DYRK1B, Active(D09-10BG)
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Description :Recombinant full-length human DYRK1B was expressed by baculovirus in Sf9 insect cells using an N-terminal GST tag.
Species :Human
Tag :GST tag
Expression System:Sf9 insect cells using baculovirus
Sequence :Full-length
Genbank Number :BC018751
Specific Activity :Sample Kinase Activity Plot. For specific information on a given lot, see related technical data sheet.
Purity :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.
Applications :Kinase Assay, Western Blot
Molecular Weight :~106 kDa
Gene Aliases :MIRK
Scientific Background :DYRK1B (Dual specificity tyrosine-phosphorylation-regulated kinase 1B) is a member of the evolutionarily conserved DYRK family with key roles in the control of cell proliferation and differentiation. DYRK1B acts in G0/G1 to maintain cells in growth arrest and quiescence by targeting cyclin D1 for proteasomal degradation by phosphorylating a threonine residue close to the C terminus. Paradoxically, DYRK1B can also stabilize other proteins by phosphorylation as illustrated by the phosphorylation by DYRK1B of p27Kip1 on Ser10 during the G0 phase of the cell cycle. Deregulation of DYRK1B such as gene amplification, overexpression and/or constitutive activation has been observed in multiple types of cancer.
References :
1. Becker W. Emerging role of DYRK family protein kinases as regulators of protein stability in cell cycle control. Cell Cycle. 2012 11:3389-94.
2. Deng X, Mercer SE, Shah S, Ewton DZ, Friedman E. The cyclin-dependent kinase inhibitor p27Kip1 is stabilized in G(0) by Mirk/dyrk1B kinase. J Biol Chem. 2004 279:22498–504.
Product Sheets (By Lot #) :
Research Areas :AKT/PKB Pathway, Apoptosis/Autophagy, Cancer, Cardiovascular Disease, Inflammation, Invasion/Metastasis, Metabolic Disorder, Neurobiology, NfkB Pathway, Ser/Thr Kinases, WNT Signaling