This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Chen, J.-J. Articles by Scully, R. Search for Related Content PubMed PubMed Citation Articles by Chen, J.-J. Articles by Scully, R.

BRCA1, BRCA2, and Rad51 Operate in a Common DNA Damage Response Pathway¹

The Dana-Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts 02115

² To whom requests for reprints should be addressed, at The Dana-Farber Cancer Institute, 44 Binney Street, Boston, MA 02115.

The two major hereditary breast cancer susceptibility genes, BRCA1 and BRCA2, are associated with early-onset breast and/or ovarian cancer and encode products that each interact with the product of the eukaryotic RecA homologue, hRad51. We have recently found that BRCA1 and BRCA2 coexist in a common biochemical complex. The two proteins also colocalize in subnuclear foci in somatic cells as well as on the axial elements of developing synaptonemal complexes in meiotic cells. Thus, BRCA1 and BRCA2 participate in a common DNA damage response pathway associated with the activation of homologous recombination and double-strand break repair. Dysfunction of this pathway may be a general phenomenon in the majority of cases of hereditary breast and/or ovarian cancer. The BRCA1/BRCA2 complex may function in postreplicational repair processes activated during the DNA synthesis stage of the cell cycle.

¹ Presented at the "General Motors Cancer Research Foundation Twentieth Annual Scientific Conference: Developmental Biology and Cancer," June 9–10, 1998, Bethesda, MD.

Received 2/ 5/99. Accepted 2/ 8/99.

This article has been cited by other articles:

				O. S. Gildemeister, J. M. Sage, and K. L. Knight Cellular Redistribution of Rad51 in Response to DNA Damage: NOVEL ROLE FOR Rad51C J. Biol. Chem., November 13, 2009; 284(46): 31945 - 31952. [Abstract] [Full Text] [PDF]

				S.E. TSUTAKAWA and P.K. COOPER Transcription-coupled Repair of Oxidative DNA Damage in Human Cells: Mechanisms and Consequences Cold Spring Harb Symp Quant Biol, January 1, 2000; 65(0): 201 - 216. [Abstract] [PDF]

				X. WU, G. RATHBUN, W.S. LANE, D.T. WEAVER, and D.M. LIVINGSTON Interactions of the Nijmegen Breakage Syndrome Protein with ATM and BRCA1 Cold Spring Harb Symp Quant Biol, January 1, 2000; 65(0): 535 - 546. [Abstract] [PDF]