Description
Protocol
Available protocols: ELISA+
Specificity / Sensitivity
The PathScan
Species Reactivity: Human, Mouse, Rat, Monkey
Background
DNA double-strand breaks (DSBs) are potentially hazardous lesions that can be induced by ionizing radiation (IR), radiomimetic chemicals, or DNA replication inhibitors. Cells sense and repair DSBs via two distinct but partly overlapping signaling pathways: nonhomologous end joining (NHEJ) and homologous recombination (HR). Research studies have shown that defects in both pathways are associated with human diseases, including cancer (reviewed in 1). DSBs that arise during S or G2 phase are repaired via homologous recombination, using the replicated sister chromatid as a repair template. Rad51 recombinase, a eukaryotic homolog of RecA, polymerizes and forms a filament along single-stranded DNA, mediating HR with the help of auxiliary proteins, including Rad54 and BRCA2 (reviewed in 2,3). BRCA2 binds Rad51 and targets it to single-stranded DNA, allowing it to displace replication protein A (RPA) (4). Five Rad51 paralogs exist in vertebrates (XRCC2, XRCC3, Rad51B, Rad51C, and Rad51D), and they all appear to be required for efficient HR (5). Researchers have found that mutations in the gene may be related to breast cancer risk (6). Some studies have implicated Rad51 as a potential marker for pancreatic cancer (7).
Alternate Names
BRCA1/BRCA2-containing complex, subunit 5; BRCC5; DNA repair protein RAD51 homolog 1; FANCR; hRAD51; HsRAD51; HsT16930; MRMV2; RAD51; RAD51 homolog (RecA homolog, E. coli) (S. cerevisiae); RAD51 homolog A; RAD51 homolog protein; RAD51 recombinase; RAD51A; RECA; RecA-like protein; RecA, E. coli, homolog of; recombination protein A
