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1 pe along with decreased expression of E- and P-cadherin.
2 rparts also expressed all these mRNAs except P-cadherin.
3 regulate the expression of endogenous E- and P-cadherin.
4 m ZO-1, alpha-, beta-, and gamma-catenin and P-cadherin.
5 d in cells with high levels of junctional E-/P-cadherin.
6 ss E-cadherin, whereas the glomeruli express P-cadherin.
7 not dependent on the cell adhesion molecule P-cadherin.
8 ot restricted to E-cadherin but is shared by P-cadherin.
10 ligand ephrin-B1, and the classical cadherin P-cadherin, all directly interact with E-cadherin ectodo
11 Cs expressed transcripts of N-, VE-, E-, and P-cadherins, alpha-, beta-, gamma-, and p120-catenins, a
13 nvolved in structural integrity (E-cadherin, P-cadherin and beta-catenin) and function (aquaporin 1 a
18 a cause-effect relationship between loss of P-cadherin and suppression of the canonical Wnt signalin
19 This effect was mediated by up-regulation of P-cadherin and the beta-catenin downstream target fascin
20 46, and 50), one adherens junction protein (P-cadherin) and eight components of desmosomes (plakophi
21 with the closely related epithelial cadherin P-cadherin), and RPE cells with different levels of junc
22 ice deficient for both a classical cadherin, P-cadherin, and a desmosomal cadherin, desmoglein 3.
23 ssion of other cadherins such as N-cadherin, P-cadherin, and the mesenchymal cadherin-11 is actually
24 ecific and not shared by either protein with P-cadherin, another integral slit diaphragm protein.
27 his mechanical regulation is mediated by the P-cadherin/beta-PIX/Cdc42 axis; P-cadherin specifically
28 on reduced cell surface CDH1 and upregulated P-cadherin (CDH3) without affecting CDH2 expression.
29 galectin 3 (LGALS3), fibronectin 1 (FN1) and p-cadherin (CDH3), and cell proliferation (CRIP1, IGFBP3
31 zed to apical microvilli, whereas in high E-/P-cadherin cells, Na/K ATPase was on basolateral surface
33 educed KC Par3 function fosters a permissive P-cadherin-dependent niche for MC transformation, invasi
34 generating an allelic series of new compound P-cadherin/E-cadherin mouse mutations disrupting combine
35 meric proteins made of functional E-, N-, or P-cadherin ectodomains fused to the Fc fragment of immun
36 epidermal basal layer responded by elevating P-cadherin, enabling these cells to maintain adherens ju
37 In agreement, low epidermal PAR3 and high P-cadherin expression correlate with human melanoma prog
38 as to determine whether the degree of E- and P-cadherin expression in melanomas correlates with the i
39 let radiation significantly decreased E- and P-cadherin expression in the human epidermal melanocytes
40 ssion in the human epidermal melanocytes and P-cadherin expression in the WM 35 melanoma cell line (p
43 nalysis, we localized and quantitated E- and P-cadherin expression on melanoma cell lines derived fro
48 cal methods to demonstrate that trapping the P-cadherin extracellular region in an X-dimer adhesive c
50 adherins is selective since cell adhesion to P-cadherin-Fc through alphaEbeta7 requires >100-fold mor
55 ate," or "advanced disease." Melanoma E- and P-cadherin immunofluorescence, as quantified by fluoresc
56 g delivery monoclonal antibody CQY684, traps P-cadherin in an X-dimer conformation and strengthens th
59 clinical model for studying the functions of P-cadherin in human epithelial biology and pathology.
60 mbrane classical cadherin (E-cadherin and/or P-cadherin in squamous epithelial cells) linked to eithe
61 the early mouse embryo corresponds to Snail2/P-cadherin in the chick, but both Snail factors and Zeb2
62 elopment, we performed expression studies on P-cadherin in the mouse embryo, and demonstrated the pre
63 he expression of E-cadherin, N-cadherin, and P-cadherin in tissues obtained from radical prostatectom
65 interference to uncover new roles for E- and P-cadherins in epidermal sheet formation in vitro and ma
72 intact human organ in vitro, and shows that P-cadherin is needed for anagen maintenance by regulatin
74 human melanoma progression, whereas elevated P-cadherin levels are associated with reduced survival o
85 d demonstrated the predominant expression of P-cadherin not only in the hair follicle placode, but al
88 and that the expression patterns of p63 and P-cadherin overlap in the hair follicle placode and AER,
89 normal urothelium such as keratin 5 (KRT5), P-cadherin (P-Cad), and epidermal growth factor receptor
90 tly P-cadherin negative, but some tumors had P-cadherin-positive areas frequently located close to ej
92 rcinoma and aggressive sarcoma; however, how P-cadherin promotes tumor malignancy remains unknown.
93 of-function mutations in CDH3, which encodes P-cadherin, result in hypotrichosis with juvenile macula
94 sequence variation, peripheral clock genes, P-cadherin signaling, neuromediators, HGF, KIT ligand se
98 iated by the P-cadherin/beta-PIX/Cdc42 axis; P-cadherin specifically activates Cdc42 through beta-PIX
99 d biophysical approaches, we determined that P-cadherin specifically induces polarization and CCM thr
101 KC-specific Par3 loss up-regulates surface P-cadherin that is essential to promote MC proliferation
103 leavage of the cell-adhesion proteins N- and P-cadherin, thus decreasing their injury-related surface
105 in We also show that Snail2 and Zeb2 repress P-cadherin transcription in the primitive streak and the
106 X-dimer cytoplasmic region, which increases P-cadherin turnover and targets the cadherin-antibody co
111 streak stages where it is substituted for by P-cadherin We also show that Snail2 and Zeb2 repress P-c
112 sociated with BLBCs such as FOXC2, CXCL1 and p-cadherin were also repressed in a similar manner.
114 ressed the slit diaphragm-associated protein P-cadherin, zonula occludens-1, and nephrin, a change co