ArticleThe Journal of biological chemistry2016
Activation of the Human Epithelial Sodium Channel (ENaC) by Bile Acids Involves the Degenerin Site.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
- Article
- Epithelial Na + Channel Activation after Bile Duct Ligation with Mineralocorticoid Receptor Blockade.Journal of the American Society of Nephrology : JASN · 2024Article
- Epithelial NaComprehensive Physiology · 2024Review
- The role of the farnesoid X receptor in kidney health and disease: a potential therapeutic target in kidney diseases.Experimental & molecular medicine · 2023Review
- Bile acid receptors and renal regulation of water homeostasis.Frontiers in physiology · 2023Review
- Bile acids regulate the epithelial NaThe Journal of physiology · 2022Article
- 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
- Bile acids and salt-sensitive hypertension: a role of the gut-liver axis.American journal of physiology. Heart and circulatory physiology · 2022Review
- Contributions of bile acids to gastrointestinal physiology as receptor agonists and modifiers of ion channels.American journal of physiology. Gastrointestinal and liver physiology · 2022Article
- Zymogen-locked mutant prostasin (Prss8) leads to incomplete proteolytic activation of the epithelial sodium channel (ENaC) and severely compromises triamterene tolerance in mice.Acta physiologica (Oxford, England) · 2021Article
- Murine epithelial sodium (NaThe Journal of biological chemistry · 2019Article
- The Biosynthesis, Signaling, and Neurological Functions of Bile Acids.Biomolecules · 2019Review
- Bile acids inhibit human purinergic receptor P2X4 in a heterologous expression system.The Journal of general physiology · 2019Article
- Bile acids are potent inhibitors of rat P2X2 receptors.Purinergic signalling · 2019Article
- Comparative electrophysiological analysis of the bile acid-sensitive ion channel (BASIC) from different species suggests similar physiological functions.Pflugers Archiv : European journal of physiology · 2019Article
- The degenerin region of the human bile acid-sensitive ion channel (BASIC) is involved in channel inhibition by calcium and activation by bile acids.Pflugers Archiv : European journal of physiology · 2018Article
- Modulation of DEG/ENaCs by Amphiphiles Suggests Sensitivity to Membrane Alterations.Biophysical journal · 2018Article
- Bile acids potentiate proton-activated currents inPhysiological reports · 2017Article
- A Cytosolic Amphiphilic α-Helix Controls the Activity of the Bile Acid-sensitive Ion Channel (BASIC).The Journal of biological chemistry · 2016Article
- Inhibition of the epithelial sodium channel (ENaC) by connexin 30 involves stimulation of clathrin-mediated endocytosis.The Journal of biological chemistryArticle
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The epithelial sodium channel (ENaC) is a member of the ENaC/degenerin ion channel family, which also includes the bile acid-sensitive ion channel (BASIC). So far little is known about the effects of bile acids on ENaC function. ENaC is probably a heterotrimer consisting of three well characterized subunits (αβγ). In humans, but not in mice and rats, an additional δ-subunit exists. The aim of this study was to investigate the effects of chenodeoxycholic, cholic, and deoxycholic acid in unconjugated (CDCA, CA, and DCA) and tauro-conjugated (t-CDCA, t-CA, t-DCA) form on human ENaC in its αβγ- and δβγ-configuration. We demonstrated that tauro-conjugated bile acids significantly stimulate ENaC in the αβγ- and in the δβγ-configuration. In contrast, non-conjugated bile acids have a robust stimulatory effect only on δβγENaC. Bile acids stimulate ENaC-mediated currents by increasing the open probability of active channels without recruiting additional near-silent channels known to be activated by proteases. Stimulation of ENaC activity by bile acids is accompanied by a significant reduction of the single-channel current amplitude, indicating an interaction of bile acids with a region close to the channel pore. Analysis of the known ASIC1 (acid-sensing ion channel) crystal structure suggested that bile acids may bind to the pore region at the degenerin site of ENaC. Substitution of a single amino acid residue within the degenerin region of βENaC (N521C or N521A) significantly reduced the stimulatory effect of bile acids on ENaC, suggesting that this site is critical for the functional interaction of bile acids with the channel.
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