MEK2 Proteins, Antibodies, cDNA Clones Research Reagents

MAP2K2 (Mitogen-Activated Protein Kinase Kinase 2, also known as CFC4; MEK2; MKK2; MAPKK2; PRKMK2), located on 19p13.3, is conserved in chimpanzee, Rhesus monkey, dog, cow, mouse, rat, chicken, zebrafish, etc. The gene produces a 44424 Da protein composed of 400 amino acids. The protein encoded by this gene is a dual-specificity protein kinase that belongs to the MAP kinase kinase family. MAP2K2 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.

MEK2 Protein (1)

    MEK2 Antibody (3)

      MEK2 cDNA Clone (30)

      NM_030662.3

      克隆载体 cDNA 产品

      In lentiviral vector

      BC014830.1

      克隆载体 cDNA 产品

      In lentiviral vector

      MEK2 Lysate (1)

        MEK2 分子背景

        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.

        MEK2 参考文献

        • MacDonald,T.J. et al., 2001, Nat Genet. 29 (2):143-52.
        • Mittal R., et al., 2006, Proc. Natl. Acad. Sci. USA. 103:18574-9.
        • Narumi,Y. et al., 2007, Am J Med Genet A. 143A (8):799-807.
        • Daub H., et al., 2008, Mol. Cell 31:438-448.
        • Catalanotti,F. et al., 2009, Nat Struct Mol Biol. 16 (3):294-303.

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