@article{a414653586f54b7f94cbfd7d4a04ce16,
title = "Stable interaction between the products of the BRCA1 and BRCA2 tumor suppressor genes in mitotic and meiotic cells",
abstract = "BRCA1 and BRCA2 account for most cases of familial, early onset breast and/or ovarian cancer and encode products that each interact with hRAD51. Results presented here show that BRCA1 and BRCA2 coexist in a biochemical complex and colocalize in subnuclear foci in somatic cells and on the axial elements of developing synaptonemal complexes. Like BRCA1 and RAD51, BRCA2 relocates to PCNA+ replication sites following exposure of S phase cells to hydroxyurea or UV irradiation. Thus, BRCA1 and BRCA2 participate, together, in a pathway(s) associated with the activation of double-strand break repair and/or homologous recombination. Dysfunction of this pathway may be a general phenomenon in the majority of cases of hereditary breast and/or ovarian cancer.",
author = "Junjie Chen and Silver, {Daniel P.} and Deepika Walpita and Cantor, {Sharon B.} and Gazdar, {Adi F.} and Gail Tomlinson and Couch, {Fergus J.} and Weber, {Barbara L.} and Terry Ashley and Livingston, {David M.} and Ralph Scully",
note = "Funding Information: We are grateful to Matt Fred for his expert technical assistance, Dr. David Hill for his gift of the CAPAN-1 cell line, Dr. Robert L. Ochs for anti-PCNA AK sera, Dr. James A. DeCaprio and Jianmin Gan for their help in generating monoclonal antibodies, and Dr. Sean V. Tavtigian and Albert Wong for providing reagents. In addition, we are grateful to all of our laboratory and divisional colleagues for many helpful and stimulating conversations. J. C. was supported by NIH training grant. R. S. was supported by DOD IDEA award. This work was supported by grants from DOD IDEA award and the National Cancer Institute to D. M. L.",
year = "1998",
month = sep,
doi = "10.1016/S1097-2765(00)80276-2",
language = "English (US)",
volume = "2",
pages = "317--328",
journal = "Molecular cell",
issn = "1097-2765",
publisher = "Cell Press",
number = "3",
}