ABSTRACT
The realisation that apoptosis is a fundamental cellular process in development and morphogenesis (Kerr et al., 1974; Kerr et al., 1987; Kerr et al., 1972; Savill et al., 1993; Smith et al., 1989; Wyllie, 1980) and moreover, that its improper regulation impacts upon the initiation and progression of disease states(Savill et al., 1989; Williams, 1991), has led to the broadening of disease model systems under consideration for intervention at the level of the apoptotic programme. For example, it has become clear that several anti-cancer agents already in use are potent inducers of apoptosis (Dive and Hickman, 1991; Fisher, 1994). Many of the studies to identify those factors regulating apoptosis, have focussed upon identification of the signal transduction pathways involved in the regulation of cell proliferation, differentiation and apoptosis. More specifically, efforts have been concentrated on determining exactly how these pathways interact and how their disregulation leads to pathogenesis (Martin, 1982; Whitehouse et al., 1982; Grigg et al., 1991; Bursch et al., 1992; Groux et al., 1992; Kerr et al., 1994). One signalling element implicated in the regulation of cell proliferation, differentiation and apoptosis, and already a target for the design of novel therapeutic modalities, is protein kinase C (Gescher, 1992).
