2. Academic Validation
  3. Embryonic lethality and radiation hypersensitivity mediated by Rad51 in mice lacking Brca2

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

  • Nature. 1997 Apr 24;386(6627):804-10. doi: 10.1038/386804a0.
S K Sharan 1,  M Morimatsu,  U Albrecht,  D S Lim,  E Regel,  C Dinh,  A Sands,  G Eichele,  P Hasty,  A Bradley
Affiliations

Affiliation

  • 1 Howard Hughes Medical Institute, Baylor College of Medicine, Houston, Texas 77030, USA.
PMID: 9126738 DOI: 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 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.

Figures