Summary: Depending on their tissue of origin, the cells of caspase-2-deficient mice can be either more or less resistant to apoptosis induction than their wild-type counterparts. This would seem to imply that caspase-2 plays more the role of an apoptosis regulator than initiator. This role may be played in part via expression of the splicing isoforms caspase-2L (proapoptotic) and caspase-2S (anti-apoptotic). A possible exception, although perhaps one that proves the rule, is Salmonella-induced macrophage apoptosis, where caspase-2 may be acting with caspase-1 as a co-initiator. Research indicates that caspase-2L promotes apoptosis by causing release of proapoptotic mitochondrial proteins such as cytochrome c and Smac. Possible mechanisms include cleavage of Bid, direct, Bid-independent, action on the mitochondria and release of an unidentified nuclear factor. The Caspase-2 Assay Kit for Drug Discovery is a complete assay system designed to measure protease activity of caspase-2. Caspase-2 is un
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