ライフサイエンスコーパス: N-cadherin

1 euroglian) and synaptic proteins (Bruchpilot/N-Cadherin).

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

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

4 gnized because of functional compensation by N-cadherin.

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

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

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

8 silencing results in enhanced proteolysis of N-cadherin.

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

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

11 berrantly expressed E-cadherin while lacking N-cadherin.

12 well as the expression of integrin beta1 or N-cadherin.

13 o such effects were obtained for Notch or E-/N-cadherin.

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

15 ess 2 members of the cadherin family, VE and N-cadherin.

16 ndent manner, the dynamic pool of junctional N-cadherin.

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

18 hymal genes characteristic of EMT, including N-cadherin (3.3-fold), vimentin (2.1-fold), and fibronec

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

20 can phosphorylate the cytoplasmic domain of N-cadherin, a major component of adherens junctions, and

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

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

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

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

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

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

27 (10(-5) m) induced a significant increase of N-cadherin AJ density at 50 mmHg, whereas vasodilatation

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

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

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

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

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

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

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

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

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

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

38 found that biomechanical stress upregulated N-cadherin and beta-catenin in p47(phox)KO hearts but di

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

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

41 N-cadherin and catenins are present in DRMs; however, th

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

43 astically and that the dynamic expression of N-cadherin and E-cadherin demarcates sharp boundaries du

44 , Vangl2, alters the dynamic distribution of N-cadherin and E-cadherin in the cochlea and causes simi

45 ll population with low surface expression of N-cadherin and enhanced adipogenic ability supports this

46 invasive behavior of melanoma cells through N-cadherin and FAK.

47 F-beta induction of the mesenchymal markers, N-cadherin and fibronectin, thereby inhibiting the migra

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

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

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

51 sing mutant B-RAF we observed high levels of N-cadherin and low levels of E-cadherin.

52 al deletion of beta1-integrins, labeling for N-cadherin and neuroligins increases.

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

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

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

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

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

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

59 Our results reveal a close interplay between N-cadherin and the Wnt-beta-catenin pathway in protectin

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

61 in, leads to the reduction of E-cadherin and N-cadherin and to characteristic cochlear CE defects but

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

77 on of a key component of adherens junctions, N-cadherin, and promotes the detachment of differentiati

78 of NFAT3 target genes, Nkx2.5 and beta-MHC), N-cadherin, and smooth muscle actin.

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

80 ating E-Cadherin, and down-regulating Snail, N-Cadherin, and Vimentin.

81 N-cadherin antagonism during regional chemotherapy has d

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

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

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

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

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

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

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

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

90 Knockdown of Cx43 and N-cadherin, but not Zonula Occludens-1, accelerated cell

91 ls junctional localization and expression of N-cadherin by limiting p120-catenin availability and red

92 is due to decreased shedding of cell-surface N-cadherin by the ADAM family protease ADAM10/Kuzbanian.

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

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

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

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

97 N-cadherin caused fibroblast growth factor receptor (FGF

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

99 <0.05) than animals expressing two wild-type N-cadherin (Cdh2) alleles.

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

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

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

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

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

105 wild type testes showed strong expression of N-cadherin (CDH2) while expression was greatly reduced i

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

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

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

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

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

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

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

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

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

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

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

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

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

119 partly due to an aberrant regulation of the N-cadherin complex in the absence of alpha-catenin.

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

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

122 N-Cadherin controls both fast filopodial dynamics and gr

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

124 We hence conclude that N-cadherin couples with distinct effectors to polarize p

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

126 oreover, engraftment of wild-type cells into N-cadherin-deleted recipients was normal.

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

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

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

130 Lack of osteoblastic N-cadherin did not block the bone anabolic or the HSC ef

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

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

133 adherin (EC) domain segments from Drosophila N-cadherin (DN-cadherin), each including the predicted N

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

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

136 the intricate regulation of Akt isoforms by N-cadherin during metastasis.

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

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

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

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

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

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

143 (5 mum) induced a progressive clustering of N-cadherin-enhanced green fluorescent protein (EGFP) on

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

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

146 Remarkably, mice with reduced N-cadherin expression (that is, Ncad(-/+)) survived 25%

147 of GSK3beta signaling was found to suppress N-cadherin expression at the messenger RNA and protein l

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

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

150 ent inactivation of RB1 and parallel loss of N-cadherin expression in OS prompted us to ask whether t

151 In this study, we observed reduced N-cadherin expression in RB1(-/-) calvarial osteoblasts.

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

153 There is evidence suggesting that N-cadherin expression on osteoblast lineage cells regula

154 ingly, the acute loss of pRb does not affect N-cadherin expression or migration or confer adipogenic

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

156 N-cadherin expression was efficiently ablated in osteobl

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

158 5 depletion results in dramatic reduction in N-cadherin expression, impaired neuronal differentiation

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

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

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

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

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

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

165 Genetic suppression of N-cadherin function interferes with basal migration of r

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

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

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

169 in which deletion of Cdh2, the gene encoding N-cadherin, has been targeted to cells of the osteoblast

170 We conclude that VE and N-cadherin have both additive and divergent effects on E

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

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

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

174 These data support a critical role for N-cadherin in PDA and its potential prognostic value.

175 Similarly, exogenous expression of N-cadherin in PyMT or MCF-7 mammary tumor cells enhanced

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

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

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

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

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

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

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

183 N-cadherin interaction with Fbxo45 is significantly abro

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

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

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

187 N-cadherin is a cell-cell adhesion molecule that plays a

188 N-cadherin is a homotypic cell-cell adhesion receptor co

189 tissue development during embryogenesis, and N-cadherin is a key factor in mediating cell-cell intera

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

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

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

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

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

195 This report demonstrates that osteoblastic N-cadherin is not required for regulation of steady-stat

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

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

198 To determine whether osteoblastic N-cadherin is required for HSC regulation, we used a gen

199 ly, it is unknown whether microenvironmental N-cadherin is required for normal marrow microarchitectu

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

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

202 have found that the adhesion molecule Cdh2 (N-cadherin) is important for interactions between the ML

203 er, these data suggest that the formation of N-cadherin junctions promotes 3D cell migration of prost

204 ions, disabling Robo function in conditional N-cadherin knock-out mice results in a wild-type-like la

205 Furthermore, Connexin43 and N-cadherin knockdown led to profound effects on fibrobla

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

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

208 am1/Rac activity resulting in an increase in N-cadherin levels and a decrease in E-cadherin levels an

209 pre-secretory to the secretory stage, while N-cadherin levels are up-regulated.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

229 it coexists with adhesively competent mature N-cadherin (N-cad), generating a spectrum of adhesive st

230 els of COLXV suppresses endogenous levels of 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 postsynaptic cell adhesion proteins such as N-Cadherin, Nectin-1, and APP may explain the postsynapt

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 bodies, confirming the contribution of these N-cadherin peptides to chondrogenesis.

240 N-cadherin potentiation of the FGFR stimulated extracell

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

242 vidence for sorting of nonadhesive precursor N-cadherin (ProN) to the neuronal surface, where it coex

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

244 We found that the N-cadherin receptor plays an important role in MSC-media

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

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

247 nical stress where cortactin interacted with N-cadherin, resulting in adaptive cytoskeletal remodelin

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

249 efit is likely due to a cumulative effect of N-cadherin's role in different aspects of tumorigenesis

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

251 ay is disrupted, diminished ADAM10-dependent N-cadherin shedding leads to increased cell-cell adhesio

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

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

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

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

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

257 between Robo and the cell adhesion molecule, N-cadherin, sorts spinal commissural axons into appropri

258 ndrogenesis was abolished via treatment with N-cadherin-specific antibodies, confirming the contribut

259 N-cadherin specifically interacts with Fbxo45 through tw

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

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

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 altogether, these findings demonstrate that N-cadherin suppresses Akt3 to promote cell motility and

265 al transition highlighted by a T-cadherin to N-cadherin switch and enhanced mesenchymal features.

266 This E- to N-cadherin switch supports epithelial migration in other

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

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

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

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

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

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

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

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

275 Nodal signaling or the cell adhesion protein N-cadherin, the left and right sides of the developing e

276 TGF-beta1-induced expression of fibronectin, N-cadherin, thrombospondin, and the notch ligand jagged-

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

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

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

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

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

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

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

284 N-cadherin upregulation has been observed in many cancer

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

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

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

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

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

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

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

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 The distribution of N-cadherin, ZO-1, and F-actin was visualized by fluoresc

300 s we found a striking upregulation of dermal N-cadherin, Zonula Occludens-1 and the gap junction prot