MASTL: Serine/threonine kinase that plays a key role in M phase by acting as a regulator of mitosis entry and maintenance. Acts by promoting the inactivation of protein phosphatase 2A (PP2A) during M phase: does not directly inhibit PP2A but acts by mediating phosphorylation and subsequent activation of ARPP19 and ENSA at 'Ser-62' and 'Ser-67', respectively. ARPP19 and ENSA are phosphatase inhibitors that specifically inhibit the PPP2R2D (PR55-delta) subunit of PP2A. Inactivation of PP2A during M phase is essential to keep cyclin-B1-CDK1 activity high. Following DNA damage, it is also involved in checkpoint recovery by being inhibited. Phosphorylates histone protein in vitro; however such activity is unsure in vivo. May be involved in megakaryocyte differentiation. Defects in MASTL are the cause of thrombocytopenia type 2 (THC2). Thrombocytopenia is defined by a decrease in the number of platelets in circulating blood, resulting in the potential for increased bleeding and decreased ability for clotting. Belongs to the protein kinase superfamily. AGC Ser/Thr protein kinase family. 3 isoforms of the human protein are produced by alternative splicing.
Protein type: Protein kinase, AGC; EC 2.7.11.1; Protein kinase, Ser/Thr (non-receptor); Kinase, protein; AGC group; MAST family
Chromosomal Location of Human Ortholog: 10p12.1
Cellular Component: nucleoplasm; centrosome; cytoplasm; nucleus; cleavage furrow
Molecular Function: protein serine/threonine kinase activity; protein phosphatase 2A binding; kinase activity; ATP binding
Biological Process: mitosis; regulation of cell cycle; cell division; mitotic cell cycle; G2/M transition of mitotic cell cycle; negative regulation of protein phosphatase type 2A activity; protein amino acid phosphorylation; response to DNA damage stimulus
Disease: Thrombocytopenia 2
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