Embryonic lethality and radiation hypersensitivity mediated by Rad51 in mice lacking Brca2
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.
- Publication:
-
Nature
- Pub Date:
- April 1997
- DOI:
- 10.1038/386804a0
- Bibcode:
- 1997Natur.386..804S