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Review
. 2002 Apr;109(8):987-91.
doi: 10.1172/JCI15429.

The cadherin-catenin adhesion system in signaling and cancer

Affiliations
Review

The cadherin-catenin adhesion system in signaling and cancer

Maralice Conacci-Sorrell et al. J Clin Invest. 2002 Apr.
No abstract available

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Figures

Figure 1
Figure 1
The dual role of β-catenin in cell adhesion and transcriptional activation. β-Catenin (β) and plakoglobin (Pg) bind to cadherin adhesion receptors, and via α-catenin (α) they associate with the actin cytoskeleton to form AJs. When the Wnt signaling pathway is inactive, free β-catenin is degraded by a complex including glycogen synthase kinase (GSK), adenomatous polyposis coli (APC), and Axin, which phosphorylate β-catenin (PP). This protein complex recruits β-TrCP, which, together with Skp1, Cul1, and the E1 and E2 ubiquitination components, mediates the ubiquitination of β-catenin (Ub) and directs it to degradation by the 26S proteasome. The binding of Wnt to Frizzled (Frz) receptors activates Wnt signaling, and disheveled (Dsh) inhibits β-catenin phosphorylation by GSK. This results in β-catenin accumulation in the nucleus, where it complexes with T cell factor (TCF) and transactivates target genes such as Cyclin D1 and Myc. Modified from ref. .

References

    1. Ben-Ze’ev A, Geiger B. Differential molecular interactions of β-catenin and plakoglobin in adhesion, signaling and cancer. Curr Opin Cell Biol. 1998;10:629–639. - PubMed
    1. Nagafuchi A. Molecular architecture of adherens junctions. Curr Opin Cell Biol. 2001;13:600–603. - PubMed
    1. Perl A, Wilgenbus P, Dahl U, Semb H, Christofori G. A causal role for E-cadherin in the transition from adenoma to carcinoma. Nature. 1998;392:190–193. - PubMed
    1. Vleminckx K, Vakaet L, Mareel M, Fiers W, van Roy F. Genetic manipulation of E-cadherin expression by epithelial tumor cells reveals an invasion suppressor role. Cell. 1991;66:107–119. - PubMed
    1. Hirohashi S. Inactivation of the E-cadherin-mediated cell adhesion system in human cancers. Am J Pathol. 1998;153:333–339. - PMC - PubMed

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