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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 (zeige GRIN2A Proteine) 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 (zeige OS9 Proteine) regulates the secretory transport of TRPV4 and appears to protect TRPV4 subunits from the precocious ubiquitination and ER-associated degradation.
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 (zeige EPHB2 Proteine) 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 (zeige CA2 Proteine)+-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 (zeige TRPC6 Proteine) was found in the digital Meissner corpuscles
TRPV4 is essential for human retinal capillary endothelial cell migration and tube formation, and maybe a potential therapeutic target for retinal vascular diseases.
TRPV4 is believed to be a mechanoreceptor in the bladder and is also involved in intercellular connectivity and structural integrity of the epithelium
this study, demonstrates for the first time that calcium exerts an oncogenic action in the stomach through activation of CaSR (zeige CASR Proteine) and TRPV4 channels. Both CaSR (zeige CASR Proteine) and TRPV4 were involved in Ca2 (zeige CA2 Proteine)+-induced proliferation, migration, and invasion of gastric cancer cells through a Ca2 (zeige CA2 Proteine)+/AKT (zeige AKT1 Proteine)/beta-catenin (zeige CTNNB1 Proteine) relay, which occurred only in gastric cancer cells or normal cells overexpressing CaSR (zeige CASR Proteine).
mediates immediate LPS (zeige TLR4 Proteine)-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 (zeige AQP4 Proteine), contributes to the calcium influx into astrocytes and neurons as well as glutamate (zeige GRIN1 Proteine) accumulation during middle cerebral artery occlusion stroke model-associated peri (zeige POSTN Proteine)-infarct depolarizations (PIDs), but that neither channel influences the threshold for PID (zeige MTA2 Proteine) 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.
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 (zeige ATP1A1 Proteine) 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 (zeige CA2 Proteine)+) and intracellular Ca(2 (zeige CA2 Proteine)+) release.
reduced tissue osmolarity, likely following proteoglycan (zeige Vcan Proteine) 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