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

Sharan, S. K.; Morimatsu, M.; Albrecht, U.; Lim, D. S.; Regel, E.; Dinh, C.; Sands, A.; Eichele, G.; Hasty, P.; Bradley, A.

doi:10.1038/386804a0

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

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Eichele, G.
Department of Molecular Embryology, Max Planck Institute for Experimental Endocrinology, Max Planck Society;

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http://www.nature.com/nature/journal/v386/n6627/pdf/386804a0.pdf
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Zitation

Sharan, S. K., Morimatsu, M., Albrecht, U., Lim, D. S., Regel, E., Dinh, C., et al. (1997). Embryonic lethality and radiation hypersensitivity mediated by Rad51 in mice lacking Brca2. Nature, 386(6627), 804-810. doi:10.1038/386804a0.

Zitierlink: https://hdl.handle.net/11858/00-001M-0000-0010-5059-F

Zusammenfassung

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.