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• W2078651408 abstract "Abstract Cell death on extended mitotic arrest is considered arguably most critical for the efficacy of microtubule-targeting agents (MTAs) in anticancer therapy. While the molecular machinery controlling mitotic arrest on MTA treatment, the spindle assembly checkpoint (SAC), appears well defined, the molecular components executing cell death, as well as factors connecting both networks remain poorly understood. Here we conduct a mini screen exploring systematically the contribution of individual BCL2 family proteins at single cell resolution to death on extended mitotic arrest, and demonstrate that the mitotic phosphorylation of BCL2 and BCLX represent a priming event for apoptosis that is ultimately triggered by NOXA-dependent MCL1 degradation, enabling BIM-dependent cell death. Our findings provide a comprehensive model for the initiation of apoptosis in cells stalled in mitosis and provide a molecular basis for the increased efficacy of combinatorial treatment of cancer cells using MTAs and BH3 mimetics." @default.
• W2078651408 created "2016-06-24" @default.
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• W2078651408 date "2015-04-29" @default.
• W2078651408 modified "2023-10-01" @default.
• W2078651408 title "The NOXA–MCL1–BIM axis defines lifespan on extended mitotic arrest" @default.
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• W2078651408 doi "https://doi.org/10.1038/ncomms7891" @default.
• W2078651408 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4423218" @default.
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