a proapoptotic member of the Bcl-2 family. Displaces Bax from binding to Bcl-2 and Bcl-xL, resulting in cell death. Survival factors such as IL-3 can inhibit the apoptotic activity of Bad inducing the phosphorylation of Bad by Akt and p90RSK. 14-3-3 proteins bind phosphorylated Bad, inhibiting its binding to Bcl-2 and Bcl-xL. Phosphorylation by mitochondria-anchored PKA in the BH3 domain can block the dimerization of Bad and Bcl-xL. Note: This description may include information from UniProtKB.
Molecular Function: caspase activator activity; lipid binding; phospholipid binding; protein binding; protein kinase binding
Biological Process: ADP metabolic process; apoptosis; ATP metabolic process; caspase activation; glucose homeostasis; negative regulation of cytolysis; pore complex biogenesis; positive regulation of apoptosis; positive regulation of autophagy; positive regulation of caspase activity; positive regulation of epithelial cell proliferation; positive regulation of glucokinase activity; positive regulation of insulin secretion; positive regulation of proteolysis; protein insertion into mitochondrial membrane during induction of apoptosis; regulation of mitochondrial membrane permeability
LTP: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.