| First Author | Katagiri T | Year | 1998 |
| Journal | Genes Chromosomes Cancer | Volume | 21 |
| Issue | 3 | Pages | 217-22 |
| PubMed ID | 9523196 | Mgi Jnum | J:46082 |
| Mgi Id | MGI:1197110 | Citation | Katagiri T, et al. (1998) Multiple possible sites of BRCA2 interacting with DNA repair protein RAD51. Genes Chromosomes Cancer 21(3):217-22 |
| abstractText | To investigate the biological consequences of aberrant BRCA2 protein during mammary carcinogenesis, we attempted to identify proteins that normally interact with BRCA2. By using a yeast two-hybrid system with a hybrid protein that contained residues 639-1,508 of BRCA2 protein fused to the GAL4 DNA-binding domain, we isolated five independent cDNA clones that encoded parts of RAD51 protein, a human homolog of bacterial RecA. In vitro experiments using anti-RAD51 antibody confirmed interaction of BRCA2 with RAD51. The RAD51-binding region of BRCA2 detected in the present study was distinct from the region reported recently. Further studies using smaller portions of BRCA2 defined at least two additional RAD51-binding domains, residues 982- 1,066 and 1,139-1,266. Our results suggest that BRCA2 can interact with RAD51 through multiple sites of BRCA2 and that control of mitotic and meiotic recombination and/or of genomic integrity through binding to RAD51 may be a crucial mechanism by which BRCA2 suppresses abnormal proliferation of mammary cells. |
