ArticleeLife2019
A hydrophobic gate in the inner pore helix is the major determinant of inactivation in mechanosensitive Piezo channels.
Article in eLife, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
What it found
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Who cites it
53 citing papers in PubMed, 88 citations in OpenAlex.
- Piezo channels in physical field therapy: From mechanotransduction mechanisms to bioelectromagnetic modulation and biomedical applications.Mechanobiology in medicine · 2026Review
- State-dependent binding of the wedge domain controls inactivation of the mechanosensitive ion channel PIEZO1.Nature communications · 2026Article
- Article
- A two-step clockwork mechanism opens a proteo-lipidic pore in PIEZO2.Nature chemical biology · 2026Article
- Lipid composition and mechanical force underlie multi-modal regulation of Piezo1 gating.Science advances · 2026Article
- The Piezo1-Ca2+-PI3k/Akt signaling axis as a context-dependent mechanotransduction node during skin wound healing.iScience · 2026Review
- Piezo channels in tumors.Journal of cancer research and clinical oncology · 2026Review
- Velocity sensitivity of mechanotransduction in the afferent terminal underlies vibration detection in the Pacinian corpuscle.Nature communications · 2026Article
- Structures of invertebrate PEZO-1 isoforms with a compact architecture and a dispensable pore-distal N-terminal blade.Cell reports · 2026Article
- PIEZO1 in Immune Cells: From Force to Function.Results and problems in cell differentiation · 2026Review
- PIEZO Force Sensing in Vascular Biology: An Explosion of New Knowledge, Concepts and Opportunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Functional evidence for early origin of tactile acuity in the vertebrate somatosensory system.Current biology : CB · 2025Article
- The fetal hydrops-associated single-residue mutation L322P disrupts mechanical but not chemical activation of the PIEZO1 ion channel.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Article
- Mechanical memory of excitable cells induced by mechanosensitive channel inactivation.Biophysical journal · 2025Article
- Article
- The inner core enables transient touch detection in the Pacinian corpuscle.Science advances · 2025Article
- The activation thresholds and inactivation kinetics of poking-evoked PIEZO1 and PIEZO2 currents are sensitive to subtle variations in mechanical stimulation parameters.Channels (Austin, Tex.) · 2024Article
- Mechanisms of mechanotransduction and physiological roles of PIEZO channels.Nature reviews. Molecular cell biology · 2024Review
- Chemical mapping of the surface interactome of PIEZO1 identifies CADM1 as a modulator of channel inactivation.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Piezo1 and Piezo2 belong to a family of mechanically-activated ion channels implicated in a wide range of physiological processes. Mechanical stimulation triggers Piezo channels to open, but their characteristic fast inactivation process results in rapid closure. Several disease-causing mutations in Piezo1 alter the rate of inactivation, highlighting the importance of inactivation to the normal function of this channel. However, despite the structural identification of two physical constrictions within the closed pore, the mechanism of inactivation remains unknown. Here we identify a functionally conserved inactivation gate in the pore-lining inner helix of mouse Piezo1 and Piezo2 that is distinct from the two constrictions. We show that this gate controls the majority of Piezo1 inactivation via a hydrophobic mechanism and that one of the physical constrictions acts as a secondary gate. Our results suggest that, unlike other rapidly inactivating ion channels, a hydrophobic barrier gives rise to fast inactivation in Piezo channels.
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Registered trials
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.