Interactions Among BRCA1, BRCA2, and Components of the Recombination Machinery
Abstract
DNA double-strand breaks are induced by endogenous free radicals and environmental agents such as ionizing radiation. The repair of DNA double-strand breaks is important for preventing possible chromosomal fragmentation, translocations, and deletions induced by these breaks. The accurate repair of Dna double-strand breaks is mediated by a group of genes called the RAD52 epistasis group and proceeds via a recombinational mechanism. In mammals, the efficiency of recombinational DNA repair is modulated by the tumor suppressors BRCA1 and BRCA2, providing compelling evidence that this DNA repair pathway functions to suppress cancer formation. Importantly, recombinational DNA repair is also required for the removal of interstrand DNA crosslinks formed by bifunctional crosslinking agents, which are commonly used to treat various malignancies. Our research efforts are directed at establishing biochemical models for examining the functions of the various RAD52 group components and for delineating the mechanism of recombinational DNA repair. Recent studies in our laboratory have established an in vitro system for examining the recombinase activity of humas Rad51 and defining the role of various recombination factors in influencing this Rad51 activity.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jun 01, 2002
- Accession Number
- ADA407213
Entities
People
- Patrick M. Sung
Organizations
- University of Texas Health Science Center at San Antonio