|Other Names||Dual specificity mitogen-activated protein kinase kinase 2, MAP kinase kinase 2, MAPKK 2, ERK activator kinase 2, MAPK/ERK kinase 2, MEK 2, MAP2K2, MEK2, MKK2, PRKMK2|
|Target/Specificity||The synthetic peptide sequence used to generate the antibody AP7961c was selected from the Center region of human MAP2K2 . A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.|
|Format||The synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder. Reconstitute with 0.1 ml deionized water for a final concentration of 1 mg/ml.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C.|
|Precautions||This product is for research use only. Not for use in diagnostic or therapeutic procedures.|
|Synonyms||MEK2, MKK2, PRKMK2|
|Function||Catalyzes the concomitant phosphorylation of a threonine and a tyrosine residue in a Thr-Glu-Tyr sequence located in MAP kinases. Activates the ERK1 and ERK2 MAP kinases (By similarity).|
|Cellular Location||Cytoplasm. Membrane; Peripheral membrane protein. Note=Membrane localization is probably regulated by its interaction with KSR1|
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Provided below are standard protocols that you may find useful for product applications.
MAP2K2 is a dual specificity protein kinase that belongs to the MAP kinase kinase family. This kinase is known to play a critical role in mitogen growth factor signal transduction. It phosphorylates and thus activates MAPK1/ERK2 and MAPK2/ERK3. The activation of this kinase itself is dependent on the Ser/Thr phosphorylation by MAP kinase kinase kinases. The inhibition or degradation of this kinase is found to be involved in the pathogenesis of Yersinia and anthrax.
Burroughs, K.D., et al., Mol. Cancer Res. 1(4):312-322 (2003).Tran, H., et al., Mol. Cell. Biol. 23(20):7177-7188 (2003).Li, S.P., et al., Cancer Res. 63(13):3473-3477 (2003).Li, Y., et al., J. Biol. Chem. 278(16):13663-13671 (2003).Liu, X., et al., J. Biol. Chem. 277(42):39312-39319 (2002).
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