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FLASH GENE
Symbol COMMD9 contributors: mct - updated : 14-04-2021
HGNC name COMM domain containing 9
HGNC id 25014
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • COMM (copper metabolism gene MURR1) domain
  • a highly conserved C-terminal domain that forms a tightly interlocked dimeric structure responsible for COMMD-COMMD interactions
  • secondary structure
  • all COMMD proteins possess an alpha-helical N-terminal domain
  • HOMOLOGY
    interspecies homolog to murine Commd9
    Homologene
    FAMILY MURR1/COMMD1 family
    CATEGORY regulatory , unknown/unspecified
    SUBCELLULAR LOCALIZATION extracellular
        intracellular
    intracellular,cytoplasm,organelle,Golgi
    intracellular,cytoplasm,cytosolic,granule
    intracellular,nucleus,nucleoplasm
    basic FUNCTION
  • suppressing NF-kappaB not by affecting nuclear translocation or binding of NF-kappaB to cognate motifs
  • only COMMD9 and its binding partner, COMMD5, have substantial effects on Notch
  • COMMD9 participates in TFDP1/E2F1 activation and plays a critical role in non-small cell lung cancer
  • COMMD proteins are a conserved family of proteins with central roles in intracellular membrane trafficking and transcription
  • COMMD proteins function as obligatory dimers with conserved domain architectures
  • CELLULAR PROCESS
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling
    a component
    INTERACTION
    DNA
    RNA
    small molecule
    protein
  • COMMD3 and COMMD9 may be endogenous regulators of SCNN1A to regulate Na&
  • 8314; transport through altering SCNN1A cell surface expression
    cell & other
    REGULATION
    ASSOCIATED DISORDERS
    corresponding disease(s)
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    tumoral       gain of function
    in several non-small cell lung cancer (NSCLC) cell lines
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    ANIMAL & CELL MODELS
  • Commd9 deletion in mice leads to embryonic lethality and complex cardiovascular alterations that bear hallmarks of Notch deficiency