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: Oncoprotein; Membrane protein, integral; Apoptosis; Autophagy
Molecular Function: identical protein binding; protein binding; protein homodimerization activity; protease binding; protein phosphatase 2A binding; protein heterodimerization activity; sequence-specific DNA binding; channel activity; ubiquitin protein ligase binding; BH3 domain binding; channel inhibitor activity; transcription factor binding
Biological Process: positive regulation of catalytic activity; focal adhesion formation; pigment granule organization and biogenesis; response to toxin; programmed cell death; ear development; female pregnancy; B cell receptor signaling pathway; negative regulation of myeloid cell apoptosis; negative regulation of ossification; regulation of transmembrane transporter activity; negative regulation of neuron apoptosis; response to drug; spleen development; positive regulation of neuron maturation; axon regeneration; cell aging; regulation of calcium ion transport; positive regulation of cell growth; DNA damage response, signal transduction resulting in induction of apoptosis; regulation of gene expression; negative regulation of osteoblast proliferation; negative regulation of apoptosis; negative regulation of autophagy; positive regulation of smooth muscle cell migration; positive regulation of skeletal muscle fiber development; negative regulation of cell migration; transmembrane transport; regulation of viral genome replication; mesenchymal cell development; CD8-positive, alpha-beta T cell lineage commitment; B cell lineage commitment; positive regulation of peptidyl-serine phosphorylation; humoral immune response; response to UV-B; peptidyl-serine phosphorylation; endoplasmic reticulum calcium ion homeostasis; homeostasis of number of cells within a tissue; ureteric bud branching; innate immune response; negative regulation of cell growth; response to nicotine; renal system process; protein polyubiquitination; response to glucocorticoid stimulus; T cell differentiation in the thymus; lymphoid progenitor cell differentiation; positive regulation of multicellular organism growth; glomerulus development; negative regulation of mitochondrial depolarization; post-embryonic development; cochlear nucleus development; cellular response to glucose starvation; regulation of mitochondrial membrane potential; positive regulation of B cell proliferation; T cell homeostasis; cell growth; defense response to virus; release of cytochrome c from mitochondria; regulation of protein homodimerization activity; actin filament organization; digestive tract morphogenesis; organ growth; induction of apoptosis via death domain receptors; gland morphogenesis; regulation of mitochondrial membrane permeability; regulation of nitrogen utilization; metanephros development; oocyte development; B cell proliferation; regulation of protein heterodimerization activity; behavioral fear response; melanin metabolic process; regulation of cell-matrix adhesion; apoptosis; negative regulation of retinal cell programmed cell death; regulation of protein stability; protein amino acid dephosphorylation; response to radiation; B cell homeostasis; ovarian follicle development; positive regulation of melanocyte differentiation; melanocyte differentiation; response to gamma radiation; negative regulation of cellular pH reduction; response to iron ion; ossification; hair follicle morphogenesis; thymus development; male gonad development; peptidyl-threonine phosphorylation; neuron apoptosis; axonogenesis; response to hydrogen peroxide; response to cytokine stimulus; response to DNA damage stimulus; induction of apoptosis by oxidative stress
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.