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. Note: This description may include information from UniProtKB.
Protein type: DNA repair, damage; Nuclear receptor co-regulator
Biological Process: positive regulation of transcription, DNA-dependent; cytokinesis; cell aging; positive regulation of mitotic cell cycle; DNA repair; inner cell mass cell proliferation; oocyte maturation; regulation of cytokinesis; negative regulation of mammary gland epithelial cell proliferation; response to UV-C; double-strand break repair via homologous recombination; DNA damage response, signal transduction by p53 class mediator resulting in transcription of p21 class mediator; male meiosis I; nucleotide-excision repair; double-strand break repair; response to gamma radiation; hemopoiesis; spermatogenesis; replication fork protection; brain development; centrosome duplication; DNA damage response, signal transduction by p53 class mediator resulting in induction of apoptosis; female gonad development; response to X-ray
Alt. Names/Synonyms: BRCA1/BRCA2-containing complex, subunit 2; BRCA2; BRCC2; breast and ovarian cancer susceptibility gene, early onset; breast cancer 2 tumor suppressor; breast cancer 2, early onset; breast cancer susceptibility protein BRCA2; Breast cancer type 2 susceptibility protein; BROVCA2; FACD; FAD; FAD1; FANCB; FANCD; FANCD1; Fanconi anemia group D1 protein; GLM3; PNCA2
SS: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.