ライフサイエンスコーパス: N-cadherin

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

2 cell remodeling which also depends on Cdh2 (N-cadherin).

3 MMP-7 promotes VSMC apoptosis by cleavage of N-cadherin.

4 e clustering of associated adhesion protein, N-cadherin.

5 disrupted the recruitment of beta-catenin to N-cadherin.

6 gnized because of functional compensation by N-cadherin.

7 or the coupling between actin and endogenous N-cadherin.

8 ied by a reduction in the levels of synaptic N-cadherin.

9 me as a direct transcriptional suppressor of N-cadherin.

10 silencing results in enhanced proteolysis of N-cadherin.

11 f Fbxo45 results in decreased proteolysis of N-cadherin.

12 in cells inhibited cell motility promoted by N-cadherin.

13 o SPRY motifs in the extracellular domain of N-cadherin.

14 or alterations in claudin-1, E-cadherin, and N-cadherin.

15 ngthened, limiting the migration of cells on N-cadherin.

16 results suggest that FGFRs are activated by N-Cadherin.

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

18 differentiation are reduced by knocking down N-cadherin, a manipulation expected to help destabilize

19 at a molecular level, but instead relies on N-cadherin, a type I cadherin whose elimination is requi

20 erin cytoplasmic domain or shRNA specific to N-cadherin abolished collective cell migration.

21 aves the extracellular domains of the E- and N-cadherin adherens junction proteins, that both E- and

22 on an optimum balance between FGFR-regulated N-cadherin adhesion and actin dynamics.

23 or (GEF) Trio as a critical component of the N-cadherin adhesion complex, which activates both Rac1 a

24 N-cadherin adhesion has been reported to enhance cancer

25 examine the mechano-responsive properties of N-cadherin adhesion sites in isolated VSMCs.

26 nstrate that a clutch-like mechanism between N-cadherin adhesions and the actin flow underlies the st

27 actin/myosin cytoskeleton and transcellular N-cadherin adhesions.

28 (10(-5) m) induced a significant increase of N-cadherin AJ density at 50 mmHg, whereas vasodilatation

29 bservations provide compelling evidence that N-cadherin AJs are sensitive to pressure and vasomotor a

30 The formation of N-cadherin AJs in the vessel wall depends on the intralu

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

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

33 significant decrease in density and size of N-cadherin AJs.

34 binding partners of beta-catenin, including N-cadherin, alpha-N-catenin, p120ctn and S-SCAM/Magi2.

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

36 We employed a panel of N-cadherin-alphaE-catenin fusion proteins to rebuild AJs

37 the level of nuclear beta-catenin, and that N-cadherin also dampens FGF activity and consequently st

38 unction proteins epithelial (E)- and neural (N)-cadherin and beta-catenin.

39 ons with relevant kinetic parameters modeled N-cadherin and actin turnover well, validating this mech

40 SVZ NPCs stimulates the interaction between N-cadherin and ADAM10.

41 ring RNA, caused a decrease in the levels of N-cadherin and an increase in the levels of E-cadherin.

42 D in the testis in which mis-localization of N-cadherin and beta-catenin was also detected at the BTB

43 ges in the localization of basal ES proteins N-cadherin and beta-catenin.

44 N-cadherin and connexin-43 in adherens junction and gap

45 gulation of E-cadherin and downregulation of N-cadherin and consequently inhibits cell migration and

46 we propose a positive feed-back loop between N-cadherin and FGFR at adhesion sites limiting N-cadheri

47 N-cadherin and GluA2-containing AMPARs are presorted to

48 To test the contribution of N-cadherin and HER2 in mammary tumor metastasis, we targ

49 N-cadherin and HER2/neu were found to be co-expressed in

50 ctivating beta-catenin signaling by cleaving N-cadherin and increasing beta-catenin nuclear transloca

51 mRNA and protein levels of metastasis marker N-cadherin and mesenchymal marker vimentin increased sig

52 osylation increases the molecular packing of N-cadherin and promotes the bone marrow homing of AML ce

53 eased E-cadherin and decreased expression of N-cadherin and snail transcription factor -2 ( SNAI2) (a

54 he upregulation of the EMT molecular markers N-cadherin and Snail, as well as the Wnt/beta-catenin ta

55 in and inhibited mesenchymal markers such as N-cadherin and snail-1.

56 thelial identity (with ectopic expression of N-cadherin and Sox2), actomyosin disorganisation, cell s

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

58 HAVDI adhesive motif from the EC1 domain of N-cadherin and the RGD adhesive motif from fibronectin.

59 pulated by clusters of the adhesion molecule N-cadherin and the VGSC NaV1.5.

60 expression of Scribble, ZO1, E-cadherin and N-cadherin and their mislocalization.

61 T by up-regulating E-cadherin and inhibiting N-cadherin and transcription factors Slug, and pluripote

62 , which undergo EMT during development, lose N-cadherin and upregulate Cadherin 6 (Cdh6) prior to EMT

63 evented the association of presenilin 1 with N-cadherin and VE-cadherin, thereby compromising pericyt

64 at MALAT1 knockdown significantly suppressed N-cadherin and Vimentin expression but induced E-cadheri

65 duced EMT in ESCC both in vivo and in vitro, N-cadherin and Vimentin expression was upregulated upon

66 sult of decreasing E-Cadherin and increasing N-Cadherin and vimentin expressions, higher clonogenicit

67 d with epithelial-to-mesenchymal transition, N-cadherin and Vimentin, were highly induced in these tM

68 n, which were associated with an increase in N-cadherin and Zeb1, and decrease in E-cadherin expressi

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

70 ated proteins such as vinculin, connexin 43, N-cadherin, and alpha-catenin showed no significant chan

71 We demonstrate that the classical cadherin, N-cadherin, and an atypical cadherin, Flamingo, act redu

72 normal organization of desmoplakin, plectin, N-cadherin, and connexin-43.

73 upregulation of matrix metalloproteinase 9, N-cadherin, and fibronectin expression with concomitant

74 irmed the differential kinetics of actin and N-cadherin, and further revealed a 20% actin population

75 including cell-surface proteins (E-cadherin, N-cadherin, and Integrins), cytoskeletal proteins (alpha

76 tly binds to and promotes internalization of N-cadherin, and N-cadherin/LLGL1 interaction is inhibite

77 cluding a decreased expression of cyclin D1, N-cadherin, and nuclear Bcl3, and an increased expressio

78 ssion of beta-catenin, Snail, Slug, Zeb1 and N-cadherin, and upregulated E-cadherin.

79 sion of the mesenchymal markers Snail, Slug, N-cadherin, and vimentin in the recipient cells, whereas

80 N-cadherin antagonism during regional chemotherapy has d

81 The vascular targeting actions of N-cadherin antagonism may not augment some regionally de

82 ografts after systemic administration of the N-cadherin antagonist, ADH-1, or saline.

83 e held together by threads labeled with anti-N-Cadherin antibodies.

84 ciprocal changes in the expression of E- and N-cadherins associated with EMT.

85 FGFR1 stabilises N-cadherin at the cell membrane through a pathway involv

86 cadherin and FGFR at adhesion sites limiting N-cadherin-based single-cell migration.

87 -like or filamentous junctions stabilized by N-cadherin, beta-catenin and p120-catenin, which undergo

88 Cs was associated with increased cytoplasmic N-cadherin-beta-catenin complex formation as well as enh

89 nd actin filament polarization depend on the N-cadherin-beta-catenin complex.

90 sal ES (ectoplasmic specialization) proteins N-cadherin/beta-catenin at stages IV-VII only.

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

92 affinity purification proteomics to identify N-cadherin-binding proteins.

93 We report that N-cadherin binds to PSD-95/SAP90/DLG/ZO-1 (PDZ) domain 2

94 At homotypic contacts, junctional N-cadherin bonds downregulate Myosin-II contractility.

95 ubstrates like amyloid precursor protein and N-cadherin, but not with its sheddases ADAM10 or BACE1 a

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

97 s' morphology and distinct markers including N-cadherin, c-Maf, Prox1, and alphaA-, alphaB-, and beta

98 xpression of different classes of cadherins (N-cadherin, cadherin 11, and protocadherin 19) results i

99 uses marked reduction of adhesion molecules (N-cadherin, cadherin6B, and alpha1-catenin) with a conco

100 ent layer through the redundant functions of N-Cadherin (CadN) and Semaphorin-1a (Sema-1a).

101 ween flowing actin filaments and immobilized N-cadherin/catenin complexes, translating into a local r

102 N-cadherin caused fibroblast growth factor receptor (FGF

103 Surprisingly, loss of N-Cadherin causes no primary targeting defects, but dest

104 sitioning, prevents FGFR degradation through N-Cadherin, causing Erk1/2 phosphorylation.

105 , HuR silencing was sufficient to upregulate N-cadherin (CDH2) and CD133 along with a migratory and m

106 this study, we examined the distribution of N-cadherin (Cdh2) during cardiac trabeculation in zebraf

107 he Polyoma Middle T mammary tumor model that N-cadherin (Cdh2) expression causes Slug (Snai2) upregul

108 ivated oncogenic K-ras(G12D) and deleted the N-cadherin (Cdh2) gene in the murine pancreas.

109 We demonstrated that deletion of N-cadherin (Cdh2) in either endothelial cells or pericyt

110 from their notochordal origin, and reside in N-cadherin (CDH2) positive cell clusters in vivo.

111 ession of E-cadherin (CDH1) and induction of N-cadherin (CDH2), and mesenchymal genes like vimentin (

112 exhibits a striking complementary pattern to N-cadherin (CDH2), marking the interface of the future s

113 N-Cadherin cell-autonomously binds FGFRs and inhibits FG

114 ly, overexpression of wild-type Akt3 in PyMT-N-cadherin cells inhibited cell motility promoted by N-c

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

116 c posttranslational modifications, regulates N-cadherin clustering and membrane density, which impact

117 n disrupts the formation and organization of N-cadherin clusters and significantly diminishes bone ma

118 at contacts between dendritic filopodia and N-cadherin-coated beads or micropatterns.

119 f pulling force ( approximately 1 nN) to the N-cadherin-coated beads via an atomic force microscope i

120 N-cadherin-coated beads were able to induce clustering o

121 AFM probes with an attached N-cadherin-coated microbead (5 mum) induced a progressiv

122 We cultured primary neurons on N-cadherin-coated micropatterned substrates, and imaged

123 Using optically manipulated N-cadherin-coated microspheres, we correlated this behav

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

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

126 The kinesin KIF5 powers GluA2/N-cadherin codelivery by using GRIP1 as a multilink inte

127 LPA exposure leads to the loss of N-cadherin concentrations at the apical endfeet, which c

128 Tumor cells that have ever expressed N-cadherin constituted the majority of metastases in lun

129 rescued by expression of a dominant negative N-cadherin construct competing for the coupling between

130 N-Cadherin controls both fast filopodial dynamics and gr

131 on, the transsynaptic cell adhesion molecule N-cadherin controls excitatory synapse function and stab

132 herin function by transfection of either the N-cadherin cytoplasmic domain or shRNA specific to N-cad

133 of rapamycin and expressed more keratin 14, N-Cadherin, DeltaNp63 and ABCG2, and less keratin 12, co

134 f the endothelium, in vitro This facilitates N-cadherin-dependent cancer cell-endothelium interaction

135 ing the internal retrograde actin flow in an N-cadherin-dependent fashion.

136 the N-cadherin extracellular domain but not N-cadherin-dependent homophilic cell-cell adhesion, sugg

137 Expression of other ID proteins like N-cadherin, desmoplakin, connexin-43, and ZO-1 was signi

138 We investigate the mechanism through which N-cadherin disruption alters the effectiveness of region

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

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

141 is precisely regulated by internalization of N-cadherin downstream of lysophosphatidic acid (LPA) rec

142 st cells, we show that the switch from E- to N-cadherin during EMT is essential for acquisition of CI

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

144 The biomarker pairs CD44/CD24, N-cadherin/E-cadherin, and CD74/CD59 stratified DCIS sam

145 ed a significant increase or decrease in the N-cadherin-EGFP clustering, respectively.

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

147 ted by insulin secretagogues and that E- and N-cadherin engagement promotes stimulated insulin secret

148 ions require the FGFR activity stimulated by N-cadherin engagement.

149 ated beads were able to induce clustering of N-cadherin-enhanced green fluorescent protein (EGFP) on

150 (5 mum) induced a progressive clustering of N-cadherin-enhanced green fluorescent protein (EGFP) on

151 oss-of-function approaches demonstrated that N-cadherin enhances the recruitment of SVZ NPCs into dem

152 variant 7 (ARV7) and the mesenchymal marker, N-cadherin, expressed on their CTCs.

153 Our results show that mesenchymal N-cadherin-expressing (Ncad+) cells and MCAs invade much

154 PFCs are marked by N-cadherin expression (NCAD(+)) and reside exclusively a

155 infected HPNCs facilitated changes in E- and N-cadherin expression and cell migration, reminiscent of

156 The modulation of N-cadherin expression had significant impact on migratio

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

158 ER2 in mammary tumor metastasis, we targeted N-cadherin expression in the mammary epithelium of the M

159 in Mmp20 ablated mice, high-level ameloblast N-cadherin expression persists during the maturation sta

160 n of tight junction proteins, E-cadherin and N-cadherin expression, and STAT3 phosphorylation in MLE-

161 uced MMP-2 and MMP-9 expression, and reduced N-cadherin expression, but increased E-cadherin levels.

162 model of germ-layer formation in which, upon N-cadherin expression, endodermal cells actively migrate

163 5 depletion results in dramatic reduction in N-cadherin expression, impaired neuronal differentiation

164 that TCF transcription may directly regulate N-cadherin expression.

165 opulation and reinstating the E-cadherin and N-Cadherin expression.

166 Remarkably, radial migration requires the N-cadherin extracellular domain but not N-cadherin-depen

167 These findings suggest N-cadherin/FGFR has a pivotal role in promoting metastas

168 xpression levels of EMT markers (E-cadherin, N-cadherin, fibronectin, vimentin, slug and snail) and s

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

170 N-cadherin formed punctate adherens junctions (AJ) along

171 junctions (AJs) in the endothelium, whereas N-cadherin forms heterotypic adhesion between endothelia

172 Perturbation of N-cadherin function by transfection of either the N-cadh

173 results demonstrate for the first time that N-cadherin functions as a growth suppressor in the conte

174 N-cadherin functions by increasing the rate of VE-cadher

175 in 6 (IL-6) that induced E-cadherin loss and N-cadherin gain and increased cell migration when added

176 Additionally, in vivo experiments using N-cadherin gain- and loss-of-function approaches demonst

177 uted to the nucleus; E-cadherin was lost and N-cadherin gained, with similar changes seen in VZV-infe

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

179 We propose that N-cadherin helps to propagate a stable neural identity t

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

181 To investigate the role of N-cadherin in mouse PanIN (mPanIN), we simultaneously ac

182 tion of beta-catenin accompanied the loss of N-cadherin in pancreatic ductal epithelial cells (PDEC).

183 t primary tumor cells activated vimentin and N-cadherin in situ, but only N-cadherin was activated an

184 promoted the recruitment of beta-catenin to N-cadherin in smooth muscle cells/tissues.

185 inished the interaction of beta-catenin with N-cadherin in smooth muscle.

186 ressed this question by studying the role of N-cadherin in the development of optimally wired neurite

187 Unexpectedly, loss of N-cadherin in the K-ras(G12D) model resulted in increase

188 ier function, as CRISPR-mediated knockout of N-cadherin in the mural cells led to loss of barrier fun

189 Here, we show that in vivo expression of N-cadherin in the PyMT mouse model, which enhances mamma

190 lopment of the mammalian neocortex depend on N-cadherin, including the radial migration of immature p

191 eterotypic contacts with E-cadherin, unbound N-cadherin induces an asymmetric accumulation of Myosin-

192 ng E-cadherin repression and fibronectin and N-cadherin induction.

193 n, suggest a physiological role for FGFR and N-Cadherin interaction in vivo and identify Reelin as an

194 N-cadherin interaction with Fbxo45 is significantly abro

195 in an evolving developmental context, HAVDI/N-cadherin interactions can alter stem cell perception o

196 eural progenitors lacking Lgl1 had decreased N-cadherin internalization and abnormal cell junctions,

197 icles in the combined delivery of AMPARs and N-cadherin into dendrites.

198 ry-based proteomic screen, we show here that N-cadherin is a novel interactor of Fbxo45.

199 adherin subtype switching from E-cadherin to N-cadherin is associated with the epithelial-to-mesenchy

200 After mediolateral cell division, N-cadherin is enriched in the post-cleavage furrow; then

201 N-cadherin is expressed at higher levels in lamina cells

202 We found that N-cadherin is expressed in human and mouse pancreatic in

203 We tested the hypothesis that N-cadherin is part of a novel mechanosensory mechanism i

204 The association of beta-catenin with N-cadherin is regulated by actin polymerization during c

205 ABSTRACT: N-cadherin is the major cell-cell adhesion molecule in v

206 strate that adhesion of beta-cells to E- and N-cadherins is regulated by insulin secretagogues and th

207 enic clusters tightly associated with Alcama/N-cadherin-labeled Muller glial radial processes.

208 Our studies using an N-cadherin lens-specific conditional knockout mouse, N-c

209 ling and that this contributes to upregulate N-cadherin levels on the surface of the endothelium, in

210 We further show that N-cadherin levels, regulated by neuronal-differentiation

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

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

213 promotes internalization of N-cadherin, and N-cadherin/LLGL1 interaction is inhibited by atypical pr

214 tins, E-cadherin) and mesenchymal (vimentin, N-cadherin) marker expression.

215 pithelial neoplasia (PanIN), suggesting that N-cadherin may also have a role in early-stage pancreati

216 N-cadherin-mediated adhesion to MSCs was associated with

217 Here we show that FGFR1 reduces N-cadherin-mediated cell migration.

218 in the direction of limb elongation via this N-cadherin-mediated coupling.

219 ipate either individually or collectively in N-cadherin-mediated development.

220 g molecular mechanisms by demonstrating that N-cadherin-mediated differential adhesion determines rel

221 esmoglein 2-mediated binding forces, whereas N-cadherin-mediated interactions were not affected.

222 the loss of Vangl2 decreased fast-diffusing N-cadherin membrane molecules and increased confined N-c

223 revealed a 20% actin population confined at N-cadherin micropatterns, contributing to local actin ac

224 s study, we functionalized HA hydrogels with N-cadherin mimetic peptides and evaluated their role in

225 ge formation in implants functionalized with N-cadherin mimetic peptides compared with controls.

226 sed N-cadherin shedding and increased intact N-cadherin molecules on the cell membrane.

227 d increased upon expression of a nonadhesive N-cadherin mutant, resulting in an inverse relationship

228 ockdown and overexpression of DIPA phenocopy N-cadherin mutations, an effect bearing functional ties

229 Genetic ablation of N-cadherin (N-cad KO) caused hyperproliferation, acceler

230 s excessive cleavage of the synaptic protein N-cadherin (N-CAD).

231 We show that the N-cadherin-NaV1.5 association is not random, that NaV1.5

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

233 rebuild AJs with specific actin linkages in N-cadherin-null cardiomyocytes.

234 actility and reveal an unprecedented role of N-cadherin on cell shapes and cell arrangements.

235 esenchymal cells, this reduction of membrane N-cadherin only triggers a partial mesenchymal phenotype

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

237 nase/Rac activities at the free end, and the N-cadherin-p120 catenin complex excludes integrin alpha5

238 Rac polarization depend specifically on the N-cadherin-p120 catenin complex, whereas myosin II light

239 N-cadherin potentiation of the FGFR stimulated extracell

240 ver, both TopoIIalpha and TCF4 ChIP with the N-cadherin promoter, which is a new discovery indicating

241 use quantitative image analysis to show that N-cadherin promotes neural differentiation independently

242 ed with increased MMP-7 activity and reduced N-cadherin protein levels in HAAA sections compared to H

243 or ADAM10 inhibits this pathway, preventing N-cadherin regulated NPC polarization and migration.

244 A switch from E- to N-cadherin regulates the transition from pluripotency to

245 on interface, as well as the crucial role of N-cadherin regulation for the involution and migration o

246 mechanism that controls the upregulation of N-cadherin remains unknown.

247 ants in CDH2 impair the adhesive activity of N-cadherin, resulting in a multisystemic developmental d

248 howed impaired interaction of cortactin with N-cadherin, resulting in loss of biomechanical stress-in

249 munofluorescence was performed for vimentin, N-cadherin, ROCK1, RhoA, ZEB1, and Snail.

250 Marimastat, which may result from decreased N-cadherin shedding and increased intact N-cadherin mole

251 Upon cleavage and activation of N-cadherin signaling by ADAM10, NPCs undergo cytoskeleta

252 found to be upregulated were members of the N-cadherin signaling pathway.

253 Our data revealed that EGFR-dependent N-cadherin signaling physically initiated by ADAM10 clea

254 , and EMT markers and transcription factors (N-cadherin, Slug, Snail and Zeb1), and upregulation of E

255 displayed enrichment in mesenchymal markers (N-cadherin, slug, snail, fibronectin) and cell invasiven

256 001) and elevated the expression of mRNA for N-cadherin, Snail, and GHRH GHRH antagonist reduced the

257 N-cadherin specifically interacts with Fbxo45 through tw

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

259 omplexes (e.g., occludin-ZO-1, CAR-ZO-1, and N-cadherin-ss-catenin), through a down-regulation of p-A

260 cell junction proteins (e.g., occluden-ZO-1, N-cadherin-ss-catenin).

261 Here, we show that the acquisition of N-cadherin stabilises neural identity by dampening anti-

262 In the context of ErbB2/Neu, N-cadherin stimulated carcinoma cell invasion, prolifera

263 ppocampal neurons on L1 substrate but not on N-cadherin substrate, thus implicating endosomal traffic

264 nd in both the strains display E-cadherin-to-N-cadherin switch, reduced expression of cellular senesc

265 epithelial-to-mesenchymal transition, E- to N-cadherin switching coincides with p120-3A to -1A alter

266 in canonical Wnt target gene expression and N-cadherin synaptic adhesion complexes, including reduce

267 N-cadherin-targeting agents may lead to differential eff

268 This migration depends on N-cadherin that, when imposed in ectodermal cells, is su

269 ing cancer-derived E-cadherin and osteogenic N-cadherin, the disruption of which abolishes niche-conf

270 y EMT markers, including vimentin, Twist and N-cadherin, the effect of TRPM7 silencing was specific f

271 that is required for pericyte cell survival; N-cadherin, the key adherens junction protein between en

272 quiescent and adhesive (via upregulation of N-cadherin) through glycolysis reduction; it also lowere

273 Moreover, FGFR1 stimulates the anchoring of N-cadherin to actin.

274 vasion and crosstalks with Eph signaling via N-cadherin to drive collective migration of the Schwann

275 tumor suppressor protein Lgl1 interacts with N-cadherin to stabilize apical junctions in brain stem c

276 in membrane molecules and increased confined N-cadherin trajectories.

277 adherens junction proteins, that both E- and N-cadherin transcripts are expressed at significantly hi

278 EMT markers assessed were Snail-1, Snail-2, N-cadherin, Twist and vimentin.

279 an abnormal proteolytic processing of L1 and N-cadherin, two ADAM10 substrates previously implicated

280 stsynaptic membranes, GluA2 physically binds N-cadherin, underlying spine growth and synaptic modulat

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

282 Notably, GluA2 and N-cadherin use different PDZ domains on GRIP1 to simulta

283 f AMPAR exocytosis affects delivery of GluA2/N-cadherin vesicles.

284 f EMT marker expression (Twist1, E-cadherin, N-cadherin, vimentin, and fibronectin) in PC cell lines,

285 l-to-mesenchymal transition (EMT) markers as N-cadherin, vimentin, and Slug, as well as metastasis-re

286 C cells reduced a cohort of molecules (ZEB1, N-cadherin, Vimentin, and/or Snail1) critical for epithe

287 g upregulation of the EMT markers FN, Snail, N-cadherin, vimentin, the matrix metalloprotease MMP2, a

288 Epcam) and repress the mesenchymal markers (N-cadherin, Vimentin, Twist2, and ZEB1).

289 ed vimentin and N-cadherin in situ, but only N-cadherin was activated and functionally required durin

290 el of bisecting GlcNAc on beta1-integrin and N-cadherin was increased in Fut8(-/-) MEFs.

291 ion (EMT) markers (Snail, Slug, vimentin and N-cadherin) were induced in human prostate, breast, lung

292 a gain of mesenchymal markers (vimentin and N-cadherin), whereas epithelial markers, such as E-cadhe

293 otein accumulation of connexin-43 (Cx43) and N-cadherin, whereas at later stages, apoptosis of sperma

294 to promote cleavage of the ADAM10 substrate N-cadherin, whereas Tspan14 was unique in reducing cleav

295 arcinoma cells, in particular PDGFR-beta and N-cadherin, which enabled EMT cells to be chemoattracted

296 diated by the recruitment of beta-catenin to N-cadherin, which may facilitate intercellular mechanotr

297 participation of the cell adhesion molecule N-cadherin, which starts to be expressed by NC cells as

298 s higher levels of SLUG, SNAIL, VIMENTIN and N-CADHERIN while show a lack of expression of E-CADHERIN

299 CDH2 encodes N-cadherin, whose essential roles in neural development

300 ehavior to a stronger mechanical coupling of N-cadherin with the actin cytoskeleton.

301 fect includes impaired binding in trans with N-cadherin-WT expressed on apposing cells.

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