Beta-Catenin Stability in Breast Cancer
Abstract
Beta-catenin is a multifunctional protein that participates in cadherin-mediated cell-cell adhesion and in transduction of the Wnt growth factor signal that regulates development. At elevated cytoplasmic levels, beta-catenin interacts with members of the LEF/TCF family of transcription factors and directly regulates gene expression. beta-catenin also binds the adenomatous polyposis coli protein (APC). The tumor suppressor function of APC is suggested to depend in part on its ability to bind beta-catenin and to facilitate beta-catenin degradation by an unknown mechanism. The general purpose of this study is to better understand regulation of beta-catenin, found aberrant in numerous cancers. We find that the cytoplasmic, signaling pool of beta-catenin is regulated at the level of protein stability by the ubiquitin- proteasome degradation pathway. Extending the studies to include APC, we find that the ubiquitination and proteasomal degradation of beta-catenin, and a serine kinase other than GSK-3 beta modulate the APC regulation of beta- catenin.
Document Details
- Document Type
- Technical Report
- Publication Date
- Sep 01, 1999
- Accession Number
- ADA375157
Entities
People
- Stephen W. Byers
- Vijay Baswaran
Organizations
- Georgetown University