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BH3-only proteins — evolutionarily conserved proapoptotic Bcl-2 family members essential for initiating programmed cell death

The Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia

View larger version (34K): [in a new window]   Fig. 1. Alignment of the BH3 domains of the proapoptotic Bcl-2 family members from mouse and C. elegans. Identical (red) and conserved (pink) amino acids are highlighted.

View larger version (24K): [in a new window]   Fig. 2. BH3-only proteins act as damage sensors in the cell. Specific insults cause the activation of specific BH3-only proteins, which then translocate, bind to and inactivate Bcl-2-like pro-survival proteins.

View larger version (17K): [in a new window]   Fig. 3. Proposed model for caspase activation: (1) Bcl-2 prevents Bax/Bak aggregation, probably indirectly; (2) BH3-only proteins inactivate Bcl-2-like molecules; (3) Bax/Bak aggregation either allows cytochrome c release by forming pores in the outer mitochondrial membrane or provides a platform for initiator caspase (X) activation through an unidentified Ced-4-like adapter (X).