Mitosis and mitochondrial priming for apoptosis

被引:9
作者
Pedley, Robert [1 ]
Gilmore, Andrew P. [1 ]
机构
[1] Univ Manchester, Wellcome Trust Ctr Cell Matrix Res, Fac Life Sci, A-3034 Michael Smith Bldg,Oxford Rd, Manchester M13 9PT, Lancs, England
基金
英国惠康基金;
关键词
apoptosis; Bcl-2; proteins; mitochondrial priming; mitosis; BCL-2 PROTEIN FAMILY; CELL-CYCLE ENTRY; DNA-DAMAGE; BH3-ONLY PROTEINS; MITOTIC ARREST; BAX; PHOSPHORYLATION; DEATH; MCL-1; MYC;
D O I
10.1515/hsz-2016-0134
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Cell division is a period of danger for cells, as inaccurate segregation of chromosomes can lead to loss of cell viability or aneuploidy. In order to protect against these dangers, cells ultimately initiate mitochondrial apoptosis if they are unable to correctly exit mitosis. A number of important chemotherapeutics exploit this response to delayed mitotic exit, but despite this, the molecular mechanism of the apoptotic timer in mitosis has proved elusive. Some recent studies have now shed light on this, showing how passage through the cell cycle fine-tunes a cell's apoptotic sensitivity such that it can respond appropriately when errors arise.
引用
收藏
页码:595 / 605
页数:11
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