Embryonic lethality and radiation hypersensitivity mediated by Rad51 in mice lacking Brca2
Embryonic lethality and radiation hypersensitivity mediated by Rad51 in mice lacking Brca2
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DOI：
10.1038/386804a0
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发表时间：
1997-04-24
期刊：
影响因子：
64.8
通讯作者：
Bradley, A
中科院分区：
文献类型：
--
作者：
Sharan, SK;Morimatsu, M;Bradley, A
人类BRCA2基因的遗传突变导致大约一半的早发性乳腺癌病例。小鼠Brca2基因的胚胎表达模式现已确定，并确定了Brca2蛋白与DNA修复蛋白Rad51的相互作用。Brca2缺陷胚胎的发育停滞、辐射敏感性以及Brca2与Rad51的关联表明，Brca2可能是Rad51依赖的DNA修复双链断裂的重要辅因子，从而解释了Brca2的肿瘤抑制功能。
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.