DYRK2 (also known as dual-specificity tyrosine-(Y)-phosphorylation regulated kinase 2) belongs to a family of protein kinases whose members are presumed to be involved in cellular growth and/or development and is defined by structural similarity of their kinase domains and their capability to autophosphorylate on tyrosine residues. DYRK2 expressed in E. coli demonstrated tyrosine autophosphorylation and catalyzed phosphorylation of histones H3 and H2B in vitro (1). DYRK2 also regulates p53 to induce apoptosis in response to DNA damage (2).
1. Becker, W. et.al: Sequence characteristics, subcellular localization, and substrate specificity of DYRK-related kinases, a novel family of dual specificity protein kinases. J. Biol. Chem. 273: 25893-25902, 1998.
2. Taira, N. et.al: DYRK2 is targeted to the nucleus and controls p53 via Ser46 phosphorylation in the apoptotic response to DNA damage. Molec. Cell 25: 725-738, 2007.
Sample Kinase Activity Plot. For specific information on a given lot, see related technical data sheet.
Sample Purity Data. For specific information on a given lot, see related technical data sheet.
Storage, Stability and Shipping:
Store product at –70oC. For optimal storage, aliquot target into smaller quantities after centrifugation and store at recommended temperature. For most favorable performance, avoid repeated handling and multiple freeze/thaw cycles.
Zheng Y et al., Regulation of folate and methionine metabolism by multisite phosphorylation of human methylenetetrahydrofolate reductase scientific reports March 2019 10.1038/s41598-019-40950-7
Sien Ong Su et al., Stability of the human pregnane X receptor is regulated by E3 ligase UBR5 and serine/threonine kinase DYRK2 Biochemical Journal January 2014 10.1042/BJ20130558
Sugatani Junko et al., Threonine-408 Regulates the Stability of the Human Pregnane X Receptor Through its Phosphorylation and the CHIP/Chaperone-Autophagy Pathway Drug Metabolism and Disposition November 2015 10.1124/dmd.115.066308
AKT/PKB Pathway, Apoptosis/Autophagy, Cancer, Cardiovascular Disease, Inflammation, Invasion/Metastasis, Metabolic Disorder, Neurobiology, NfkB Pathway, Ser/Thr Kinases, WNT Signaling