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FLASH GENE
Symbol GSTO1 contributors: mct - updated : 09-09-2011
HGNC name glutathione S-transferase omega 1
HGNC id 13312
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • N terminal 19-20AA extension
  • thioredoxin-like domains
  • a glutathione binding site where glutathione can form a disulfide bond with a conserved active site cysteine residue positioned near the N-terminal end of helix 1
  • an active site cysteine residue that is essential for its primary catalytic activities
  • seven alpha helices abriting the C terminal
    • mono polymer monomer
    HOMOLOGY
    interspecies homolog to murine P28
    intraspecies homolog to GSTO2
    Homologene
    FAMILY
  • cytosolic glutathione transferase super family
    • CATEGORY enzyme
    SUBCELLULAR LOCALIZATION extracellular
        intracellular
    intracellular,cytoplasm,cytosolic
    basic FUNCTION
  • small stress response protein likely involved in cellular redox homeostasis
  • implicated in the post-translational processing and activation of the proinflammatory mediator interleukin-1B
  • inhibitor of cardiac muscle ryanodine receptor Ca2+ channels
  • nuclear translocation could be potentially involved in the stress response of human cells playing a role in the cancer progression of Barrett esophagus
  • two isozymes (GSTO1 and GSTO2) have significant DHA reductase (DHAR) activity
  • participates in the glutathionylation cycle and targets specific proteins
    • CELLULAR PROCESS
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling
    a component
    INTERACTION
    DNA
    RNA
    small molecule
    protein
    cell & other
    REGULATION
    ASSOCIATED DISORDERS
    corresponding disease(s)
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    constitutional     --over  
    appears to be associated with activation of survival pathways (Akt and ERK1/2) and inhibition of apoptotic pathways (JNK1), as well as protection against cisplatin-induced apoptosis
    Susceptibility
  • to variation of the age at onset of Alzheimer disease
  • to hepatocellular carcinoma, cholangiocarcinoma and breast cancer
    • Variant & Polymorphism insertion/deletion
  • polymorphic deletion of Glu-155 causes a deficiency of GSTO1 (by its low stability, resulting from its increased propensity to unfold), may contribute to the observed association of GSTO1 with the age at onset of Alzheimer disease
  • GSTO1*A140D polymorphism could play an important role as a risk factor for the development ofhepatocellular carcinoma, cholangiocarcinoma and breast cancer
    • Candidate gene
    Marker
    Therapy target
    ANIMAL & CELL MODELS