Apoptosis — the regulated destruction of a cell — is a complicated process. The decision to die cannot be taken lightly, and the activity of many genes influence a cell's likelihood of activating its self-destruction programme. Once the decision is taken, proper execution of the apoptotic programme requires the coordinated activation and execution of multiple subprogrammes. Here I review the basic components of the death machinery, describe how they interact to regulate apoptosis in a coordinated manner, and discuss the main pathways that are used to activate cell death.
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It is impossible to circumscribe the field of apoptosis in such a short review. I apologize to my many colleagues for having failed to cite their seminal papers and/or the critical results that clearly demonstrate their favourite model to be right. Many thanks to Y. Lazebnik for contributions to Box 3, and to Y.L., S. Lowe and members of the apoptosis community at Cold Spring Harbor Laboratory for many stimulating discussions. I dedicate this review to W. Hengartner on the occasion of his retirement from active mathematical duty.
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Hengartner, M. The biochemistry of apoptosis. Nature 407, 770–776 (2000). https://doi.org/10.1038/35037710
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