Embryonic lethality and radiation hypersensitivity mediated by Rad51 in mice lacking Brca2
Open Access
- 24 April 1997
- journal article
- research article
- Published by Springer Nature in Nature
- Vol. 386 (6627), 804-810
- https://doi.org/10.1038/386804a0
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.Keywords
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