ArticleThe Journal of general physiology2011
Voltage- and temperature-dependent activation of TRPV3 channels is potentiated by receptor-mediated PI(4,5)P2 hydrolysis.
Article in The Journal of general physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 99 citations in OpenAlex.
- Orally available Colivin traps TRPV3 in an inactive state and suppresses intestinal inflammation.The EMBO journal · 2026Article
- PIP2 regulation of TRPV4 channels: Binding sites and dynamic coupling.Biophysical journal · 2025Article
- CaBiomedicines · 2025Review
- TRP Channels in Stroke.Neuroscience bulletin · 2024Review
- TRPV3 activation by different agonists accompanied by lipid dissociation from the vanilloid site.Science advances · 2024Article
- The Effect of Osthole on Transient Receptor Potential Channels: A Possible Alternative Therapy for Atopic Dermatitis.Journal of inflammation research · 2024Article
- Functions of TRPs in retinal tissue in physiological and pathological conditions.Frontiers in molecular neuroscience · 2024Review
- Novel Insights into the Role of Keratinocytes-Expressed TRPV3 in the Skin.Biomolecules · 2023Review
- Regulation of ThermoTRP Channels by PIP2 and Cholesterol.Advances in experimental medicine and biology · 2023Article
- Beyond CaPflugers Archiv : European journal of physiology · 2021Article
- Structural mechanism of heat-induced opening of a temperature-sensitive TRP channel.Nature structural & molecular biology · 2021Article
- Structural basis for promiscuous action of monoterpenes on TRP channels.Communications biology · 2021Article
- Deficiency of Inositol Monophosphatase Activity Decreases Phosphoinositide Lipids and Enhances TRPV1 FunctionThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Th2 Modulation of Transient Receptor Potential Channels: An Unmet Therapeutic Intervention for Atopic Dermatitis.Frontiers in immunology · 2021Review
- TRPV3 expression and purification for structure determination by Cryo-EM.Methods in enzymology · 2021Article
- PIPProceedings of the National Academy of Sciences of the United States of America · 2020Review
- PAR2 Mediates Itch via TRPV3 Signaling in Keratinocytes.The Journal of investigative dermatology · 2020Observational
- The structure of lipid nanodisc-reconstituted TRPV3 reveals the gating mechanism.Nature structural & molecular biology · 2020Article
- Gating of human TRPV3 in a lipid bilayer.Nature structural & molecular biology · 2020Article
- The TRPV3 channel of the bovine rumen: localization and functional characterization of a protein relevant for ruminal ammonia transport.Pflugers Archiv : European journal of physiology · 2020Article
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
TRPV3 is a thermosensitive channel that is robustly expressed in skin keratinocytes and activated by innocuous thermal heating, membrane depolarization, and chemical agonists such as 2-aminoethyoxy diphenylborinate, carvacrol, and camphor. TRPV3 modulates sensory thermotransduction, hair growth, and susceptibility to dermatitis in rodents, but the molecular mechanisms responsible for controlling TRPV3 channel activity in keratinocytes remain elusive. We show here that receptor-mediated breakdown of the membrane lipid phosphatidylinositol (4,5) bisphosphate (PI(4,5)P(2)) regulates the activity of both native TRPV3 channels in primary human skin keratinocytes and expressed TRPV3 in a HEK-293-derived cell line stably expressing muscarinic M(1)-type acetylcholine receptors. Stimulation of PI(4,5)P(2) hydrolysis or pharmacological inhibition of PI 4 kinase to block PI(4,5)P(2) synthesis potentiates TRPV3 currents by causing a negative shift in the voltage dependence of channel opening, increasing the proportion of voltage-independent current and causing thermal activation to occur at cooler temperatures. The activity of single TRPV3 channels in excised patches is potentiated by PI(4,5)P(2) depletion and selectively decreased by PI(4,5)P(2) compared with related phosphatidylinositol phosphates. Neutralizing mutations of basic residues in the TRP domain abrogate the effect of PI(4,5)P(2) on channel function, suggesting that PI(4,5)P(2) directly interacts with a specific protein motif to reduce TRPV3 channel open probability. PI(4,5)P(2)-dependent modulation of TRPV3 activity represents an attractive mechanism for acute regulation of keratinocyte signaling cascades that control cell proliferation and the release of autocrine and paracrine factors.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.