Embryonic lethality and radiation hypersensitivity mediated by Rad51 in mice lacking Brca2

Shyam K. Sharan, Masami Morimatsu, Urs Albrecht, Dae-Sik Lim, Eva Regel, Christopher Dinh, Arthur Sands, Gregor Eichele, Paul Hasty and Allan Bradley
Additional contact information
Shyam K. Sharan: Baylor College of Medicine
Masami Morimatsu: Lexicon Genetics Inc.
Urs Albrecht: Baylor College of Medicine
Dae-Sik Lim: Lexicon Genetics Inc.
Eva Regel: Baylor College of Medicine
Christopher Dinh: Baylor College of Medicine
Arthur Sands: Lexicon Genetics Inc.
Gregor Eichele: Baylor College of Medicine
Paul Hasty: Lexicon Genetics Inc.
Allan Bradley: Baylor College of Medicine

Nature, 1997, vol. 386, issue 6627, 804-810

Abstract: Abstract Inherited mutations in the human BRCA2 gene cause about half of the cases of early-onset breast cancer. The embryonic expression pattern of the mouse Brca2 gene is now defined and an interaction identified of the Brca2 protein with the DMA-repair protein Rad51. Developmental arrest in Brca2-deficient embryos, their radiation sensitivity, and the association of Brca2 with Rad51 indicate that Brca2 may be an essential cofactor in the Rad51-dependent DNA repair of double-strand breaks, thereby explaining the tumour-suppressor function of Brca2.

Date: 1997
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DOI: 10.1038/386804a0

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