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