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FLASH GENE
Symbol TMED2 contributors: mct - updated : 12-09-2015
HGNC name transmembrane emp24 domain trafficking protein 2
HGNC id 16996
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • a GOLD domain
  • HOMOLOGY
    interspecies ortholog to rattus Rnp24
    Homologene
    FAMILY
  • EMP24/GP25L family
  • CATEGORY receptor , transport carrier
    SUBCELLULAR LOCALIZATION     plasma membrane
        intracellular
    intracellular,cytoplasm,organelle,membrane
    intracellular,cytoplasm,organelle,Golgi
    intracellular,cytoplasm,cytosolic,microsome
    text
  • type I membrane protein
  • Golgi-derived coatomer-coated vesicles
  • crucial constituent of the Golgi apparatus, associates with F2RL1 at the Golgi apparatus
  • basic FUNCTION
  • could have a role in the budding of coatomer-coated and other species of coated vesicles
  • could bind cargo molecules to collect them into budding vesicles
  • inhibiting the GTPase-activating activity of ARFGAP1
  • involved in vesicular targeting
  • cargo receptor facilitating calcium sensing receptor maturation and stabilization in the early secretory pathway
  • TMED2, TMED10 are specific cargo receptors of GPCRs and differentially control GPCR trafficking in the biosynthetic pathway, and thereby, TMED2 and TMED10 regulate GPCR signaling in astrocytes
  • required for transport of proteins between the endoplasmic reticulum and the Golgi
  • may play a role during placental development
  • CELLULAR PROCESS
    PHYSIOLOGICAL PROCESS cellular trafficking transport
    text
  • intracellular protein transport
  • PATHWAY
    metabolism
    signaling
    a component
    INTERACTION
    DNA
    RNA
    small molecule
    protein
  • ARFGAP1
  • F2RL1 and TMED2 interaction occurs between the N-terminal region of TMED2 p24A-GL (GOLD domain with a small linker) and the second extracellular loop of F2RL1, and after receptor activation, F2RL1 dissociates from TMED2
  • regulator of signal-dependent trafficking that regulates the life cycle of F2RL1
  • interactors of GCGR, LDLR and TMED2, significantly enhanced glucagon-stimulated glucose production, while YWHAB inhibited glucose production
  • cell & other
    REGULATION
    ASSOCIATED DISORDERS
    ANIMAL & CELL MODELS