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FLASH GENE
Symbol MAP2K2 contributors: npt/mct/pgu - updated : 14-09-2013
HGNC name mitogen-activated protein kinase kinase 2
HGNC id 6842
Corresponding disease
CFC4 cardio-facio-cutaneous syndrome 4
Location 19p13.3      Physical location : 4.090.328 - 4.124.126
Synonym name
  • dual specificity mitogen-activated protein kinase kinase 2
  • ERK activator kinase 2
  • MAPK/ERK kinase 2
    • Synonym symbol(s) MEK2, MKK2, PRKMK2, MAPKK2
    EC.number 2.7.1.-, 2.7.12.2
    DNA
    TYPE functioning gene
    STRUCTURE 33.81 kb     11 Exon(s)
    10 Kb 5' upstream gene genomic sequence study
    MAPPING cloned Y linked N status provisional
    RNA
    TRANSCRIPTS type messenger
    identificationnb exonstypebpproduct
    ProteinkDaAAspecific expressionYearPubmed
    11 - 1759 44.3 400 - 2000 10828601
    EXPRESSION
    Type
       expressed in (based on citations)
    organ(s)
    SystemOrgan level 1Organ level 2Organ level 3Organ level 4LevelPubmedSpeciesStageRna symbol
    Digestiveintestinelarge intestinecolon highly
     salivary gland   highly
    Lymphoid/Immunelymph node   highly
    Reproductivefemale systemovary  highly
    Skin/Tegumentskin   highly
    cell lineage
    cell lines
    fluid/secretion
    at STAGE
    PROTEIN
    PHYSICAL PROPERTIES
    STRUCTURE
    motifs/domains
    conjugated PhosphoP
    HOMOLOGY
    interspecies homolog to murine Map2k2
    homolog to C.elegans Y54e10bl.6
    intraspecies homolog to MAP2K1/MEK1
    Homologene
    FAMILY
  • protein kinase superfamily
  • STE Ser/Thr protein kinase family
  • MAP kinase kinase subfamily
    • CATEGORY enzyme
    SUBCELLULAR LOCALIZATION extracellular
        intracellular
    intracellular,cytoplasm,organelle,mitochondria
    intracellular,cytoplasm,organelle,endoplasmic reticulum
    intracellular,cytoplasm,organelle,Golgi
    intracellular,cytoplasm,organelle,endosome
    intracellular,cytoplasm,cytosolic
    intracellular,cytoplasm,cytoskeleton,microtubule
    intracellular,nucleus
    basic FUNCTION
  • serine/threonine protein kinase
  • play a critical role in mitogen growth factor signal transduction
  • activating ERK1 and ERK2 MAP kinases
  • dual-specificity kinase that mediate ERK1 and ERK2 activation during adhesion and growth factor signaling
  • have a crucial role in cardiac hypertrophy
  • crucial modulator of Mek and Erk signaling and have potential implications for the role of MAP2K1 and MAP2K2 in tumorigenesis
  • MAP2K1 levels are upregulated at transcriptional level whereas MAP2K2 levels are downregulated at posttranslational level
    • CELLULAR PROCESS protein
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling
    a component
  • MAP2K1–MAP2K2 heterodimerize and form a stable complex in fibroblasts
    • INTERACTION
    DNA
    RNA
    small molecule nucleotide,
  • ATP
    • protein
  • interacting with ERK1, ERK2
  • MAP2K1 conditionally compensates for loss of MAP2K2 only in the presence of other mitogen-activated protein kinase kinases
  • interaction of DLG1 with the activated form of MAP2K2 of the canonical RAF/MEK/ERK pathway, a protein that is found at the midbody during cytokinesis
  • MAP2K2 is an endogenous regulator of RRM2B, suggesting that it may associate with RRM2B and upregulate its activity
  • PAK1 can stimulate MAP2K1/MAP2K2 activity in a kinase-independent manner, probably by serving as a scaffold to facilitate interaction of RAF1
    • cell & other
    REGULATION
    activated by Ser/Thr phosphorylation by MAP kinase kinase kinases
    Other inhibition or degradation of this kinase is found to be involved in the pathogenesis of Yersinia and anthrax
    ASSOCIATED DISORDERS
    corresponding disease(s) CFC4
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    constitutional germinal mutation      
    missense mutation in CFC
    tumoral somatic mutation      
    in melanomas
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    ANIMAL & CELL MODELS
    Mek2-deficient mice were viable and fertile and showed no phenotypic abnormalities. Mutant embryonic fibroblasts and purified lymphocytes proliferated normally, demonstrating that Mek2 is not required for reentry into the cell cycle or for T-cell development concluding that MEK1 can compensate for a lack of MEK2 function