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Caspase-2 redux

Authors :
Michael L. Shelanski
Carol M. Troy
Source :
Cell Death & Differentiation. 10:101-107
Publication Year :
2003
Publisher :
Springer Science and Business Media LLC, 2003.

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.

Details

ISSN :
14765403 and 13509047
Volume :
10
Database :
OpenAIRE
Journal :
Cell Death & Differentiation
Accession number :
edsair.doi.dedup.....4da09abf555dab55264772fcdf2b92c2
Full Text :
https://doi.org/10.1038/sj.cdd.4401175