In the presence of an appropriate stimulus, accelerates programmed cell death by binding to, and antagonizing the anti- apoptotic action of BCL2 or its adenovirus homolog E1B 19k protein. Low micromolar levels of zinc ions inhibit the promotion of apoptosis. Interacts with BCL2A1. Homodimer. Formation of the homodimer is zinc-dependent. Forms heterodimers with BCL2, E1B 19k protein, and BCL2L1 isoform Bcl-X(L). Interacts with myxoma virus protein M11L. Expressed in a wide variety of tissues, with highest levels in the heart and skeletal muscle. Belongs to the Bcl-2 family. Note: This description may include information from UniProtKB.
Protein type: Apoptosis; Membrane protein, integral; Endoplasmic reticulum; Mitochondrial
Cellular Component: integral to mitochondrial outer membrane; mitochondrial outer membrane; mitochondrion; pore complex
Molecular Function: identical protein binding; protein binding; protein heterodimerization activity; protein homodimerization activity
Biological Process: cytolysis; DNA damage response, signal transduction resulting in induction of apoptosis; endoplasmic reticulum calcium ion homeostasis; establishment and/or maintenance of transmembrane electrochemical gradient; positive regulation of apoptosis; positive regulation of proteolysis; regulation of mitochondrial membrane permeability; regulation of mitochondrial membrane potential; regulation of protein heterodimerization activity; regulation of protein homodimerization activity; release of cytochrome c from mitochondria; unfolded protein response, activation of signaling protein activity
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.