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FLASH GENE
Symbol NDUFA13 contributors: mct - updated : 31-03-2014
HGNC name NADH dehydrogenase (ubiquinone) 1 alpha subcomplex, 13
HGNC id 17194
Location 19p13.11      Physical location : 19.627.018 - 19.639.013
Synonym name
  • gene associated with retinoid-IFN-induced mortality 19
  • cell death-regulatory protein GRIM19
  • retinoid-IFN-induced mortality 19
  • complex I B16.6 subunit
  • NADH-ubiquinone oxidoreductase B16.6 subunit
  • Synonym symbol(s) B16.6, CDA016, CGI-39, GRIM-19, GRIM19, FLJ58045, FLJ59191
    DNA
    TYPE functioning gene
    STRUCTURE 11.99 kb     5 Exon(s)
    MAPPING cloned Y linked N status provisional
    RNA
    TRANSCRIPTS type messenger
    identificationnb exonstypebpproduct
    ProteinkDaAAspecific expressionYearPubmed
    5 - 557 16 144 - 2000 10924506
    EXPRESSION
    Type ubiquitous
       expressed in (based on citations)
    organ(s)
    SystemOrgan level 1Organ level 2Organ level 3Organ level 4LevelPubmedSpeciesStageRna symbol
    Cardiovascularheart   highly
    Endocrineneuroendocrinepituitary  highly
     parathyroid   highly
    tissue
    SystemTissueTissue level 1Tissue level 2LevelPubmedSpeciesStageRna symbol
    Blood / hematopoieticbone marrow   
    Muscularstriatumskeletal  
    cell lineage
    cell lines
    fluid/secretion
    at STAGE
    physiological period fetal
    Text numerous fetal tissues
    PROTEIN
    PHYSICAL PROPERTIES
    STRUCTURE
    motifs/domains
  • mitochondrial localization sequences at the N-terminus, having a major role in mediating its tumor-suppressive actions
  • HOMOLOGY
    Homologene
    FAMILY
    CATEGORY regulatory , tumor suppressor
    SUBCELLULAR LOCALIZATION     intracellular
    intracellular,cytoplasm,organelle,mitochondria,inner
    intracellular,cytoplasm,organelle,membrane
    intracellular,nucleus,nucleoplasm
    text primarily a nuclear protein
    basic FUNCTION
  • death-inductive role in the IFN retinoid regulated pathway
  • involved in transfer of electrons from NADH to the respiratory chain
  • required for electron transfer activity of complex I, and essential for maintenance of mitochondrial membrane potential
  • inhibits SRC-induced oncogenic transformation and metastatic behavior of cells
  • promotes the inhibitory effect of CDKN2A on CDK4
  • regulatory gene necessary for interferon-beta and retinoic acid-induced cell death
  • acts as a chaperone to recruit STAT3 into mitochondria
  • critical role as a tumor suppressor
  • has a major role in tumor suppression by acting as an essential regulator of antioncogenic transcription and metabolism
  • CELLULAR PROCESS cell life, cell death/apoptosis
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling
    a component
  • functional component of mitochondrial complex I and essential for early embryonic development
  • INTERACTION
    DNA
    RNA
    small molecule
    protein
  • NDUFA13/CDKN2A synergistically suppressed cell cycle progression via inhibiting E2F1-driven gene expression (N- terminus of NDUFA13 and the fourth ankyrin repeat of CDKN2A are crucial for their interaction)
  • interact physically with STAT3 and inhibit STAT3-dependent signal transduction
  • NDUFA13-mediated translocation of STAT3 to mitochondria is necessary for TNF-induced necroptosis
  • SRC downregulated the expression of PAG1, a lipid raft-associated inhibitor of SRC, which was restored by wild-type NDUFA13
  • cell & other
    REGULATION
    induced by interferon beta combined with all-trans-retinoic acid
    ASSOCIATED DISORDERS
    corresponding disease(s)
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    tumoral     --low  
    in primary renal cell carcinomas (RCCs) and in some urinogenital tumors
    constitutional       loss of function
    caused mitochondrial electron transport dysfunction resulting from failure to assemble electron transport chain complexes and altered the expression of several cellular genes involved in glycolysis
    tumoral     --low  
    in several primary tumors of lung, kidney, prostate, thyroid, ovary, colon, esophagus, and brain
    tumoral        
    significantly associated with lymph node metastasis and advanced tumor-node-metastasis stage
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
  • overexpression in cancer cells suppresses STAT3-mediated signal transduction and cancer growth, having potential as a novel anticancer therapy in STAT3c cancer
  • suppressed the expression of tumor invasion- and angiogenesis-associated factors to limit tumor growth in cervical cancer
  • deletion of Grim-19 in the skin significantly increased the susceptibility of mice to chemical carcinogenesis, resulting in development of squamous cell carcinomas
  • ANIMAL & CELL MODELS