Greater than 95.0% as determined by: (a) Analysis by RP-HPLC. (b) Analysis by SDS-PAGE.
The BID gene encodes a protein that contains only the BH3 domain, one of the four characteristic domains of the Bcl-2 family. Unlike other Bcl-2 family members, BID lacks a C-terminal signal-anchor segment and is found in both cytosolic and membrane locations . The mouse BID gene is located on chromosome 6 and has several alternatively spliced transcript variants .
BID is a mediator of mitochondrial damage induced by caspase-8 (CASP8). Upon apoptotic signaling, CASP8 cleaves BID, and the COOH-terminal part translocates to the mitochondria. This translocation triggers the release of cytochrome c, leading to the activation of caspases and apoptosis .
BID interacts with other Bcl-2 family proteins, such as Bax, leading to the insertion of Bax into organelle membranes, primarily the outer mitochondrial membrane. This interaction is believed to induce the opening of the mitochondrial voltage-dependent anion channel (VDAC) or form an oligomeric pore, resulting in the release of pro-apoptotic factors .
BID acts as a direct activator of Bax, a role common to some pro-apoptotic Bcl-2 proteins containing only the BH3 domain. The anti-apoptotic Bcl-2 proteins, including Bcl-2 itself, can bind BID and inhibit its ability to activate Bax, thereby inhibiting apoptosis .
The expression of BID is upregulated by the tumor suppressor p53, and BID has been shown to be involved in p53-mediated apoptosis. The p53 protein is a transcription factor that regulates many downstream target genes, including BID, as part of the cell’s response to stress .