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Bax-induced apoptotic cell death.

Apoptosis is an ordered cascade of enzymatic events that culminates in cell death and the cleavage of DNA into characteristic nucleosomal fragments. It is operative during embryonic development and, during adult life, plays a key role in various physiological processes, such as tissue remodeling and execution and regulation of the immune response. The consequences of inappropriate apoptotic responses are profound; for example, the failure of cells to initiate apoptosis in response to DNA damage has been implicated in the development and progression of cancer, whereas inappropriate activation of apoptosis is thought to be a contributing factor in Alzheimer's disease and Parkinson's disease. Rigorous signaling requirements and a complex network of inhibitory molecules maintain tight control of the apoptotic process, while permitting rapid and effective responses to diverse extracellular and intracellular signals. Growth-factor withdrawal, specific peptide hormones (e.g., tumor necrosis factor α, Fas ligand, and TRAIL), changes in intracellular or extracellular calcium, drugs (e.g., staurosporine and phorbol esters), DNA damage, and mitochondrial poisons can all induce apoptosis, with each of these triggers activating a different portion of the pathway. As our knowledge of the apoptotic cell death cascade increases, it is becoming apparent that the system is more complex than first thought. In a recent issue of PNAS, Khaled and colleagues (1) have addressed how cells might accomplish this fine-tuning of the apoptosis cascade by analyzing the regulation of the proapoptotic molecule Bax in response to the withdrawal of growth factors.