Involved in the activation cascade of caspases responsible for apoptosis execution. At the onset of apoptosis it proteolytically cleaves poly(ADP-ribose) polymerase (PARP) at a '216-Asp-|-Gly-217' bond. Cleaves and activates sterol regulatory element binding proteins (SREBPs) between the basic helix-loop- helix leucine zipper domain and the membrane attachment domain. Cleaves and activates caspase-6, -7 and -9. Involved in the cleavage of huntingtin. Triggers cell adhesion in sympathetic neurons through RET cleavage. Heterotetramer that consists of two anti-parallel arranged heterodimers, each one formed by a 17 kDa (p17) and a 12 kDa (p12) subunit. Interacts with BIRC6/bruce. Highly expressed in lung, spleen, heart, liver and kidney. Moderate levels in brain and skeletal muscle, and low in testis. Also found in many cell lines, highest expression in cells of the immune system. Inhibited by isatin sulfonamides. Belongs to the peptidase C14A family. Note: This description may include information from UniProtKB.
Protein type: Protease; Motility/polarity/chemotaxis; EC 126.96.36.199; Apoptosis; EC 3.4.22.-
Molecular Function: peptidase activity; cyclin-dependent protein kinase inhibitor activity; protein binding; cysteine-type endopeptidase activity; aspartic-type endopeptidase activity
Biological Process: extracellular matrix organization and biogenesis; nerve growth factor receptor signaling pathway; positive regulation of apoptosis; apoptosis; negative regulation of activated T cell proliferation; heart development; negative regulation of B cell proliferation; proteolysis; regulation of caspase activity; neuron differentiation; regulation of apoptosis; extracellular matrix disassembly; sensory perception of sound; B cell homeostasis; positive regulation of neuron apoptosis; response to wounding; erythrocyte differentiation; T cell homeostasis; DNA fragmentation during apoptosis; response to UV; cell structure disassembly during apoptosis; release of cytochrome c from mitochondria; cell fate commitment; negative regulation of cyclin-dependent protein kinase activity; keratinocyte differentiation; neuron apoptosis; induction of apoptosis via death domain receptors; platelet formation; caspase activation via cytochrome c; response to DNA damage stimulus; induction of apoptosis by oxidative stress; negative regulation of apoptosis
SS: 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.