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FLASH GENE
Symbol TRPC1 contributors: mct/npt/pgu - updated : 22-01-2015
HGNC name transient receptor potential cation channel, subfamily C, member 1
HGNC id 12333
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • cytoplasmic N terminus
  • ankyrin repeats and a coiled coil structure
  • six transmembrane segments
  • a cytoplasmic C terminus with a dystrophin (coiled-coil) domain
  • a highly conserved TRP (EWKFHR) domain
  • conjugated GlycoP
    mono polymer homomer , heteromer , tetramer , heptamer
    HOMOLOGY
    interspecies ortholog to Drosophila store-operated channel (Soc)
    Homologene
    FAMILY
  • TRP superfamily of Ca2+ cation channels, classic subfamily
  • transient receptor family
  • STrpC subfamily
  • CATEGORY transport channel
    SUBCELLULAR LOCALIZATION     plasma membrane
        intracellular
    intracellular,cytoplasm
    text
  • perisynaptic region of the cerebellar parallel fibre-purkinje cell synapse
  • mostly associated to the surface of spermatogenic cells
  • co-localizes and could be co-immunoprecipitated with beta-tubulin
  • forms functional endoplasmic reticulum (ER) homotetrameric channels, and is localized exclusively in the sarcoplasmic reticulum
  • basic FUNCTION
  • transient receptor potential non voltage-channel
  • involved in calcium homeostasis in megakaryocytes and platelets
  • plays fundamental roles in processes ranging from sensory physiology to male fertility
  • may influence flagellar movement
  • encoding a non-selective cation channel involved directly or indirectly in the regulation of cell volume
  • having a function in retinal epithelium cells, dependent on its interaction with beta-tubulin
  • showing a pattern of single-channel conductance, amiloride sensitivity and ion permeability distinct from that of TRPC1 alone
  • operates as a sarcoplasmic reticulum Ca2+ leak channel in skeletal muscle
  • deeply involved in intracellular Ca2+ homeostasis at rest and during muscle activation by potentially regulating SR Ca2+ content, resting cytosolic Ca2+ and kinetics of the voltage-evoked Ca2+ transients
  • necessary mediator of pathologic cardiac hypertrophy, in part through a calcineurin/NFAT signaling pathway
  • critical aspects of the TRPC1 channelosome that are involved in the regulation of TRPC1 function and TRPC1-SOC-generated Ca2+ signals
  • cationic channel with functional effects that include stimulation of cardiovascular remodelling
  • is potentially a molecular mediator for postsynaptic Ca2+ elevation required for BDNF-induced synaptic plasticity
  • TRPC1 and TRPC5 have critical roles in neurite outgrowth
  • acts as a scaffold at the cell surface to assemble a signaling complex to stimulate neurite outgrowth
  • both TRPC1 and TRPC4 are essential for an intrinsic membrane conductance mediating the plateau potential in lateral septal neurons, possibly as heteromeric channels
  • reduces calcium permeability in heteromeric channel complexes
  • TRPC1-mediated Ca2+ influx enhances PI3K/Akt pathway during muscle regeneration
  • regulates cell proliferation and motility, two processes underlying cancer progression
  • TRPC1-mediated increase in store-operated Ca2+ entry is required for the proliferation of adult hippocampal neural progenitor cells
  • down-regulation of TRPV6 currents by TRPC1 may increase the cellular diversity to fine-tune Ca2+ homeostasis
  • TRPC1 is able to suppress TRPV6 dependent currents/entry because of a reduction of TRPV6 plasma membrane expression
  • TRPC5 and TRPC1/4 contribute to seizure and excitotoxicity by distinct cellular mechanisms
  • heteromeric TRPC3/TRPC1 could participate in regulating the resting cytosolic Ca(2+) levels in skeletal muscle
  • contribution of heteromultimeric channels from TRPC1, TRPC4, and TRPC5 subunits to the regulation of mechanisms underlying spatial working memory and flexible relearning by facilitating proper synaptic transmission in hippocampal neurons
  • CELLULAR PROCESS cell migration & motility
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling
    a component
  • forming with PKD2 a channel with a unique constellation of new and TRPP2/TRPC1-specific properties, activated in response to G-protein-coupled receptor activation
  • in glomerular mesangial cells, the TRPC1/TRPC4 complexes constitute the functional subunits of UBXN11 and the interaction between STIM1 and TRPC4 may be the mechanism for the activation of the channels
  • comprised of homo- or heterotetramers between either TRPC1/4/5
  • is a component of a Ca(2+)-dependent amplification of EGF-dependent cell proliferation
  • INTERACTION
    DNA
    RNA
    small molecule
    protein
  • HOMER and ITPR1 (interaction TRPC1/ITPR1 regulated by HOMER)
  • interacting with C10orf63
  • interacting with STIM1
  • CAV1 interacts with TRPC1 and ITPR3 to regulate Ca2+ store release-induced Ca2+ entry in endothelial cells
  • interacting with PKD2(form homotetramers, with distinct functional and regulatory properties, among which there are the presence of four subconductance states in PKD2)
  • binds directly to KL and KDR and strengthens the association to promote their cointernalization (
  • functional interaction of TRPC1 with TRPV6 that negatively regulates Ca2+ influx (
  • MARCKS coordinates native TRPC1 channel activation in VSMCs by acting as a reversible PI(4,5)P2 buffer, which is regulated by PRKCA-mediated TRPC1 phosphorylation
  • cell & other
    REGULATION
    activated by by depletion of intracellular Ca2+ stores (store-operated Ca2+ entry) or by stretch
    GRM1
    induced by TNF-alpha through an NF-kappaB-dependent pathway in endothelial cells, which can trigger augmented Ca2+ entry following Ca2+ store depletion
    Other stimulated by a G protein coupled receptor from extracellular space by a process called calcium capacitative entry (CCE)
    regulated by REST
    at least in certain cell types, TRPC1 is regulated during cell cycle progression
    ASSOCIATED DISORDERS
    corresponding disease(s)
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    SystemTypeDisorderPubmed
    neurologyepilepsy 
    TRPC channels could be an unsuspected but critical molecular target for clinical intervention for excitotoxicity
    ANIMAL & CELL MODELS