Apoptosis, or programmed cell death, is a well-documented phenomenon in many cellular systems.2 It plays a key role in tissue and organ development as well as in adult tissues during cell turnover. Apoptosis can be induced by a variety of internal and external stimuli including growth factor deprivation, cytokine treatment, antigen-receptor engagement, cell-cell interactions, irradiation and glucocorticoid treatment.3 Bcl- 2 and one of its homologues, Bcl-xL, protect cells from apoptosis4,5, while other homologues of Bcl-2 such as Bax, Bad and Bak have been shown to enhance apoptosis.6-9 Bcl-xL has been shown to block apoptosis which is induced by a variety of stimuli and, under certain conditions, offers greater protection against apoptosis than Bcl-2.10-14 In contrast, Bad and Bax inhibit the protective functions of Bcl-xL and Bcl-2, respectively. Although heterodimerization between Bcl-xL/Bad and Bcl-2/Bax was originally thought to be essential for the differential anti-apoptotic activity of Bcl-xL and Bcl-2,5,14 other results suggest that the formation of heterodimers may not be necessary for this death-repressing activity.16,17
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