摘要：An increase of mitochondrial membrane permeability is one of the key events in apoptosis, since it leads to the release of mitochondrial apoptogenic factors, such as cytochrome c , into the cytoplasm that activate downstream target of apoptotic cell death. Bcl-2 family is one of the best-characterized proteins that directly regulate mitochondrial functions. A major role of the Bcl-2 family of proteins is to alter mitochondrial membrane permeability, thus controlling the release of caspase-activating cytochrome c . Recent reports describe about involvement of interesting apoptogenic regulators other than Bcl-2 family in regulation of mitochondrial function. Tumor necrosis factor receptor-associated protein 1 (TRAP1) is a member of the heat-shock family of mitochondrial proteins, and substantially homologous to members of the 90-kDa families of heat-shock proteins (HSP90). TRAP1 seems to have specific functions differ from those of other members of the HSP90 family. Downregulation of TRAP1 expression enhances the release of cytochrome c from mitochondria. Moreover, reactive oxygen species (ROS) are involved in the regulation of the TRAP1 expression, indicating that TRAP1 is a sensor that involved in ROS mediated regulation of apoptosis. Here, we describe the mechanisms underlying the regulation of mitochondrial functions during apoptosis by TRAP1.
