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Bax activation by Bim?Czabotar PE; Colman PM; Huang DCCell Death Differ 2009[Sep]; 16 (9): 1187-91The mechanism by which the cell death mediator Bax becomes activated to cause mitochondrial damage, a key step for the intrinsic pathway to apoptosis, remain highly contentious. Although some data support a role for certain BH3-only proteins, such as Bim or tBid, to directly activate Bax, others have led to the conclusion that BH3-only proteins act indirectly by antagonizing the prosurvival Bcl-2 proteins, thereby allowing Bax activation to proceed. A recent paper in Nature by Gavathiotis et al. provides the first biophysical evidence for a direct interaction between a BH3 domain, that of Bim, with Bax. Here, we review these intriguing observations and discuss their implications for our understanding of how the BH3-only proteins initiate apoptosis.|Apoptosis[MESH]|Apoptosis Regulatory Proteins/*metabolism[MESH]|Bcl-2-Like Protein 11[MESH]|Membrane Proteins/*metabolism[MESH]|Peptide Fragments/metabolism[MESH]|Protein Structure, Tertiary[MESH]|Proto-Oncogene Proteins c-bcl-2/metabolism[MESH]|Proto-Oncogene Proteins/*metabolism[MESH]|bcl-2-Associated X Protein/*metabolism[MESH] |
