Functions of Human Rad51 and Other Recombination Factors in DNA Double-Strand Break Repair
Abstract
The genetic material of all cells is frequently damaged by both exogenous and endogenous factors. Cells have evolved distinct mechanisms to remove different types of DNA damage. Perhaps the most serious form of DNA damage is the double strand break, where both the DNA strands are broken. This type of DNA lesion, if left intact, can lead to cell death, chromosomal translocations, chromosome loss and cancer. The accurate repair of DNA double-strand breaks is mediated by a group of genes called the RAD52 epistasis group and proceeds by means of a recombinational mechanism. Interestingly, the tumor suppressors BRCA1 and BRCA2 have been shown to be important for this DNA repair pathway, underscoring the importance of dissecting the molecular basis of the human homologous recombination machinery. The human Rad51 protein is capable of catalyze homologous DNA pairing and strand exchange reaction. The reaction is stimulated by RPA and molecular mediators like the Rad51B-Rad51C complex. However, the importance of specific protein-protein interactions in the reaction is currently unknown. Here I describe initial studies that should contribute to defining the hierarchy of protein-protein interactions that control the functional integrity of the human recombination machinery.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jun 01, 2003
- Accession Number
- ADA417432
Entities
People
- Stefan Sigurdsson
Organizations
- University of Texas Health Science Center at San Antonio