BH3结构域凋亡诱导蛋白抗体
2015-01-28 09:07
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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: Apoptic death agonist; Apoptotic death agonist; Apoptotic death agonist BID; BH3 interacting domain death agonist; BH3 interacting domain death agonist; BH3 interacting domain death agonist p11; BH3 interacting domain death agonist p13; BH3 interacting domain death agonist p15; BH3-interacting domain death agonist p11; BID; BID isoform ES(1b); BID isoform L(2); BID isoform Si6; BID_HUMAN; Desmocollin type 4; FP497; HGNC:1050; Human BID coding sequence; MGC15319; MGC42355; p11 BID; p13 BID; p15 BID; p22 BID.BH3结构域凋亡诱导蛋白抗体
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