Anti-BRCA2, clone BRCA2/2158

0.2 mg/ml in 1X PBS with 0.1 mg/ml BSA (US sourced), 0.05% sodium azide. In 1990, a breast cancer susceptibility gene designated BRCA1 was localized to chromosome 17q. Mutations within this gene are believed to account for approximately 45% of families with high incidence of breast cancer and at least 80% of families with increased incidence of both early-onset breast cancer and ovarian cancer. A second breast cancer susceptibility gene, BRCA2 (breast cancer 2, early onset), located on chromosome 13q13.1, also confers a high incidence of breast cancer but, unlike BRCA1, does not confer a substantially elevated risk of ovarian cancer. Both BRCA1 and BRCA2 play a role in the maintainance of genome stability, particularly in the homologous recombination pathway for double-strand DNA repair. BRCA2 is regarded as a tumor suppressor gene, tumors with BRCA2 mutations exhibit loss of heterozygosity (LOH) of the wildtype allele. The protein encoded by the BRCA2 gene contains multiple copies of a 70 amino acid motif called the BRC motif. These motifs effect binding to the Rad51 recombinase, which operates in DNA repair. Protein function: Involved in double-strand break repair and/or homologous recombination. Binds RAD51 and potentiates recombinational DNA repair by promoting assembly of RAD51 onto single-stranded DNA (ssDNA). Acts by targeting RAD51 to ssDNA over double-stranded DNA, enabling RAD51 to displace replication protein-A (RPA) from ssDNA and stabilizing RAD51- ssDNA filaments by blocking ATP hydrolysis. Part of a PALB2-scaffolded HR complex containing RAD51C and which is thought to play a role in DNA repair by HR. May participate in S phase checkpoint activation. Binds selectively to ssDNA, and to ssDNA in tailed duplexes and replication fork structures. May play a role in the extension step after strand invasion at replication-dependent DNA double-strand breaks, together with PALB2 is involved in both POLH localization at collapsed replication forks and DNA polymerization activity. In concert with NPM1, regulates centrosome duplication. Interacts with the TREX-2 complex (transcription and export complex 2) subunits PCID2 and SEM1, and is required to prevent R-loop-associated DNA damage and thus transcription-associated genomic instability. Silencing of BRCA2 promotes R-loop accumulation at actively transcribed genes in replicating and non-replicating cells, suggesting that BRCA2 mediates the control of R-loop associated genomic instability, independently of its known role in homologous recombination (PubMed:24896180). [The UniProt Consortium]