Embryonic lethality and radiation hypersensitivity mediated by Rad51 in mice lacking Brca2
- PMID: 9126738
- DOI: 10.1038/386804a0
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 DNA-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.
Comment in
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Cancer-susceptibility genes. Gatekeepers and caretakers.Nature. 1997 Apr 24;386(6627):761, 763. doi: 10.1038/386761a0. Nature. 1997. PMID: 9126728 No abstract available.
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