MAP2K2 Proteins

MAP2K2 (Mitogen-Activated Protein Kinase Kinase 2) is a Protein Coding gene. Diseases associated with MAP2K2 include Cardiofaciocutaneous Syndrome 4 and Cardiofaciocutaneous Syndrome 1. Among its related pathways are Oxytocin signaling pathway and MicroRNAs in cardiomyocyte hypertrophy. Gene Ontology (GO) annotations related to this gene include transferase activity, transferring phosphorus-containing groups and protein tyrosine kinase activity. An important paralog of this gene is ENSG00000230626.

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MAP2K2 Proteins Catalog

MAP2K2 Proteins for Homo sapiens (Human)

MAP2K2 Proteins for Rattus norvegicus (Rat)

MAP2K2 Proteins for Canis lupus familiaris (Dog) (Canis familiaris)

MAP2K2 Proteins for Mus musculus (Mouse)

MAP2K2 Proteins for Cyprinus carpio (Common carp)

MAP2K2 Proteins for Gallus gallus (Chicken)

MAP2K2 Background

Dual specificity mitogen-activated protein kinase kinase 2 is a protein in humans that is encoded by the MAP2K2 gene [1]. It is more commonly known as MEK2. The MAP2K/MEK2 protein bears substantial sequence homology to MEK1, except at its amino terminus, and a proline-rich region inserts between the conserved kinase subdomains 9 and 10 [2]. Northern analysis indicates that MEK2 is expressed at low levels in the adult mouse brain and heart tissue and at higher levels in other tissues examined [2]. However, MEK2 is expressed at high levels in the neonatal brain [2]. MAP2K/MEK2 plays a critical role in mitogen growth factor signal transduction. As a part of the RAS/MAPK pathway, MAP2K/MEK2 transmits chemical signals from outside the cell to the cell's nucleus. MAP2K/MEK2 is activated through Ser/Thr phosphorylation by MAP kinase kinase kinases. Activated MAP2K/MEK2 phosphorylates and activates MAPK1/ERK2 and MAPK3/ERK1, leading to their activation and further transduction of the signal within the MAPK/ERK cascade [3-7]. RAS/MAPK signaling helps control the proliferation of cells, the process by which cells mature to carry out differentiation, cell movement, and apoptosis. Bélanger LF et al. demonstrated that MEK2 is not necessary for the normal development of the embryo and T-cell lineages, suggesting that the loss of MEK2 can be compensated for by MEK1 [8].

[1] Zheng CF, Guan KL. Cloning and characterization of two distinct human extracellular signal-regulated kinase activator kinases, MEK1 and MEK2 [J]. J Biol Chem. 1993, 268 (15): 11435-9.
[2] Brott B. K., A. Alessandrini, et al. MEK2 is a kinase related to MEK1 and is differentially expressed in murine tissues [J]. Cell Growth Differ. 1993, 4:921-929.
[3] Crews, C. M., Alessandrini, A. et al. The primary structure of MEK, a protein kinase that phosphorylates the ERK gene product [J]. Science 1992, 258,478 -480.
[4] Buscà R, Pouysségur J and Lenormand P: ERK1 and ERK2 Map Kinases: Specific Roles or Functional Redundancy [J]? Front Cell Dev Biol. 2016, 4:53.
[5] Wang Y, Nie H, Zhao X, Qin Y and Gong X: Bicyclol induces cell cycle arrest and autophagy in HepG2 human hepatocellular carcinoma cells through the PI3K/AKT and Ras/Raf/MEK/ERK pathways [J]. BMC Cancer. 2016, 16:742.
[6] Asati V, Mahapatra DK and Bharti SK: PI3K/Akt/mTOR and Ras/Raf/MEK/ERK signaling pathways inhibitors as anticancer agents: Structural and pharmacological perspectives [J]. Eur J Med Chem. 2016, 109:314-341.
[7] Scholl FA, Dumesic PA, et al. Mek1/2 gene dosage determines tissue response to oncogenic Ras signaling in the skin [J]. Oncogene 2009; 28: 1485-95.
[8] Bélanger LF, Sophie Roy, et al. Mek2 is dispensable for mouse growth and development [J]. Molecular and Cellular Biology, 01 Jul 2003, 23(14):4778-4787.


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