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Sci. Signal., 23 September 2008
Vol. 1, Issue 38, p. pe42
[DOI: 10.1126/scisignal.138pe42]

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Caspase-2: Vestigial Remnant or Master Regulator?

Carol M. Troy* and Elena M. Ribe

Columbia University College of Physicians and Surgeons, Departments of Pathology and Neurology, Taub Center for the Study of Alzheimer’s Disease and the Aging Brain, 630 West 168th Street, New York, NY 10032, USA.

Abstract: Caspase-2, the second mammalian caspase to be identified and the most evolutionarily conserved caspase, has eluded classification. The lack of a profound phenotype in the caspase-2–deficient mouse resulted in decreased interest in caspase-2 for many years. However, advances in the field, including the identification of a potential activation complex and the development of methods to detect active caspase-2, now illuminate our understanding of the function of this caspase. These studies suggest that caspase-2 induces death through two pathways. First, caspase-2 induces cell death independently of the mitochondrial pathway, in a manner similar to that of ced-3, a caspase in Caenorhabditis elegans. Second, caspase-2 also induces cell death upstream of the mitochondrial pathway. The choice of pathway may depend on the type of death stimulus. The placing of caspase-2 upstream and independent of mitochondrial dysfunction provides a potentially new therapeutic target for aberrant cell death.

* Corresponding author. E-mail: cmt2{at}columbia.edu

Citation: C. M. Troy, E. M. Ribe, Caspase-2: Vestigial Remnant or Master Regulator? Sci. Signal. 1, pe42 (2008).

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