a CAMK protein kinase of the Death-associated protein kinase (DAPK) family. Mediates autophagy and is a positive mediator of ER stress-induced and gamma-interferon induced programmed cell death. Catalytic activity is increased by ER stress. Inhibited by autophosphorylation of S308. DAPK -/- cells are protected from ER stress-induced cell death, and both apoptosis and autophagy are decreased. Colocalizes with the actin filament system. It is a tumor suppressor candidate, activating p53-dependent apoptosis. Expression is reduced in some cancers, and the promoter is frequently hypermethylated in invasive cancers. Increased expression and mislocalization is seen in epilepsy, where it may regulate neuronal death. A structurally unique serine-threonine kinase that carries eight ankyrin repeats and two putative P-loop consensus sites. Two isoforms of the human protein are produced by alternative splicing. Note: This description may include information from UniProtKB.
Protein type: Apoptosis; Autophagy; Kinase, protein; Protein kinase, Ser/Thr (non-receptor); Protein kinase, CAMK; EC 220.127.116.11; CAMK group; DAPK family
Molecular Function: ATP binding; calmodulin binding; calmodulin-dependent protein kinase activity; GTP binding; identical protein binding; protein binding; protein kinase activity; protein serine/threonine kinase activity; syntaxin-1 binding
Biological Process: apoptosis; induction of apoptosis via death domain receptors; negative regulation of translation; positive regulation of caspase activity; protein amino acid autophosphorylation; protein amino acid phosphorylation; regulation of apoptosis; regulation of autophagy
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.