ArticleThe Journal of physiology2002
An external site controls closing of the epithelial Na+ channel ENaC.
Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 71 citations in OpenAlex.
- Analysis of sodium self-inhibition of the epithelial sodium channel (ENaC) using classical and medium-throughput automated two-electrode voltage-clamp recordings.Pflugers Archiv : European journal of physiology · 2026Article
- Guinea pig δβγ-ENaC is locked in an open state and uncoupled from regulation by proteases.Pflugers Archiv : European journal of physiology · 2026Article
- SECS, drugs, and Rac1&Rho: regulation of EnNaC in vascular endothelial cells.Pflugers Archiv : European journal of physiology · 2025Article
- Ion channel function of polycystin-2/polycystin-1 heteromer revealed by structure-guided mutagenesis.FEBS letters · 2025Article
- Transmembrane serine protease 2 (TMPRSS2) proteolytically activates the epithelial sodium channel (ENaC) by cleaving the channel's γ-subunit.The Journal of biological chemistry · 2022Article
- The M1 and pre-M1 segments contribute differently to ion selectivity in ASICs and ENaCs.The Journal of general physiology · 2021Article
- Paraoxonase 3 functions as a chaperone to decrease functional expression of the epithelial sodium channel.The Journal of biological chemistry · 2020Article
- Shear force sensing of epithelial NaProceedings of the National Academy of Sciences of the United States of America · 2020Article
- Thumb domains of the three epithelial NaThe Journal of biological chemistry · 2018Article
- The N terminus of α-ENaC mediates ENaC cleavage and activation by furin.The Journal of general physiology · 2018Article
- Pore-lining residues of MEC-4 and MEC-10 channel subunits tune theThe Journal of biological chemistry · 2018Article
- The Epithelial Sodium Channel Is a Modifier of the Long-Term Nonprogressive Phenotype Associated with F508del CFTR Mutations.American journal of respiratory cell and molecular biology · 2017Article
- TNF Lectin-Like Domain Restores Epithelial Sodium Channel Function in Frameshift Mutants Associated with Pseudohypoaldosteronism Type 1B.Frontiers in immunology · 2017Article
- Endogenous Isoquinoline Alkaloids Agonists of Acid-Sensing Ion Channel Type 3.Frontiers in molecular neuroscience · 2017Article
- Activation of the Human Epithelial Sodium Channel (ENaC) by Bile Acids Involves the Degenerin Site.The Journal of biological chemistry · 2016Article
- Review
- Unbiased View of Synaptic and Neuronal Gene Complement in Ctenophores: Are There Pan-neuronal and Pan-synaptic Genes across Metazoa?Integrative and comparative biology · 2015Article
- Gamma subunit second transmembrane domain contributes to epithelial sodium channel gating and amiloride block.American journal of physiology. Renal physiology · 2013Article
- Benzamil sensitive ion channels contribute to volume regulation in canine chondrocytes.British journal of pharmacology · 2013Article
- The genetic architecture of degenerin/epithelial sodium channels in Drosophila.G3 (Bethesda, Md.) · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Members of the ENaC/degenerin family of ion channels include the epithelial sodium channel (ENaC), acid-sensing ion channels (ASICs) and the nematode Caenorhabditis elegans degenerins. These channels are activated by a variety of stimuli such as ligands (ASICs) and mechanical forces (degenerins), or otherwise are constitutively active (ENaC). Despite their functional heterogeneity, these channels might share common basic mechanisms for gating. Mutations of a conserved residue in the extracellular loop, namely the 'degenerin site' activate all members of the ENaC/degenerin family. Chemical modification of a cysteine introduced in the degenerin site of rat ENaC (betaS518C) by the sulfhydryl reagents MTSET or MTSEA, results in a approximately 3-fold increase in the open probability. This effect is due to an 8-fold shortening of channel closed times and an increase in the number of long openings. In contrast to the intracellular gating domain in the N-terminus which is critical for channel opening, the intact extracellular degenerin site is necessary for normal channel closing, as illustrated by our observation that modification of betaS518C destabilises the channel closed state. The modification by the sulfhydryl reagents is state- and size-dependent consistent with a conformational change of the degenerin site during channel opening and closing. We propose that the intracellular and extracellular modulatory sites act on a common channel gate and control the activity of ENaC at the cell surface.
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