ABSTRACT
Apoptosis or programmed cell death is a morphologically distinct form of cell death, highly conserved in multicellular organisms. It is characterised by a precisely orchestrated sequence of morphological changes which result in the engulfment of the dying cell by macrophages in the absence of inflammation. These changes include cell shrinkage, plasma membrane blebbing, chromatin condensation, nuclear segmentation and formation of apoptotic bodies. A variety of death signals including DNA damage, ionizing or UV radiation, cytotoxic agents, growth factor withdrawal, and cytokines can induce apoptosis. The cellular signalling pathways involved in controlling apoptosis remain poorly defined and little is known about the biochemical mechanisms underlying the dramatic changes that accompany cell death. The importance of proteases in the execution of apoptosis has become increasingly apparent, in particular the cysteine proteases of the interleukin 1β-converting enzyme (ICE)-like family (caspases) (Martin and Green, 1995; Kumar and Lavin, 1996; Cohen, 1997) and the serine proteases of the granzyme B family (Greenberg, 1996). A role for calpain (Squier and Cohen, 1996) and the proteasome has also been described (Grimm et al., 1996).
