Potent inhibitor of cell death. Inhibits activation of caspases. Appears to regulate cell death by blocking the voltage-dependent anion channel (VDAC) by binding to it and preventing the release of the caspase activator, CYC1, from the mitochondrial membrane. Also acts as a regulator of G2 checkpoint and progression to cytokinesis during mitosis.
Isoform Bcl-X(L) also regulates presynaptic plasticity, including neurotransmitter release and recovery, number of axonal mitochondria as well as size and number of synaptic vesicle clusters. During synaptic stimulation, increases ATP availability from mitochondria through regulation of mitochondrial membrane ATP synthase F(1)F(0) activity and regulates endocytic vesicle retrieval in hippocampal neurons through association with DMN1L and stimulation of its GTPase activity in synaptic vesicles. May attenuate inflammation impairing NLRP1-inflammasome activation, hence CASP1 activation and IL1B release .
Isoform Bcl-X(S) promotes apoptosis.
Subcellular locations: Mitochondrion inner membrane, Mitochondrion outer membrane, Mitochondrion matrix, Cytoplasmic vesicle, Secretory vesicle, Synaptic vesicle membrane, Cytoplasm, Cytosol, Cytoplasm, Cytoskeleton, Microtubule organizing center, Centrosome, Nucleus membrane
After neuronal stimulation, translocates from cytosol to synaptic vesicle and mitochondrion membrane in a calmodulin-dependent manner (By similarity). Localizes to the centrosome when phosphorylated at Ser-49.
Bcl-X(S) is expressed at high levels in cells that undergo a high rate of turnover, such as developing lymphocytes. In contrast, Bcl-X(L) is found in tissues containing long-lived postmitotic cells, such as adult brain.