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Details for receptor: TrpV4-A

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EndoNet ID: ENR01238

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Synonyms

  • TrpV4-1
  • Transient receptor potential cation channel subfamily V member 4
  • Osm-9-like TRP channel 4
  • Vanilloid receptor-like channel 2
  • Vanilloid receptor-like protein 2
  • VRL-2
  • Vanilloid receptor-related osmotically-activated channel
  • VR-OAC
  • Transient receptor potential protein 12
  • TRP12
  • TrpV4-A

General information

  • TRPV4-A and TRPV4-D are fully processed and reach the plasma membrane where they produce functional channels. [1]
  • TRPV4 shows multiple modes of activation and regulatory sites, enabling it to respond to various stimuli, including osmotic cell swelling, mechanical stress, heat, acidic pH, endogenous ligands, high viscous solutions, and synthetic agonists. [1]
  • TRPV4-A and TRPV4-D proteins displayed a robust cell surface expression. [1]

Links to other resources

UniProt Q9HBA0-1
Ensembl ENST00000418703

Subunit information

Isoform 1

Sequence 
MADSSEGPR AGPGEVAEL PGDESGTPG 
GEAFPLSSL ANLFEGEDG SLSPSPADA 
SRPAGPGDG RPNLRMKFQ GAFRKGVPN 
PIDLLESTL YESSVVPGP KKAPMDSLF 
DYGTYRHHS SDNKRWRKK IIEKQPQSP 
KAPAPQPPP ILKVFNRPI LFDIVSRGS 
TADLDGLLP FLLTHKKRL TDEEFREPS 
TGKTCLPKA LLNLSNGRN DTIPVLLDI 
AERTGNMRE FINSPFRDI YYRGQTALH 
IAIERRCKH YVELLVAQG ADVHAQARG 
RFFQPKDEG GYFYFGELP LSLAACTNQ 
PHIVNYLTE NPHKKADMR RQDSRGNTV 
LHALVAIAD NTRENTKFV TKMYDLLLL 
KCARLFPDS NLEAVLNND GLSPLMMAA 
KTGKIGIFQ HIIRREVTD EDTRHLSRK 
FKDWAYGPV YSSLYDLSS LDTCGEEAS 
VLEILVYNS KIENRHEML AVEPINELL 
RDKWRKFGA VSFYINVVS YLCAMVIFT 
LTAYYQPLE GTPPYPYRT TVDYLRLAG 
EVITLFTGV LFFFTNIKD LFMKKCPGV 
NSLFIDGSF QLLYFIYSV LVIVSAALY 
LAGIEAYLA VMVFALVLG WMNALYFTR 
GLKLTGTYS IMIQKILFK DLFRFLLVY 
LLFMIGYAS ALVSLLNPC ANMKVCNED 
QTNCTVPTY PSCRDSETF STFLLDLFK 
LTIGMGDLE MLSSTKYPV VFIILLVTY 
IILTFVLLL NMLIALMGE TVGQVSKES 
KHIWKLQWA TTILDIERS FPVFLRKAF 
RSGEMVTVG KSSDGTPDR RWCFRVDEV 
NWSHWNQNL GIINEDPGK NETYQYYGF 
SHTVGRLRR DRWSSVVPR VVELNKNSN 
PDEVVVPLD SMGNPRCDG HQQGYPRKW 
RTDDAPL

Binding hormones

    Anatomical structures with this receptor

    • continuous_vascular_endothelial_cell_of_blood_vessels_and_lymphatics

      Induced phenotypes

      • regulation of cell communication
        • EETs are biologically important signal transduction molecules that have been implicated in numerous biological processes including communication between endothelial and vascular smooth muscle cells. [2]
        • TRPV4 has a potential role in the regulation of vascular homeostasis and in the regulation of endothelial cell signaling. [3]
        • TRPV4 is a possible epoxyeicosatrienoic acid(EET)-regulated Ca2+ entry channel in mouse aorta endothelium. [3]

    • smooth_muscle

      Induced phenotypes

      • positive regulation of smooth muscle contraction
        • Functional TRPV4 is expressed in human airway smooth muscle cells and may act as an osmolarity sensor in the airway. [4]
        • Activation of TRPV4 on airway smooth muscle cells increases intracellular Ca2+ level, which may induce smooth muscle contraction. [4]
        • TRPV4 is the most plausible channel involved in hypotonic stimulation-induced airway contraction. [4]

    • keratinocyte

      Induced phenotypes

      • thermoception
        • TRPV4 is essential for the desensitizing warmth-evoked current responses. [5]
        • Keratinocytes can detect warm temperatures by mechanisms that are apparently TRPV4-dependent. [5]

    • dorsal_root_ganglion

      Induced phenotypes

      • multicellular organismal water homeostasis
        • Blockers of TRPV4 Attenuate the Hypotonic Stimulus-Induced [Ca2+]i Increase in Nociceptors, this suppoprt the involvement of TRPV4 in nociceptor osmosensitivity.
        • TRPV4 is a transducer of osmotic stimulation in primary afferent nociceptive nerve fibers, and a transducer involved in inflammatory pain.

    • epithelial_cell

      Induced phenotypes

      • negative regulation of cell volume
        • TRPV4 channel is the only pathway mediating the swelling-activated Ca2+ entry required to achieve a full RVD in human tracheal epithelial cells. [6]
        • Human airway epithelia show a typical Ca2+-dependent cell regularoty volume decrease (RVD) under hypotonic conditions. [7]
        • Impaired RVD response in Cystic Fibrosis airway epithelia is caused by a misregulation of TRPV4, suggesting that hypotonic activation of TRPV4 channels is cystic fibrosis transmembrane conductance regulator-dependent. [6]
    Reference