Developing Strategies to Block Beta-Catenin Action in Signaling and Cell Adhesion during Carcinogenesis
Abstract
To understand abnormal cell behavior in cancer, we must understand normal cell behavior. We focus on Drosophila Armadillo (Arm) and its human homolog beta-catenin. Both are key players in two processes: 1) They are components of cell-cell adhesive junctions, and 2) they act in transduction of Wingless - (Wg)/Wnt cell-cell signals. Mutations in beta-catenin or its regulators are early steps in certain cancers. Our working hypotheses are: 1) Several protein partners compete to bind to the same site on Arm, and 2) The Arm:dTCF complex activates Wg-responsive genes; dTCF can represses the same genes. Our Aims are to understand: 1) how different partners interact with and compete with one another for binding Arm, and 2) how the Arm partner dTCF positively and negatively regulates Wg responsive genes.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jul 01, 1999
- Accession Number
- ADA384233
Entities
People
- Mark A. Peifer
Organizations
- University of North Carolina at Chapel Hill