MAP2K1 Antibodies

MAP2K1 (Mitogen-Activated Protein Kinase Kinase 1) is a Protein Coding gene. Diseases associated with MAP2K1 include Cardiofaciocutaneous Syndrome 3 and Cardiofaciocutaneous Syndrome 1. Among its related pathways are Oocyte meiosis and Oxytocin signaling pathway. 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 MAP2K2.

CUSABIO has supplied high-quality antibodies to researchers worldwide for more than 13 years. The MAP2K1 antibodies in the following catalog are manufactured under our strict standards. They have the features of high specificity and sensitivity, high reproducibility, multiple immunogen and host species options,
validation in various applications, etc. And above all, CUSABIO provides 100% Risk-free Performance Guarantee. In addition, CUSABIO also offers MAP2K1 antibody custom service for researchers who need more specific needs.

MAP2K1 Antibodies Catalog

MAP2K1 Antibodies for Homo sapiens (Human)

MAP2K1 Background

Dual specificity mitogen-activated protein kinase kinase 1 is a protein in humans that is encoded by the MAP2K1 gene [1][2]. MAP2K1 is also called MEK1. Dual specificity protein kinase which acts as an essential component of the MAP kinase signal transduction pathway. Binding of extracellular ligands such as growth factors, cytokines, and hormones to their cell-surface receptors activates RAS and this initiates RAF1 activation. RAF1 further activates the dual-specificity protein kinases MAP2K1/MEK1 and MAP2K2/MEK2. Both MAP2K1/MEK1 and MAP2K2/MEK2 function specifically in the MAPK/ERK cascade, and catalyze the concomitant phosphorylation of a threonine and a tyrosine residue in a Thr-Glu-Tyr sequence located in the extracellular signal-regulated kinases MAPK3/ERK1 and MAPK1/ERK2, leading to their activation and further transduction of the signal within the MAPK/ERK cascade [3-7]. The Ras/Raf/Mek/Erk mitogen-activated protein kinase pathway regulates fundamental processes in normal and malignant cells, including proliferation, differentiation, and cell survival, even apoptosis [8]. The inactivation of the MEK1 gene leads to embryonic lethality, suggesting an unique role of MEK1 during embryogenesis. Florence A. Scholl et al. demonstrated that disruption of MEK1, but not of MEK2, decreases tumor burden [9]. And their study also uncovered that MEK1 function is important for the early stages of skin tumor formation and that MEK2 cannot compensate for its absence [9].

[1] Rampoldi L, Zimbello R, et al. Chromosomal localization of four MAPK signaling cascade genes: MEK1, MEK3, MEK4 and MEKK5 [J]. Cytogenet Cell Genet. 1998, 78 (3-4): 301-3.
[2] 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.
[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. Oncogene 2009; 28: 1485-95.
[8] Huynh H, Nguyen TT, et al. Over-expression of the mitogen-activated protein kinase (MAPK) kinase (MEK)-MAPK in hepatocellular carcinoma: its role in tumor progression and apoptosis [J]. BMC Gastroenterol. 2003, Aug 8; 3():19.
[9] Florence A. Scholl, Phillip A. Dumesic, et al. Selective Role for Mek1 but not Mek2 in the Induction of Epidermal Neoplasia [J]. Cell, Tumor, and Stem Cell Biology, Volume 69, Issue 9, pp. 3772-3778.

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