磷酸化BH3结构域凋亡诱导蛋白抗体

磷酸化BH3结构域凋亡诱导蛋白抗体 Background: Bid, a BH3 domain containing proapoptotic Bcl2 family member, is localized in the cytosolic fraction of cells as an inactive precursor. Its active form is generated upon proteolytic cleavage by caspase 8 in the Fas signaling pathway. Cleaved Bid translocates to mitochondria and releases its potent proapoptotic activity, which in turn induces cytochrome c release and mitochondrial damage. The cytochrome c releasing activity of Bid was antagonized by Bcl2. Mutation in the SH3 domain can diminish the cytochrome c releasing activity. In animal model studies, Bid deficient mice are found resistant to the lethal effects of death factor signals relayed through Fas. Also known as: Bid (phospho S65); p-Bid (phospho S65); BH3 interacting domain death agonist; p22 BID; BID;) BH3-interacting domain death agonist; AltName: BH3-interacting domain death agonist p15; BH3-interacting domain death agonist p13; p13 BID; BH3-interacting domain death agonist p11; p11 BID磷酸化BH3结构域凋亡诱导蛋白抗体