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FLASH GENE
Symbol TMEM38A contributors: mct - updated : 16-12-2015
HGNC name transmembrane protein 38A
HGNC id 28462
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • four transmembrane-spanning alpha helices
  • C-terminal domain faces the cytoplasmic side of the endo(sarco)plasmic reticulum
    • HOMOLOGY
    Homologene
    FAMILY
    CATEGORY transport channel
    SUBCELLULAR LOCALIZATION     plasma membrane
        intracellular
    intracellular,cytoplasm,organelle,endoplasmic reticulum
    intracellular,nucleus
    intracellular,nuclear envelope
    text
  • distributed in both longitudinal tubules and terminal cisternae of the sarcoplasmic reticulum, as well as in the perinuclear membrane systems and the nuclear envelope of myotubes and adult fibres
  • predominantly expressed in the sarcoplasmic reticulum (SR) of muscle cells
    • basic FUNCTION
  • TMEM38A, TMEM38B channels are likely to act as counter-ion channels that function in synchronization with Ca2+ release from intracellular stores
  • may be involved in the structural organization or function of the molecular machinery underlying excitation-contraction coupling
  • act as novel monovalent cation-specific channels on intracellular membrane systems
  • TMEM38A, TMEM38B, seem to have differential functions in Ca(2+) signaling in excitable and nonexcitable cells
  • directly modulates the function of the cardiac ryanodine receptor 2 Ca(2+) release channel, which in turn controls store-overload-induced Ca(2+) release from the SR
    • CELLULAR PROCESS
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling
    a component
  • part of TRIC channels that are likely to act as counter-ion channels that function in synchronization with Ca2+ release from intracellular stores
  • constituent of the skeletal muscle SR (sarcoplasmic reticulum)
    • INTERACTION
    DNA
    RNA
    small molecule
    protein
    cell & other
    REGULATION
    ASSOCIATED DISORDERS
    corresponding disease(s)
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    ANIMAL & CELL MODELS
  • Tric-a(-/-) mice display defective Ca(2+) sparks and spontaneous transient outward currents in arterial smooth muscle and develop hypertension, in addition to skeletal muscle dysfunction