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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.
9 Cs expressed transcripts of N-, VE-, E-, and P-cadherins, alpha-, beta-, gamma-, and p120-catenins, a
11 nvolved in structural integrity (E-cadherin, P-cadherin and beta-catenin) and function (aquaporin 1 a
16 a cause-effect relationship between loss of P-cadherin and suppression of the canonical Wnt signalin
17 This effect was mediated by up-regulation of P-cadherin and the beta-catenin downstream target fascin
18 46, and 50), one adherens junction protein (P-cadherin) and eight components of desmosomes (plakophi
19 with the closely related epithelial cadherin P-cadherin), and RPE cells with different levels of junc
20 ice deficient for both a classical cadherin, P-cadherin, and a desmosomal cadherin, desmoglein 3.
21 ssion of other cadherins such as N-cadherin, P-cadherin, and the mesenchymal cadherin-11 is actually
22 ecific and not shared by either protein with P-cadherin, another integral slit diaphragm protein.
24 his mechanical regulation is mediated by the P-cadherin/beta-PIX/Cdc42 axis; P-cadherin specifically
25 on reduced cell surface CDH1 and upregulated P-cadherin (CDH3) without affecting CDH2 expression.
26 galectin 3 (LGALS3), fibronectin 1 (FN1) and p-cadherin (CDH3), and cell proliferation (CRIP1, IGFBP3
28 zed to apical microvilli, whereas in high E-/P-cadherin cells, Na/K ATPase was on basolateral surface
30 educed KC Par3 function fosters a permissive P-cadherin-dependent niche for MC transformation, invasi
31 meric proteins made of functional E-, N-, or P-cadherin ectodomains fused to the Fc fragment of immun
32 epidermal basal layer responded by elevating P-cadherin, enabling these cells to maintain adherens ju
33 In agreement, low epidermal PAR3 and high P-cadherin expression correlate with human melanoma prog
34 as to determine whether the degree of E- and P-cadherin expression in melanomas correlates with the i
35 let radiation significantly decreased E- and P-cadherin expression in the human epidermal melanocytes
36 ssion in the human epidermal melanocytes and P-cadherin expression in the WM 35 melanoma cell line (p
39 nalysis, we localized and quantitated E- and P-cadherin expression on melanoma cell lines derived fro
44 adherins is selective since cell adhesion to P-cadherin-Fc through alphaEbeta7 requires >100-fold mor
49 ate," or "advanced disease." Melanoma E- and P-cadherin immunofluorescence, as quantified by fluoresc
52 clinical model for studying the functions of P-cadherin in human epithelial biology and pathology.
53 mbrane classical cadherin (E-cadherin and/or P-cadherin in squamous epithelial cells) linked to eithe
54 the early mouse embryo corresponds to Snail2/P-cadherin in the chick, but both Snail factors and Zeb2
55 elopment, we performed expression studies on P-cadherin in the mouse embryo, and demonstrated the pre
56 he expression of E-cadherin, N-cadherin, and P-cadherin in tissues obtained from radical prostatectom
58 interference to uncover new roles for E- and P-cadherins in epidermal sheet formation in vitro and ma
65 intact human organ in vitro, and shows that P-cadherin is needed for anagen maintenance by regulatin
67 human melanoma progression, whereas elevated P-cadherin levels are associated with reduced survival o
78 d demonstrated the predominant expression of P-cadherin not only in the hair follicle placode, but al
81 and that the expression patterns of p63 and P-cadherin overlap in the hair follicle placode and AER,
82 normal urothelium such as keratin 5 (KRT5), P-cadherin (P-Cad), and epidermal growth factor receptor
83 tly P-cadherin negative, but some tumors had P-cadherin-positive areas frequently located close to ej
85 rcinoma and aggressive sarcoma; however, how P-cadherin promotes tumor malignancy remains unknown.
86 of-function mutations in CDH3, which encodes P-cadherin, result in hypotrichosis with juvenile macula
90 iated by the P-cadherin/beta-PIX/Cdc42 axis; P-cadherin specifically activates Cdc42 through beta-PIX
91 d biophysical approaches, we determined that P-cadherin specifically induces polarization and CCM thr
93 KC-specific Par3 loss up-regulates surface P-cadherin that is essential to promote MC proliferation
96 in We also show that Snail2 and Zeb2 repress P-cadherin transcription in the primitive streak and the
101 streak stages where it is substituted for by P-cadherin We also show that Snail2 and Zeb2 repress P-c
102 sociated with BLBCs such as FOXC2, CXCL1 and p-cadherin were also repressed in a similar manner.
104 ressed the slit diaphragm-associated protein P-cadherin, zonula occludens-1, and nephrin, a change co
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