anti-Bid, mAb (21F10)

Bcl-2 (B-cell lymphoma 2) family govern mitochondrial outer membrane permeabilization (MOMP) and can be either pro-apoptotic (Bax, BAD, Bak, Bid and Bok) or anti-apoptotic (Bcl-2, Bcl-xL, and Bcl-w). Mitochondrial membrane permeabilization and subsequent release of apoptotic factors are key mechanisms during this process. The members of the Bcl-2 family share one or more of the four characteristic domains of homology entitled the Bcl-2 homology (BH) domains (named BH1, BH2, BH3 and BH4). Bid consists of only one Bcl-2 homology domain, BH3. Bid cleavage to tBid (truncated Bid) activates apoptotic pathway at the mitochondrial level. Cleavage of cytosolic Bid and subsequent mitochondrial translocation have been detected in neuronal cell death related to acute or chronic neurodegeneration. Pharmacological inhibition of Bid can be a promising therapeutic strategy in neurological diseases where programmed cell death is prominent. After Bid activation and mitochondrial translocation, the most prominent downstream mechanisms of Bid-dependent neuronal apoptosis involve disruption of mitochondrial membrane integrity and intracellular calcium homoeostasis and the release of pro-apoptotic mitochondrial factors such as cytochrome c. The major proteolytic product p15 BID allows the release of cytochrome c. Isoform 1, isoform 2 and isoform 4 induce ICE-like proteases and apoptosis. Isoform 3 does not induce apoptosis. Counters the protective effect of Bcl-2.