Bid，a BH3 domain-containing proapoptotic Bcl-2 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 Bcl-2. Mutation in the SH3 domain can diminish the cytochrome c releasing activity. In the animal model studies，Bid-deficient mice are found resistant to the lethal effects of death factor signals relayed throμgh Fas.
应用类型
Western blot, Immunoprecipitation, Immunohistochemistry
免疫原
Synthetic peptide surrounding amino acid 37 of human Bid
