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FLASH GENE
Symbol ME2 contributors: mct - updated : 15-05-2013
HGNC name malic enzyme 2, NAD(+)-dependent, mitochondrial
HGNC id 6984
EXPRESSION
Type ubiquitous
   expressed in (based on citations)
organ(s)
SystemOrgan level 1Organ level 2Organ level 3Organ level 4LevelPubmedSpeciesStageRna symbol
Endocrineneuroendocrinepituitary  highly
 pancreas   highly Homo sapiensAdult
Nervousbrain   highly
Reproductivemale systemprostate  moderately
Respiratorylung   moderately
Urinarykidney   moderately
Visualeye   highly
tissue
SystemTissueTissue level 1Tissue level 2LevelPubmedSpeciesStageRna symbol
Connectivebone   
cells
SystemCellPubmedSpeciesStageRna symbol
Endocrineislet cell (alpha,beta...) Homo sapiensAdult
cell lineage
cell lines
fluid/secretion
at STAGE
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
mono polymer homomer , tetramer
HOMOLOGY
Homologene
FAMILY malic enzyme family
CATEGORY enzyme
SUBCELLULAR LOCALIZATION     intracellular
intracellular,cytoplasm,organelle,mitochondria,matrix
basic FUNCTION
  • mitochondrial NAD-dependent malic enzyme, catalyzing the oxidative decarboxylation of malate to pyruvate
  • converting malate to pyruvate and is involved in neuronal synthesis of the neurotransmitter gamma-aminobutyric acid (GABA)
  • ME1, ME2 use only NADP as a cofactor and have lower Kms for malate
  • ME1, ME2 are important for NADPH production, lipogenesis and glutamine metabolism, but ME2 has a more profound effect
  • CELLULAR PROCESS
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling
    a component
    INTERACTION
    DNA
    RNA
    small molecule
    protein
  • TP53 represses the expression of the tricarboxylic-acid-cycle-associated malic enzymes ME1 and ME2 in human and mouse cells
  • cell & other
    REGULATION
    inhibited by ATP
    ASSOCIATED DISORDERS
    corresponding disease(s)
    related resource MITOP database
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    constitutional       loss of function
    modulates the outcome of TP53 activation, leading to strong induction of senescence, but not apoptosis
    constitutional       gain of function
    suppresses senescence
    Susceptibility to adolescent-onset idiopathic generalized epilepsy
    Variant & Polymorphism SNP increases the risk for adolescent-onset idiopathic generalized epilepsy
    Candidate gene
    Marker
    Therapy target
    ANIMAL & CELL MODELS