Skip Navigation
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Your Environment. Your Health.

Publication Detail

Title: Recombination mediator and Rad51 targeting activities of a human BRCA2 polypeptide.

Authors: San Filippo, Joseph; Chi, Peter; Sehorn, Michael G; Etchin, Julia; Krejci, Lumir; Sung, Patrick

Published In J Biol Chem, (2006 Apr 28)

Abstract: BRCA2 likely exerts its tumor suppressor function by enhancing the efficiency of the homology-directed repair of injured chromosomes. To help define the DNA repair role of BRCA2, we expressed and purified a polypeptide, BRC3/4-DBD, that harbors its BRC3 and BRC4 repeats and DNA binding domain. BRC3/4-DBD interacted with hRad51 and bound DNA with a distinct preference for single-stranded (ss) DNA. Importantly we demonstrated by biochemical means and electron microscopy that BRC3/4-DBD nucleates hRad51 onto ssDNA and acts as a recombination mediator in enabling hRad51 to utilize replication protein A-coated ssDNA as recombination substrate. These functions of BRC3/4-DBD required both the BRC repeats and the BRCA2 DNA binding domain. The results thus clarify the role of BRCA2 in Rad51-dependent DNA recombination and repair, and the experimental strategies described herein should be valuable for systematically deciphering this BRCA2 function.

PubMed ID: 16513631 Exiting the NIEHS site

MeSH Terms: BRCA2 Protein/genetics; BRCA2 Protein/metabolism*; DNA Damage; DNA Primers/chemistry; DNA Repair*; DNA, Single-Stranded/genetics; DNA, Single-Stranded/metabolism*; Humans; Peptide Fragments/genetics; Peptide Fragments/metabolism*; Rad51 Recombinase/genetics*; Rad51 Recombinase/metabolism; Recombination, Genetic*; Replication Protein A/metabolism

Back
to Top