Breast Cancer Susceptibility Protein 2 (BRCA2) Antibody – Rabbit Polyclonal

Inherited mutations in BRCA1 and this gene, BRCA2, confer increased lifetime risk of developing breast or ovarian cancer. Both BRCA1 and BRCA2 are involved in maintenance of genome stability, specifically the homologous recombination pathway for double-strand DNA repair. The BRCA2 protein contains several copies of a 70 aa motif called the BRC motif, and these motifs mediate binding to the RAD51 recombinase which functions in DNA repair. BRCA2 is considered a tumor suppressor gene, as tumors with BRCA2 mutations generally exhibit loss of heterozygosity (LOH) of the wild-type allele. [provided by RefSeq, Dec 2008]

BRCA2: involved in double-strand break repair and/or homologous recombination. May participate in S phase checkpoint activation. Interacts with RAD51 and DSS1. Interacts with ubiquitinated FANCD2. Interacts with PALB2, enables the recombinational repair and checkpoint functions. Interacts with WDR16. Defects in BRCA2 are a cause of genetic susceptibility to breast cancer and may underlie susceptibility to uveal melanoma.

Protein type: DNA repair, damage; Nuclear receptor co-regulator; Tumor suppressor

Chromosomal Location of Human Ortholog: 13q13.1

Cellular Component: BRCA2-MAGE-D1 complex; centrosome; cytosol; lateral element; nuclear chromosome, telomeric region; nucleoplasm; nucleus; protein complex; secretory granule

Molecular Function: gamma-tubulin binding; H3 histone acetyltransferase activity; H4 histone acetyltransferase activity; histone acetyltransferase activity; identical protein binding; protease binding; protein binding; protein C-terminus binding; single-stranded DNA binding

Biological Process: brain development; cell aging; centrosome duplication; cytokinesis; DNA damage response, signal transduction by p53 class mediator resulting in transcription of p21 class mediator; DNA synthesis involved in DNA repair; double-strand break repair; double-strand break repair via homologous recombination; female gonad development; hemopoiesis; inner cell mass cell proliferation; intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediator; male meiosis I; mitotic recombination-dependent replication fork processing; negative regulation of mammary gland epithelial cell proliferation; nucleotide-excision repair; oocyte maturation; positive regulation of mitotic cell cycle; positive regulation of transcription, DNA-templated; regulation of cytokinesis; replication fork protection; response to gamma radiation; response to UV-C; response to X-ray; spermatogenesis; strand displacement; telomere maintenance via recombination

Disease: Breast Cancer; Breast-ovarian Cancer, Familial, Susceptibility To, 2; Fanconi Anemia, Complementation Group D1; Glioma Susceptibility 3; Medulloblastoma; Pancreatic Cancer, Susceptibility To, 2; Prostate Cancer; Tracheoesophageal Fistula With Or Without Esophageal Atresia; Wilms Tumor 1