a antiapoptotic member of the Bcl-2 family. Regulates cell death by controlling the mitochondrial membrane permeability. Inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF-1). Phosphorylation by JNKs may increase its antiapoptotic functions. Note: This description may include information from UniProtKB.
Protein type: Autophagy; Oncoprotein; Membrane protein, integral; Apoptosis
Molecular Function: BH3 domain binding; channel activity; channel inhibitor activity; identical protein binding; protease binding; protein binding; protein heterodimerization activity; protein homodimerization activity; sequence-specific DNA binding; ubiquitin protein ligase binding
Biological Process: apoptosis; B cell proliferation; B cell receptor signaling pathway; defense response to virus; DNA damage response, signal transduction resulting in induction of apoptosis; endoplasmic reticulum calcium ion homeostasis; humoral immune response; induction of apoptosis via death domain receptors; negative regulation of apoptosis; negative regulation of autophagy; negative regulation of cellular pH reduction; negative regulation of mitochondrial depolarization; negative regulation of neuron apoptosis; neuron apoptosis; positive regulation of B cell proliferation; positive regulation of cell growth; protein polyubiquitination; regulation of calcium ion transport; regulation of mitochondrial membrane permeability; regulation of mitochondrial membrane potential; regulation of protein heterodimerization activity; regulation of protein homodimerization activity; regulation of transmembrane transporter activity; release of cytochrome c from mitochondria; response to cytokine stimulus; response to DNA damage stimulus; response to drug; response to iron ion; response to nicotine; response to toxin
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.