Cells are hard-wired to undergo programmed cell death or apoptosis to literally shape the organism during development and maintain tissue homeostasis throughout the normal lifespan. BCL-2 family proteins participate in a web of pro-life and pro-death interactions that adjudicate cell fate in response to apop-totic stimuli. When a death sentence is rendered, one of the key executioner proteins named BAX is activated to form toxic mitochondrial pores that effectively lance the cell's power plants. Deciphering the explicit mechanism of BAX activation is fundamental to advancing our understanding of the mitochondrial death pathway and how the apoptotic machinery can be manipulated for therapeutic benefit in diseases of uncontrolled cell survival or premature cell death.
展开▼
