ArticleThe Journal of biological chemistry2009
Extracellular chloride regulates the epithelial sodium channel.
Article in The Journal of biological chemistry, 2009. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
53 citing papers in PubMed, 72 citations in OpenAlex.
- The small molecule activator S3969 stimulates the epithelial sodium channel by interacting with a specific binding pocket in the channel's β-subunit.The Journal of biological chemistry · 2024Article
- Epithelial NaComprehensive Physiology · 2024Review
- A proton-inhibited DEG/ENaC ion channel maintains neuronal ionstasis and promotes neuronal survival under stress.iScience · 2023Article
- Accessibility of ENaC extracellular domain central core residues.The Journal of biological chemistry · 2022Article
- Differential Chloride Secretory Capacity in Transepithelial Ion Transport Properties in Chronic Rhinosinusitis.American journal of rhinology & allergy · 2020Article
- Engineered mutant α-ENaC subunit mRNA delivered by lipid nanoparticles reduces amiloride currents in cystic fibrosis-based cell and mice models.Science advances · 2020Article
- ENaC in Salt-Sensitive Hypertension: Kidney and Beyond.Current hypertension reports · 2020Review
- ClAmerican journal of physiology. Cell physiology · 2020Review
- Regulating ENaC's gate.American journal of physiology. Cell physiology · 2020Review
- New insights regarding epithelial Na+ channel regulation and its role in the kidney, immune system and vasculature.Current opinion in nephrology and hypertension · 2019Review
- Thumb domains of the three epithelial NaThe Journal of biological chemistry · 2018Article
- Epithelial NaAnnual review of physiology · 2018Review
- Divalent cation and chloride ion sites of chicken acid sensing ion channel 1a elucidated by x-ray crystallography.PloS one · 2018Article
- Current-direction/amplitude-dependent single channel gating kinetics of mouse pannexin 1 channel: a new concept for gating kinetics.Scientific reports · 2017Article
- Specific Palmitoyltransferases Associate with and Activate the Epithelial Sodium Channel.The Journal of biological chemistry · 2017Article
- Expression and purification of the alpha subunit of the epithelial sodium channel, ENaC.Protein expression and purification · 2016Article
- The Epithelial Sodium Channel and the Processes of Wound Healing.BioMed research international · 2016Review
- CPT-cGMP Is A New Ligand of Epithelial Sodium Channels.International journal of biological sciences · 2016Review
- Albuterol Improves Alveolar-Capillary Membrane Conductance in Healthy Humans.Clinical medicine insights. Circulatory, respiratory and pulmonary medicine · 2016Article
- Functional Roles of Clusters of Hydrophobic and Polar Residues in the Epithelial Na+ Channel Knuckle Domain.The Journal of biological chemistry · 2015Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The extracellular domain of the epithelial sodium channel ENaC is exposed to a wide range of Cl(-) concentrations in the kidney and in other epithelia. We tested whether Cl(-) alters ENaC activity. In Xenopus oocytes expressing human ENaC, replacement of Cl(-) with SO4(2-), H2PO4(-), or SCN(-) produced a large increase in ENaC current, indicating that extracellular Cl(-) inhibits ENaC. Extracellular Cl(-) also inhibited ENaC in Na+-transporting epithelia. The anion selectivity sequence was SCN(-) < SO4(2-) < H2PO4(-) < F(-) < I(-) < Cl(-) < Br(-). Crystallization of ASIC1a revealed a Cl(-) binding site in the extracellular domain. We found that mutation of corresponding residues in ENaC (alpha(H418A) and beta(R388A)) disrupted the response to Cl(-), suggesting that Cl(-) might regulate ENaC through an analogous binding site. Maneuvers that lock ENaC in an open state (a DEG mutation and trypsin) abolished ENaC regulation by Cl(-). The response to Cl(-) was also modulated by changes in extracellular pH; acidic pH increased and alkaline pH reduced ENaC inhibition by Cl(-). Cl(-) regulated ENaC activity in part through enhanced Na+ self-inhibition, a process by which extracellular Na+ inhibits ENaC. Together, the data indicate that extracellular Cl(-) regulates ENaC activity, providing a potential mechanism by which changes in extracellular Cl(-) might modulate epithelial Na+ absorption.
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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.