous levels of E-cadherin in cancer cell lines exhibiting strong or int

165 These findings demonstrate a crucial role of E-cadherin in efficient DNA repair of UV-induced DNA dam

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

167 respiratory distress syndrome but preserved E-cadherin in lung tissue only in extrapulmonary acute r

168 Interference with the function of E-cadherin in macrophages disorganized the granulomas an

169 ropatterns; meanwhile, introducing exogenous E-cadherin in metastatic MDA-MB-231 cells increases the

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

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

172 ir of ultraviolet (UV)-induced DNA damage in E-cadherin-inhibited cells.

173 n expression, demonstrating that the type of E-cadherin inhibitor employed dictates the cellular phen

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

175 reted where it cleaves the tumour-suppressor E-cadherin interfering with gastric disease development,

176 E-cadherin is a cell adhesion molecule best known for it

177 E-cadherin is a central molecule in the process of gastr

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

179 Mechanistic studies demonstrated that E-cadherin is closely associated with claudin-1 (CLDN1)

180 It is generally regarded that E-cadherin is downregulated during tumorigenesis via Sna

181 d premalignant and malignant skin neoplasia, E-cadherin is downregulated in association with reduced

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

183 Our results show that E-cadherin is intensely expressed in germline cysts, and

184 ach, we determined that molecular tension on E-cadherin is lower than dsDNA unzipping force (nominal

185 While E-cadherin is not known to participate in cellular fusio

186 Here we reveal a novel mechanism that E-cadherin is post-transcriptionally regulated by Slug-p

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

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

189 functions as both a structural component of E-cadherin junctions and as a co-transcriptional activat

190 primordial follicle formation by regulating E-cadherin junctions between oocytes in mouse ovaries.

191 Mechanotransduction at E-cadherin junctions has been postulated to be mediated

192 beta-catenin concentration and stability of E-cadherin junctions in response to DPAGT1 inhibition.

193 oupling is propagated through the tissue via E-cadherin junctions, which in turn depend on tissue-wid

194 ERbeta2, ERbeta5, PR, AR, Bcl-2, HER2, p53, E-cadherin, Ki67, survivin, prolactin, FOXA1) for surviv

195 E-cadherin knockdown reversed Galpha13 siRNA-induced cel

196 and Wnt signaling, genes downregulated after E-cadherin knockdown, and genes related to increased ext

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

198 ced cleavage of desmoglein-2 (DSG-2) but not E-cadherin, leading to disruption of IEC intercellular a

199 R-221, which level inversely correlated with E-cadherin level in breast cancer cells, targeted E-cadh

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

201 EEF1A, an actin bundling protein, increases E-cadherin levels at junctions without a corresponding r

202 P10 or the Rho GTPase activator VAV2 reduces E-cadherin levels at junctions.

203 PTK6 downregulation restored E-cadherin levels via proteasome-dependent degradation o

204 thology and HDAC activity, and reduced renal E-cadherin levels.

205 While cell-cell E-cadherin ligandation reduced mitogenesis, this chemopr

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

207 Molecularly, E-cadherin localizes and tunes EGFR activity and junctio

208 PSGR-Pten(Delta/Delta) tumors exhibited E-cadherin loss and increased stromal androgen receptor

209 pair and suggest a mechanistic link of early E-cadherin loss in tumor initiation.

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

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

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

213 emulsion system to characterize the passive E-cadherin-mediated adhesion between droplets.

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

215 ion, Wnt/beta-catenin signaling pathway, and E-cadherin-mediated cell-cell adhesion plays pivotal rol

216 n in three-dimensional collagen and enhanced E-cadherin-mediated cell-cell adhesion.

217 to the basal extracellular matrix (ECM) and E-cadherin-mediated cell-cell adhesions on the orthogona

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

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

220 on, and second, to a downstream reduction in E-cadherin-mediated inter-SC adhesion.

221 PIIY domain has a separate role in Rho1- and E-cadherin-mediated polarization at the initiation stage

222 In addition, an E-cadherin monoclonal antibody effectively blocked HCV e

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

224 herin level in breast cancer cells, targeted E-cadherin mRNA open reading frame (ORF) and suppressed

225 tic breast cancer cells after overexpressing E-cadherin mRNA.

226 Consistent with destabilization of E-cadherin, NCX1 knockdown cells showed an increase in b

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

228 wild-type astrocytes were mesenchymal (i.e. E-cadherin negative and highly motile).

229 Here we show that mESCs treated with the E-cadherin neutralising antibody DECMA-1 or the E-cadher

230 to cell death by chemotherapeutic drugs but E-cadherin null cells or those expressing E-cadherin onl

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

232 hermore, ATAD3A-mediated suppression of CDH1/E-cadherin occurs through its regulation of GRP78-mediat

233 s by confining the movement of bilayer-bound E-cadherin on nanopatterned substrates reduced the level

234 ut E-cadherin null cells or those expressing E-cadherin only in the cytoplasm were sensitive to death

235 n of genes involved in structural integrity (E-cadherin, P-cadherin and beta-catenin) and function (a

236 Our findings indicate that E-cadherin plays a key role in sensing polarized tensile

237 various hepatic cell lines, indicating that E-cadherin plays an important regulatory role in CLDN1/O

238 ghtly adherent, less motile, and epithelial (E)-cadherin positive), whereas wild-type astrocytes were

239 ng GnT-V, resulted in a protective effect on E-cadherin, precluding its functional dysregulation and

240 These results indicate that E-cadherin presented in the proper 3D context constitute

241 association of acetylated H3 and H4 with the E-cadherin promoter in kidneys from AT-, relative to EZT

242 s increased binding of CUX1 to Snail and the E-cadherin promoter in mesenchymal cells compared to epi

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

244 Here we show that E-cadherin promotes nucleotide excision repair through p

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

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

247 mRNA open reading frame (ORF) and suppressed E-cadherin protein expression.

248 nism cannot explain the failure of producing E-cadherin protein in metastatic breast cancer cells aft

249 rin and demonstrate that complete absence of E-cadherin protein is likely required for hierarchical s

250 in breast cancer cells induced or decreased E-cadherin protein level, leading to suppressing or prom

251 overexpression was associated with decreased E-cadherin protein levels; increased expression of SNAIL

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

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

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

255 hese data demonstrate the role of a paRNA in E-cadherin regulation and the impact of a noncoding gene

256 via proteasome-dependent degradation of the E-cadherin repressor SNAIL.

257 junction protein ZO-1 and adherens junction E-cadherin, resulting in the dysfunction of the epitheli

258 ive image analysis, we track the behavior of E-cadherin-rich junction clusters, demonstrating that in

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

260 pulmonary E-cadherin expression and soluble E-cadherin shedding compared with WT mice.

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

262 E-cadherin silencing significantly inhibited HCV infecti

263 R1), connective tissue growth factor (CTGF), E-cadherin, SRY-box 7 (SOX7), and NFAT (nuclear factor o

264 E-cadherin stability depends on F-actin, but the mechani

265 in HF development, including failure of the E-cadherin suppression required for follicle down-growth

266 Profiling the predicted E-cadherin-targeting miRNAs in breast cancer tissues and

267 e show that p100 amotL2 forms a complex with E-cadherin that associates with radial actin filaments c

268 An activating monoclonal antibody to E-cadherin that induces a high adhesive state significan

269 iously unappreciated host factors, including E-cadherin, that mediate HCV entry.

270 ectin, and Twist1, and lowered expression of E-cadherin, thereby facilitating epithelial-mesenchymal

271 data indicate that a dynamic interplay among E-cadherin, tight junctions, and EMT exists and mediates

272 with Rho kinase to promote the transport of E-cadherin to adherens junctions and myotactin to hemide

273 eting alphaE-catenin, which indirectly links E-cadherin to F-actin, did not decrease L. monocytogenes

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

275 Cadherin subtype switching from E-cadherin to N-cadherin is associated with the epitheli

276 icroscopy, we demonstrated redistribution of E-cadherin to plasma membrane in colon cancer cells tran

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

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

279 ic and adult tissues by direct repression of E-cadherin transcription.

280 during tumorigenesis via Snail/Slug-mediated E-cadherin transcriptional reduction.

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

282 ermined that the molecular mechanism is that E-cadherin triggers expression of the miRs in pre-EMT ce

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

284 At heterotypic contacts with E-cadherin, unbound N-cadherin induces an asymmetric acc

285 SNAIL downregulation and E-cadherin upregulation mediated by PTK6 inhibition indu

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

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

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

289 However, E-cadherin was found to be downregulated.

290 Surprisingly, E-cadherin was not spontaneously expressed by these cell

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

292 s junction (AJ) components, beta-catenin and E-cadherin, was increased, and electron micrographs reve

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

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

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 nockdown specifically diminished adhesion to E-cadherin without altering adhesion to fibronectin matr

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

300 concentrations of vitamin D receptor (VDR), E-cadherin, zonula occluden 1 (ZO-1), occludin, claudin-