| BCL2L11/Bod is a pro-apoptotic protein belonging to the BH3-only group of Bcl-2 family members including Bad, Bid, Bik, Hrk and Noxa that contain a BH3 domain but lack other conserved BH1 or BH2 domains (1,2). BCL2L11 induces apoptosis by binding to and antagonizing anti-apoptotic members of the Bcl-2 family. Interactions have been observed with Bcl-2, Bcl-xL, Mcl-1, Bcl-w, Bfl-1 and BHRF-1 (1,2). BCL2L11 functions in regulating apoptosis associated with thymocyte negative selection and following growth factor withdrawal, during which BCL2L11 expression is elevated (3-6). Three major isoforms of BCL2L11 are generated by alternative splicing: BCL2L11EL, BCL2L11L and BCL2L11S (1). The shortest form, BCL2L11S, is the most cytotoxic and is generally only transiently expressed during apoptosis. The BCL2L11EL and BCL2L11L isoforms may be sequestered to the dynein motor complex through an interaction with the dynein light chain and released from this complex during apoptosis (7). Apoptotic activity of these longer isoforms may be regulated by phosphorylation (8,9). Environmental stress triggers BCL2L11 phosphorylation by JNK and results in its dissociation from the dynein complex and increased apoptotic activity. |
