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FLASH GENE
Symbol MERTK contributors: mct/shn - updated : 12-10-2010
HGNC name c-mer proto-oncogene tyrosine kinase
HGNC id 7027
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • N glycosylation sites
  • two Ig-like C2-type (immunoglobulin-like) domains
  • two fibronectin type III domains
  • one tyrosine kinase domain
  • HOMOLOGY
    interspecies ortholog to Mertk, Rattus norvegicus
    ortholog to Mertk, Mus musculus
    ortholog to MERTK, Pantroglodytes
    ortholog to mertk, Danio rerio
    Homologene
    FAMILY
  • MER/AXL/TYRO3 receptor kinase family
  • TAM receptor tyrosine kinase (RTK) subfamily
  • CATEGORY enzyme , regulatory , protooncogene , receptor membrane
    SUBCELLULAR LOCALIZATION     plasma membrane
    text transmembrane protein
    basic FUNCTION
  • participates in an inhibitory pathway in macrophages important for regulating TNF-alpha secretion and attenuating endotoxic shock
  • critical for the engulfment and efficient clearance of apoptotic cells
  • plays an essential immunoregulatory role
  • an integral component of the retinal pigmentary epithelium phagocytic process tnat triggers ingestion of bound outer segments
  • CELLULAR PROCESS
    PHYSIOLOGICAL PROCESS immunity/defense
    PATHWAY
    metabolism
    signaling sensory transduction/vision
    a component
    INTERACTION
    DNA
    RNA
    small molecule nucleotide,
  • ATP
  • protein
  • growth arrest-specific gene 6, GAS6 (
  • C-terminal region of the guanine nucleotide-exchange factor (GEF) V,av1 (
  • TULP1 interacts with TYRO3, AXL and MERTK of the TAM receptor tyrosine kinase subfamily, whereas tubby binds only to MERTK (
  • tubby and TULP1 are new MERTK ligands and facilitate phagocytosis in a MERTK-dependent manner (
  • cell & other
    REGULATION
    activated by growth arrest-specific gene 6, GAS6 and protein S
    TUB and TULP1 potentially (activation induced by tubby and TULP1 facilitate MERTK-dependent cytoskeletal reorganization)
    Other cleaved in the extracellular domain via a metalloproteinase
    ASSOCIATED DISORDERS
    corresponding disease(s) RPMR
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    constitutional     --over  
    may reflect an increased demand for removal of apoptotic cells in smokers, an observation with implications for the development of chronic obstructive pulmonary disease, a disorder associated with dysregulated apoptosis of lung parenchymal cells
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    SystemTypeDisorderPubmed
    bloodcoagulation 
    potential therapeutic use for soluble MERTK in the treatment of clotting disorders
    ANIMAL & CELL MODELS
  • mice that lack the Merk signaling tyrosine kinase domain exhibit edema, leukocyte infiltration, and signs of endotoxic shock then die of endotoxic shock
  • viral gene transfer of Mertk to a RCS rat retina can correct both functional cellular defect (phagocytosis) and photoreceptor degeneration
  • mutation of the Mertk in Royal College of Surgeons (RCS) rat leads to retinal degeneration in which the RPE fails to phagocytose shed outer segments
  • mer(kd) mice with a cytoplasmic truncation of Mer have macrophages deficient in the clearance of apoptotic thymocytes
  • mice with disruption of Mertk gene manifest a retinal dystrophy phenotype similar to RCS rats
  • MerTK-deficient mice develop retinal degeneration due to defective RPE phagocytosis, whereas ablation of Axl or Tyro3 appears to have minimal impact on retinal homeostasis