Functional Interactions of Human Rad54 With the Rad51 Recombinase
Abstract
Chromosomal DNA breaks occur in cells during normal metabolism and are induced by continual exposure to harmful radiation and other environmental insults. Homologous recombination represents a major pathway for the elimination of these chromosomal breaks. As such, homologous recombination is indispensable for the maintenance of genome stability in all organisms. Importantly, emerging evidence implicates the homologous recombination machinery in the suppression of cancer formation. In fact, defective homologous recombination represents one of the most prominent phenotypes of hereditary breast cancer patients mutated for BRCA1 and BRCA2, and mutations in key recombination factors have been found in various other tumor types as well. This research project will use a variety of mechanistic approaches to decipher the functions of human Rad51 and human Rad54, key protein factors that mediate homologous recombination, specifically focusing on the role of these factors in DNA remodeling and the formation of DNA joints which facilitated the genetic exchange between recombining homologous chromosomes during the break repair reaction.
Document Details
- Document Type
- Technical Report
- Publication Date
- May 01, 2003
- Accession Number
- ADA417023
Entities
People
- Stephen J. Van Komen
Organizations
- University of Texas Health Science Center at San Antonio