Bcl2 antagonist of cell death; BAD; Bcl-2-binding component 6; Bcl-2-like protein 8; Bcl2-L-8; Bcl-XL/Bcl-2-associated death promoter (BAD, BBC6, BCL2L8)

^[1]^[2]^[3]^[4]^[5]^[6]

Function

promotes apoptosis
competes for binding to Bcl-XL, Bcl-2 & Bcl-W, thus affecting the level of heterodimerization of these proteins with BAX.
can reverse death repressor activity of Bcl-XL, but not that of Bcl-2
appears to act as a link between growth factor receptor signaling & the apoptotic pathways
phosphorylated on one or more of Ser-75, Ser-99, Ser-118 & Ser-134 in response to survival stimuli, which blocks its pro-apoptotic activity
phosphorylation on Ser-99 or Ser-75 promotes heterodimerization with 14-3-3 proteins; this then facilitates phosphorylation at Ser-118, a site within the BH3 domain, leading to the release of Bcl-XL & the promotion of cell survival
Ser-99 is the major site of AKT/PKB phosphorylation, Ser-118 the major site of protein kinase A (CAPK) phosphorylation (putative)
phosphorylation at Ser-112 by raf1 kinase or ribosomal S6 kinase
forms heterodimers with the anti-apoptotic proteins, Bcl-XL, Bcl-2 & Bcl-W
also binds protein S100A10 (putative)
the Ser-75/Ser-99 phosphorylated form binds 14-3-3 proteins

intact BH3 motif is required by BIK, BID, BAK, BAD & BAX for their pro-apoptotic activity & for their interaction with anti-apoptotic members of the Bcl-2 family
belongs to the Bcl-2 family

expressed in a wide variety of tissues