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Human MEK2 / MAP2K2 / MKK2 Protein (GST Tag)

CFC4,FLJ26075,MAPKK2,MEK2,MKK2,PRKMK2

Catalog Number P10678-H09B
Organism Species Human
Host Baculovirus-Insect Cells
Synonyms CFC4,FLJ26075,MAPKK2,MEK2,MKK2,PRKMK2
Molecular Weight The recombinant human MAP2K2/GST chimera consists of 624 amino acids and has a calculated molecular mass of 70.7 kDa. It migrates as an approximately 66 kDa band in SDS-PAGE under reducing conditions.
predicted N Met
SDS-PAGE
Purity > 92 % as determined by SDS-PAGE
Protein Construction A DNA sequence encoding the human MAP2K2 (NP_109587.1) (Met 1-Val 400) was fused with the GST tag at the N-terminus.
Bio-activity No Kinase Activity
Research Area Immunology |Inflammation / Inflammatory Mediator |Pattern Recognition Receptors |C-type Lectin Receptors
Formulation Lyophilized from sterile 20mM Tris, 500mM NaCl, 2mM GSH, pH 7.4
1. Normally 5 % - 8 % trehalose and mannitol are added as protectants before lyophilization. Specific concentrations are included in the hardcopy of COA.
Background Dual specificity mitogen-activated protein kinase kinase 2, also known as MAP kinase kinase 2, MAPKK2, ERK activator kinase 2, MAPK / ERK kinase 2, MEK2 and MAP2K2, is a member of the protein kinase superfamily, STE Ser/Thr protein kinase family and MAP kinase kinase subfamily. MAP2K2 / MEK2 contains one protein kinase domain. MEK1 and MEK2 (also known as MAP2K1 and MAP2K2, respectively) are evolutionarily conserved, dual-specificity kinases that mediate Erk1 and Erk2 activation during adhesion and growth factor signaling. MAP2K1 / MEK1 is a crucial modulator of Mek and Erk signaling and have potential implications for the role of MEK1 and MEK2 in tumorigenesis. MAP2K2 / MEK2 catalyzes the concomitant phosphorylation of a threonine and a tyrosine residue in a Thr-Glu-Tyr sequence located in MAP kinases. It also activates the ERK1 and ERK2 MAP kinases. Defects in MAP2K2 are a cause of cardiofaciocutaneous syndrome (CFC syndrome) which is characterized by a distinctive facial appearance, heart defects and mental retardation. Heart defects include pulmonic stenosis, atrial septal defects and hypertrophic cardiomyopathy.
Reference
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  • Daub H., et al., 2008, Mol. Cell 31:438-448.
  • Catalanotti,F. et al., 2009, Nat Struct Mol Biol. 16 (3):294-303.