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PubMed · 12655298

Caspase-2 redux.

C M Troy·M L Shelanski
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Abstract

It has been difficult to assign caspase-2 to the effector or initiator caspase groups. It bears sequence homology to initiators (caspase-9 and CED-3), but its cleavage specificity is closer to the effectors (caspase-3 and -7). Interest in caspase-2 was dampened by the lack of a dramatic phenotype in the caspase-2 null mouse. Studies have been inhibited by the lack of knowledge about its mechanism of activation and the lack of specific methods to assay its activity. Molecular studies have defined a unique role for caspase-2 in apoptosis initiated by beta-amyloid toxicity or by trophic factor deprivation. Recently, a role for caspase-2 as an upstream initiator of mitochondrial permeabilization has been proposed. Thus, while much remains to be deciphered about caspase-2, most critically the mode of activation, it is clear that caspase-2 plays critical and singular roles in the control of programmed cell death.

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Amyloid beta-PeptidesAnimalsApoptosisCaspase 2CaspasesCell Membrane PermeabilityGrowth SubstancesHumansMitochondriaNerve DegenerationSignal TransductionJournal ArticleResearch Support, Non-U.S. Gov'tResearch Support, U.S. Gov't, P.H.S.Review

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C M Troy, M L Shelanski. 2003. Caspase-2 redux.. https://doi.org/10.1038/sj.cdd.4401175

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