S118 (BAD) Antibody – Rabbit

BAD: 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.

Protein type: Apoptosis

Chromosomal Location of Human Ortholog: 11q13.1

Cellular Component: mitochondrial outer membrane; mitochondrion; cytosol

Molecular Function: protein kinase B binding; protein binding; protein heterodimerization activity; phospholipid binding; caspase activator activity; lipid binding; protein kinase binding; protein phosphatase 2B binding

Biological Process: response to oleate; nerve growth factor receptor signaling pathway; positive regulation of apoptosis; positive regulation of proteolysis; apoptosis; response to glucocorticoid stimulus; positive regulation of caspase activity; glucose homeostasis; cellular process regulating host cell cycle in response to virus; response to estradiol stimulus; positive regulation of apoptosis by virus; response to glucose stimulus; pore complex biogenesis; positive regulation of autophagy; positive regulation of glucokinase activity; caspase activation; response to drug; epidermal growth factor receptor signaling pathway; release of cytochrome c from mitochondria; fibroblast growth factor receptor signaling pathway; phosphoinositide-mediated signaling; cytokine and chemokine mediated signaling pathway; suppression by virus of host apoptosis; ADP metabolic process; positive regulation of insulin secretion; response to testosterone stimulus; response to amino acid stimulus; ATP metabolic process; glucose catabolic process; response to ethanol; positive regulation of T cell differentiation; induction of apoptosis via death domain receptors; DNA damage response, signal transduction resulting in induction of apoptosis; response to hydrogen peroxide; innate immune response; positive regulation of B cell differentiation; regulation of mitochondrial membrane permeability; response to progesterone stimulus; response to calcium ion; positive regulation of epithelial cell proliferation