What are the caspase-independent death effectors?
The mitochondria are central relaying stations for both caspase-dependent and caspase-independent death pathways (reviewed in Tsujimoto, 2003). Mitochondria respond to multiple death stimuli including those in which proapoptotic Bcl2 family proteins such as Bax/Bak induce mitochondrial membrane permeabilization and cause the release of apoptotic molecules (reviewed in Gross et al., 1999; Newmeyer and Ferguson-Miller, 2003) (Goping et al., 1998; Gross et al., 1998; Ruffolo et al., 2000). These proapoptotic molecules can also be released from the mitochondria independent of Bax/Bak by cellular perturbations that cause a sudden increase in intracellular calcium levels as seen following acute injuries such as myocardial infarction or stroke (reviewed in Weiss et al., 2003; Yu et al., 2003). Thus, multiple death stimuli with or without the involvement of the classical Bcl family proteins converge on the mitochondria to trigger the release of proapoptotic molecules to initiate the death casc
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