Journal
CELL CYCLE
Volume 9, Issue 11, Pages 2097-2101Publisher
TAYLOR & FRANCIS INC
DOI: 10.4161/cc.9.11.11840
Keywords
cell cycle checkpoint; DNA damage; Plk1; 53BP1; Chk2; mitosis
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Funding
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [P30ES002109] Funding Source: NIH RePORTER
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In order to maintain genetic integrity, cells are equipped with cell cycle checkpoints that detect DNA damage, orchestrate repair, and if necessary, eliminate severely damaged cells by inducing apoptotic cell death. The mitotic machinery is now emerging as an important determinant of the cellular responses to DNA damage where it functions as both the downstream target and the upstream regulator of the G(2)/M checkpoint. Cell cycle kinases and the DNA damage checkpoint kinases appear to reciprocally control each other. Specifically, cell cycle kinases control the inactivation of DNA damage checkpoint signaling. Termination of a DNA damage response by mitotic kinases appears to be an evolutionary conserved mechanism that allows resumption of cell cycle progression. Here we review recent reports in which molecular mechanisms underlying checkpoint silencing at the G(2)/M transition are elucidated.
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