a proline-directed protein kinase of the GSK family. Implicated in the control of several regulatory proteins including glycogen synthase, Myb, and c-Jun. GSK3 and GSK3 have similar functions. GSK3 phophorylates tau, the principal component of neurofibrillary tangles in Alzheimer disease and is required for maximal production of amyloid plaque peptides by secretase. A GSK3 promoter SNP effects progression of bipolar disorder. The GSK3 inhibitor, lithium, is used to treat bipolar disorder and is seen to block plaque formation. GSK3 generally opposes the action of insulin, and GSK3 hyperactivity is thought to contribute to insulin resistant (type II) diabetes. GSK3 also negatively regulates cardiac hypertrophy. A tumor suppressor role is indicated by the oncogenic potential of stabilized -catenin mutants that lack GSK3 phosphorylation sites. Inhibitor: AR-A014418 Note: This description may include information from UniProtKB.
Protein type: Kinase, protein; EC 126.96.36.199; Protein kinase, Ser/Thr (non-receptor); EC 188.8.131.52; Protein kinase, CMGC; CMGC group; GSK family; GSK subfamily
Molecular Function: transferase activity; protein serine/threonine kinase activity; protein binding; tau-protein kinase activity; nucleotide binding; kinase activity; ATP binding; protein kinase activity
Biological Process: glycogen metabolic process; proteasomal ubiquitin-dependent protein catabolic process; nervous system development; cell migration; negative regulation of TOR signaling pathway; genetic imprinting; Wnt receptor signaling pathway; negative regulation of insulin receptor signaling pathway; positive regulation of peptidyl-serine phosphorylation; protein amino acid phosphorylation; negative regulation of signal transduction; negative regulation of glucose import; cellular response to insulin stimulus; positive regulation of cAMP biosynthetic process; carbohydrate metabolic process; insulin receptor signaling pathway; regulation of systemic arterial blood pressure; positive regulation of transcription from RNA polymerase II promoter; phosphorylation; positive regulation of heart contraction
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.