Radiation enhances caspase 3 cleavage of rad51 in BRCA2-defective cells
Radiation enhances caspase 3 cleavage of rad51 in BRCA2-defective cells
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DOI：
10.1667/rr1129.1
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发表时间：
2008-05-01
影响因子：
3.4
通讯作者：
Holt, Jeffrey T.
中科院分区：
文献类型：
--
作者：
Brown, Erika T.;Robinson-Benion, Cheryl;Holt, Jeffrey T.
Brown, E. T., Robinson-Benion, C. and Holt, J. T. Radiation Enhances Caspase 3 Cleavage of Rad51 in BRCA2-Defective Cells. Radiat. Res. 169, 595-601 (2008).After DNA damage, caspases cleave and activate proteins involved in cell death by apoptosis but also cleave and inactivate proteins implicated in DNA repair. Here we report a rapid onset of Rad51 cleavage by caspase 3 in BRCA2-defective mouse and human cells. This rapid cleavage was reduced markedly by transfer of full-length human BRCA2 into BRCA2-defective mouse or human cells, which also blocked the association of caspase 3 and Rad51 proteins. Overall caspase 3 activity was increased in BRCA2-defective cells, but the time course was much slower than that for Rad51. cleavage. We further showed that caspase 3 cleavage of Rad51 resulted in a functional decrease in Rad51 strand exchange activity and that inhibition of caspase 3 activity increased Rad51 protein levels and Rad51 foci. These findings indicate that BRCA2 inhibits Rad51. cleavage and subsequent apoptosis. (c) 2008 by Radiation Research Society.
