Overview:

β-catenins are cytoplasmic proteins that are ubiquitously expressed. These proteins associate with E-cadherin at cellular junctions (1). β-catenin interacts with TCF and LEF transcription factors and is an essential member of the Wingless-Wnt signal transduction pathway. The adenomatous polyposis coli (APC) tumor-suppressor protein, together with Axin and GSK3β, form a Wnt-regulated signaling complex that mediates phosphorylation-dependent degradation of β-catenin by the proteasome. APC and Siah-1 mediate a novel β-catenin degradation pathway linking p53 activation to cell cycle control. Activating mutations in the human β-catenin gene have been found in human colon cancer and melanomas (2).

Gene Aliases:

CTNNB, FLJ25606

Genbank Number:

NM_001904

References:

1. Morin, P.J. et al: Activation of beta-catenin-Tcf signaling in colon cancer by mutations in beta-catenin or APC. Science 1997; 275(5307):1787-1790.

2. Liu, J. et al: Siah-1 mediates a novel beta-catenin degradation pathway linking p53 to the adenomatous polyposis coli protein. Mol. Cell. 2001;7(5):927-36.