期刊
EMBO JOURNAL
卷 29, 期 14, 页码 2255-2257出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/emboj.2010.150
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资金
- NCI NIH HHS [K99 CA140948, K99 CA140948-01A1] Funding Source: Medline
- NIGMS NIH HHS [R01 GM080333] Funding Source: Medline
Microtubule poisons induce mitotic arrest that leads to apoptotic cell death if not resolved in a timely manner, but the mechanisms that directly link this cell cycle arrest to apoptosis have been elusive. In this issue of The EMBO Journal, Clarke and colleagues show thatMcl-1, an anti-apoptotic Bcl-2 family protein, is phosphorylated by the mitotic kinase CDK1/cyclin B1. This targets the protein for degradation by anaphase-promoting complex/cyclosome (APC/C)-mediated ubiquitination, in a manner such that only prolonged arrest allows sufficient Mcl-1 phosphorylation and degradation to trigger apoptosis. Thus, the APC/C, a major effector of the spindle assembly checkpoint (SAC), not only ensures cell cycle arrest upon spindle disruption, but promotes cell death when the duration of mitotic arrest is too long.
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