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FLASH GENE
Symbol GARS contributors: mct - updated : 27-08-2012
HGNC name glycyl-tRNA synthetase
HGNC id 4162
EXPRESSION
Type ubiquitous
   expressed in (based on citations)
organ(s)
SystemOrgan level 1Organ level 2Organ level 3Organ level 4LevelPubmedSpeciesStageRna symbol
Cardiovascularheart    
Digestiveliver    
 mouthgingiva   
 stomach    
Endocrineadrenal gland    
Lymphoid/Immunespleen    
Nervousbrain   highly
Reproductivefemale systemuteruscervix highly
Respiratorylung    
Skin/Tegumentskin   highly
tissue
SystemTissueTissue level 1Tissue level 2LevelPubmedSpeciesStageRna symbol
Muscularstriatumskeletal  
cells
SystemCellPubmedSpeciesStageRna symbol
Endocrineislet cell (alpha,beta...)
cell lineage
cell lines
fluid/secretion
at STAGE
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • N-terminal WHEP-TRS domain
  • a catalytic domain containing the characteristic three conserved motifs (1, 2, and 3) of class II tRNA synthetases and, in addition, three insertions (I, II, and III) between the motifs
  • a C-terminal anticodon binding domain
  • mono polymer homomer , dimer
    HOMOLOGY
    interspecies homolog to C.elegans T10f2.1
    Homologene
    FAMILY aminoacyl-t RNA synthetase family, class 2
    CATEGORY enzyme
    SUBCELLULAR LOCALIZATION     intracellular
    intracellular,cytoplasm,organelle,mitochondria,matrix
    intracellular,cytoplasm,cytosolic
    basic FUNCTION
  • acting as a target of autoantibodies in the human autoimmune diseases
  • . essential component of the translation apparatus, circulates in serum and can be secreted from macrophages in response to FAS ligand that is released from tumor cells
  • CELLULAR PROCESS
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling
    a component
    INTERACTION
    DNA
    RNA
    small molecule
    protein
    cell & other
    REGULATION
    ASSOCIATED DISORDERS
    corresponding disease(s) CMT2D , DSMAVA
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    ANIMAL & CELL MODELS
  • although missense mutations of Gars may cause some loss of function, the dominant neuropathy phenotype observed in mice is caused by a dose-dependent gain of function that is not mitigated by over-expression of functional wild-type protein