Figure 1.

Interplay of cellular stress signals with apoptosis pathways. Signaling via the death receptor pathway can be inhibited by downregulation or epigenetic silencing of death receptors (DRs) or upregulation of cFLIP by hyperoxia. In the mitochondrial pathway, Bcl-2 favors a prooxidant milieu that promotes survival, while the reduced form of cytochrome c is inhibited in its activity to trigger caspase activation via the apoptosome. At the postmitochondrial level, translation of XIAP and cIAP1 is sustained via an IRES-dependent mechanism even under cellular stress conditions. See text for more details.