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lüll Signal transduction mediated by Bid, a pro-death Bcl-2 family proteins, connects the death receptor and mitochondria apoptosis pathways Yin XMCell Res 2000[Sep]; 10 (3): 161-7Two major apoptosis pathways have been defined in mammalian cells, the Fas/TNF-R1 death receptor pathway and the mitochondria pathway. The Bcl-2 family proteins consist of both anti-apoptosis and pro-apoptosis members that regulate apoptosis, mainly by controlling the release of cytochrome c and other mitochondrial apoptotic events. However, death signals mediated by Fas/TNF-R1 receptors can usually activate caspases directly, bypassing the need for mitochondria and escaping the regulation by Bcl-2 family proteins. Bid is a novel pro-apoptosis Bcl-2 family protein that is activated by caspase 8 in response to Fas/TNF-R1 death receptor signals. Activated Bid is translocated to mitochondria and induces cytochrome c release, which in turn activates downstream caspases. Such a connection between the two apoptosis pathways could be important for induction of apoptosis in certain types of cells and responsible for the pathogenesis of a number of human diseases.|Animals[MESH]|Antigens, CD/*metabolism[MESH]|Apoptosis/*physiology[MESH]|BH3 Interacting Domain Death Agonist Protein[MESH]|Carrier Proteins/*metabolism[MESH]|Caspases/metabolism[MESH]|Hepatocytes/metabolism/ultrastructure[MESH]|Humans[MESH]|Liver Diseases/metabolism/pathology/physiopathology[MESH]|Mitochondria/*metabolism/ultrastructure[MESH]|Proto-Oncogene Proteins c-bcl-2/*metabolism[MESH]|Receptors, Tumor Necrosis Factor, Type I[MESH]|Receptors, Tumor Necrosis Factor/*metabolism[MESH]|Signal Transduction/*physiology[MESH]|Tumor Necrosis Factor-alpha/*metabolism[MESH]|fas Receptor/*metabolism[MESH] |