catalytic subunit of cAMP-dependent protein kinase alpha, an AGC kinase. A number of inactive tetrameric holoenzymes are produced by the combination of homo- or heterodimers of the different regulatory subunits associated with two catalytic subunits. cAMP causes the dissociation of the inactive holoenzyme into a dimer of regulatory subunits bound to four cAMP and two free monomeric catalytic subunits. Two splice-variant isoforms have been described. Note: This description may include information from UniProtKB.
Protein type: EC 22.214.171.124; Protein kinase, AGC; Kinase, protein; Protein kinase, Ser/Thr (non-receptor); AGC group; PKA family
Cellular Component: centrosome; membrane; mitochondrion; plasma membrane; cytosol; nucleus; neuromuscular junction; cAMP-dependent protein kinase complex; AMP-activated protein kinase complex; cilium
Molecular Function: protein binding; cAMP-dependent protein kinase activity; ubiquitin protein ligase binding; protein kinase binding; ATP binding
Biological Process: nerve growth factor receptor signaling pathway; water transport; protein amino acid autophosphorylation; signal transduction; protein amino acid phosphorylation; positive regulation of protein export from nucleus; triacylglycerol catabolic process; G2/M transition of mitotic cell cycle; transmembrane transport; sperm capacitation; regulation of synaptic transmission; epidermal growth factor receptor signaling pathway; cytosolic calcium ion homeostasis; fibroblast growth factor receptor signaling pathway; regulation of osteoblast differentiation; regulation of heart rate; activation of protein kinase A; glucose metabolic process; gluconeogenesis; peptidyl-serine phosphorylation; mesoderm formation; phospholipase C activation; regulation of protein binding; carbohydrate metabolic process; energy reserve metabolic process; innate immune response; mitotic cell cycle; blood coagulation; regulation of insulin secretion
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.