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TRPP2 and TRPV4 are mechanosensitive channels in the endocardium.Oscillatory flow modulates mechanosensitive klf2a expression through trpv4 and trpp2 during heart valve development.
TRPP2 utilizes TRPV4 to form a mechano- and thermosensitive molecular sensor in the cilium.
Age-dependence of heat-activated seizure susceptibility mimicks the mRNA expression of TRPV4 and glutamate receptors.
TRPV4 present in all sensory organs of adult zebrafish.
Study reports cloning of a zebrafish trpv4 cDNA and assaying its expression during embryogenesis; trpv4 is expressed as maternal mRNA in 4-cell embryos and later zygotic expression is first observed in the forming notochord at the one somite stage.
OS-9 regulates the secretory transport of TRPV4 and appears to protect TRPV4 subunits from the precocious ubiquitination and ER-associated degradation.
TRPV4 variant was found in the family with intermediate skeletal dysplasia. Molecular modeling confirmed the pathogenicity of the unique TRPV4 variant.
5',6'-epoxyeicosatrienoic acid binding pocket was identified on a site formed by residues from the S2-S3 linker, S4 and S4-S5 linker.
Stimulation of TRPV4 releases ATP via Pannexin channels in human pulmonary fibroblasts.
Gain-of-function mutations in KRAS, FGFR1, and TRPV4 are present in 72% of giant cell lesions of the jaw (GCLJ). TRPV4 mutations induce sustained activation of ERK1/2, indicating that their effects converge with that of KRAS and FGFR1 mutations on the activation of the MAPK pathway in GCLJ.
expression of TRPV4 and VNUT in normal human gastrointestinal cell derived cell lines
TRPV4 is the temperature-sensitive ion channel of human sperm.
TRPV4 might be a target for the maintenance of the intestinal epithelial barrier.
TRPV4 is expressed in skin keratinocytes and plays a role in inflammation has increased expression after irradiation of human epidermal keratinocytes HaCaT cells
TRPV4 glycosylation and channel activity are diminished in human ADPKD cells compared with NHK cells.
Wildtype and mutant TRPV4 channels were expressed in human coronary artery endothelial cells (HCAECs). AA-induced TRPV4 activation was blunted in the S824A mutant but was enhanced in the phosphomimetic S824E mutant, whereas the channel activation by the synthetic agonist GSK1016790A was not affected.
TRPV4 mediates Ca(2+) influx and nuclear accumulation of DDX3X in cells exposed to the Zika virus. Targeting of TRPV4 reduces infectivity of dengue, hepatitis C and Zika viruses. Our results highlight the role of TRPV4 in the regulation of DDX3X-dependent control of RNA metabolism and viral infectivity.
Results suggest that transient receptor potential vanilloid 4 (TRPV4) accelerates glioma migration and invasion through the AKT/Rac1 signaling, and TRPV4 might be considered as a potential target for glioma therapy.
study for the first time demonstrated an abnormal TRPV4-related mechanosensitive Ca(2+) signaling in Dilated cardiomyopathy induced-pluripotent stem cells-derived cardiomyocytes.
There is expression of TRPV4 channels on the nerve fibers of human dental pulp. Findings suggest upregulation of TRPV4 expression under inflammatory conditions in the pulp. The upregulation of TRPV4 channels may be associated with the exaggerated response of dental pulp to innocuous mechanical, thermal and osmotic stimuli under inflammatory conditions.
the antitumor effects caused by TRPV4 channel inhibition in hepatocellular carcinoma cell lines might be attributed to the suppression of epithelial-mesenchymal transition process and inactivation of phospho-ERK which induced subsequent cell apoptosis.
Hypothermia-mediated increase in AQP4 surface abundance on human astrocytes, which was blocked using either calmodulin antagonist; TRPV4 antagonist or calcium chelation. A TRPV4 agonist mimicked the effect of hypothermia compared with untreated normothermic astrocytes. Hypothermia increased surface localization of AQP4 in human astrocytes likely through TRPV4 calcium channels and calmodulin activation.
our study suggests a role for compound heterozygosity and loss-of-function as a potential novel disease mechanism for this group of disorders. Profound intellectual disability was also noted in both affected children, suggesting that TRPV4 may be necessary for normal brain development.
Findings indicate that TRPV4 channels function as a critical component of mechano-sensitive, Ca2+-signaling machinery within the trabecular meshwork (TM), and that TRPV4-dependent cytoskeletal remodeling regulates TM stiffness and outflow. Thus, TRPV4 is a potential IOP sensor within the conventional outflow pathway.
These results identify an essential role of TRPV4 in flow shear stress-induced early osteogenic differentiation of human mesenchymal stem cells.
axonal colocalization of TRPV4 and TRPC6 was found in the digital Meissner corpuscles
Outer retinal morphology is unaffected by the ablation of the Trpv4 gene. Selective TRPV4 stimulation of Muller glial cells induces oscillatory calcium signals in adjacent rods. No differences in scotopic or photopic light-evoked signaling in the distal retina were observed in TRPV4-/- eyes, suggesting that TRPV4 signaling in healthy Muller cells does not modulate light-evoked signal transmission at rod/cone synapses.
Results indicate that surgical incision activates the paraventricular hypothalamus and that Trpv1 and Trpv4 might be involved in neuronal activity in the dorsal horn laminae III-IV after surgical incision.
Muscularis macrophages (MMs) expressing the transient receptor potential vanilloid 4 (TRPV4) channel are required to maintain normal gastrointestinal motility. Stimulation of MMs via TRPV4 promotes the release of prostaglandin E2 and elicits colon contraction in a paracrine manner via prostaglandin E receptor signaling in intestinal smooth muscle cells without input from the enteric nervous system.
Data suggest that transient receptor potential vanilloid type 4 channels are not involved in astrocyte volume regulation in situ; however, they play a protective role during the ischemia-induced brain edema formation.
These findings collectively support the concept that Gq-protein-coupled receptor activation functions as a molecular switch to favor capillary TRPV4 activity over Kir2.1 signaling, an observation with potentially profound significance for the control of cerebral blood flow.
Smooth muscle cell Gq protein-coupled receptor stimulation triggers inositol 1,4,5-trisphosphate-dependent activation of endothelial TRPV4 channels to limit vasoconstriction.
Muscarinic stimulation of saliva and tear secretion was down-regulated in TRPV4-deficient mice. Temperature dependence of muscarinic salivation was depended mainly on TRPV4.
STIM1 and TRPV4 act as mechanical transduction channels for osteoclasts during the early and late differentiation stages, respectively.
mediates immediate LPS-induced increases in ciliary beat frequency and the production of bactericidal nitric oxide
that TRPV4 activation results in the proliferation of stem cells in the adult hippocampal dentate gyrus
a role of TRPV4 in skin diseases such as systemic scleroderma.
TRPV4 plays a key role in LL37- driven mast cell activation in rosacea.
High TRPV4 expression is associated with maternal fever-associated birth defects.
Cartilage-specific knockout of TRPV4 decreases age-related osteoarthritis.
TRPV4 was shown to be required for breast cancer cell invasion and transendothelial migration but not growth/proliferation. Knockdown of Trpv4 significantly reduced the number of metastatic nodules in mouse xenografts leaving the size unaffected.
Study found that TRPV4, but not AQP4, contributes to the calcium influx into astrocytes and neurons as well as glutamate accumulation during middle cerebral artery occlusion stroke model-associated peri-infarct depolarizations (PIDs), but that neither channel influences the threshold for PID in the first hours after stroke.
The findings identify a novel role for TRPV4 in regulating macrophage foam cell formation by modulating uptake of oxLDL.
Fluorescence resonance energy transfer experiments showed that FliI-NMMIIA interactions require Ca(2+) influx. We conclude that Ca(2+) influx through the TRPV4 channel regulates FliI-NMMIIA interaction, which in turn enables generation of the cell extensions essential for collagen remodeling
findings also indicate that TRPV4 channels are mechanosensors in neonatal pig preglomerular vascular SMCs and contribute to renal myogenic autoregulation
Data indicate a physiologic function of transient receptor potential vanilloid 4 (TRPV4) in the regulation of blood-cerebrospinal fluid barrier (BCSFB) permeability.
Hyposmotic shock-induced TRPV4 channel activation regulates hemichannel-mediated ATP release and Na-K-ATPase activity in lens epithelium.
The large amounts of transported calcium and the short signaling ways suggest a potentially important role of TRPV4 in many physiological processes.
TRPV4 is present in articular chondrocytes in swine, and chondrocyte response to hypo-osmotic stress is mediated by this channel, which involves both an extracellular Ca(2+) and intracellular Ca(2+) release.
reduced tissue osmolarity, likely following proteoglycan degradation, can increase TRPV4 signalling and enhance pro-inflammatory cytokine production.
TRPV4 channels activity in bovine articular chondrocytes are regulated by obesity-associated mediators.
TRPV4 channels mediate cyclic strain-induced endothelial cell reorientation through integrin-to-integrin signaling.
This gene encodes a member of the OSM9-like transient receptor potential channel (OTRPC) subfamily in the transient receptor potential (TRP) superfamily of ion channels. The encoded protein is a Ca2+-permeable, nonselective cation channel that is thought to be involved in the regulation of systemic osmotic pressure. Mutations in this gene are the cause of spondylometaphyseal and metatropic dysplasia and hereditary motor and sensory neuropathy type IIC. Multiple transcript variants encoding different isoforms have been found for this gene.
transient receptor potential cation channel subfamily V member 4
, transient receptor potential cation channel, subfamily V, member 4
, transient receptor potential cation channel subfamily V member 4-like
, OSM9-like transient receptor potential channel 4
, osm-9-like TRP channel 4
, osmosensitive transient receptor potential channel 4
, transient receptor potential protein 12
, vanilloid receptor-like channel 2
, vanilloid receptor-related osmotically activated channel
, vanilloid receptor-like protein 2
, vanilloid receptor-related osmotically-activated channel
, transient receptor potential cation channel, subfamily 5, member 4
, vanilloid receptor-related osmotically activated channel (Vroac)
, vanilloid receptor-related osmotically activated channel protein