Overview:

BAD is a member of the BCL-2 family of proteins that are known to be regulators of programmed cell death. BAD is a pro-apoptotic protein that forms a heterodimer complex with BCL-xL and BCL-2 which reverses the prosurvival activity of these proteins (1). The proapoptotic activity of BAD is regulated through its phosphorylation and this inhibits the pro-apoptosis function of BAD. Protein kinases such as AKT, RAF and RSK1 can phosphorylate BAD and RSK1-induced phosphorylation of BAD at ser112 suppresses BAD-mediated apoptosis in neurons. BAD inhibits G(1) to S phase transition in MCF7 breast cancer cells and overexpression of BAD inhibits cell growth as well as cyclin D1 expression (2).

References:

1. Yang E, et al: Bad, a heterodimeric partner for Bcl-X(L) and Bcl-2, displaces Bax and promotes cell death. Cell 80: 285-291, 1995.

2. Fernando R, et al: Breast cancer cell proliferation is inhibited by BAD: regulation of cyclin D1. J Biol Chem. 2007 Sep 28;282(39):28864-73.