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Inhibition of the epithelial sodium channel (ENaC) by connexin 30 involves stimulation of clathrin-mediated endocytosis

The Journal of biological chemistry, 2021-01, Vol.296, p.100404-100404, Article 100404

2021

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Contributions of bile acids to gastrointestinal physiology as receptor agonists and modifiers of ion channels

American journal of physiology: Gastrointestinal and liver physiology, 2022-02, Vol.322 (2), p.G201-G222

2022

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Disease-associated missense mutations in the pore loop of polycystin-2 alter its ion channel function in a heterologous expression system

The Journal of biological chemistry, 2024-08, Vol.300 (8), p.107574, Article 107574

2024

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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, 2024-04, Vol.300 (4), p.105785-105785, Article 105785

2024

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Bile acids inhibit human purinergic receptor P2X4 in a heterologous expression system

The Journal of general physiology, 2019-06, Vol.151 (6), p.820-833

2019

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Transmembrane serine protease 2 (TMPRSS2) proteolytically activates the epithelial sodium channel (ENaC) by cleaving the channel’s γ-subunit

The Journal of biological chemistry, 2022-06, Vol.298 (6), p.102004-102004, Article 102004

2022

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Activation of the Human Epithelial Sodium Channel (ENaC) by Bile Acids Involves the Degenerin Site

The Journal of biological chemistry, 2016-09, Vol.291 (38), p.19835-19847

2016

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Transmembrane Serine Protease 2 and Proteolytic Activation of the Epithelial Sodium Channel in Mouse Kidney

Journal of the American Society of Nephrology, 2024-10

2024

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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, 2021-05, Vol.232 (1), p.e13640-n/a

2021

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Proteolytic activation of the epithelial sodium channel (ENaC) by factor VII activating protease (FSAP) and its relevance for sodium retention in nephrotic mice

Pflügers Archiv, 2022-02, Vol.474 (2), p.217-229

2022

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Urokinase‐type plasminogen activator (uPA) is not essential for epithelial sodium channel (ENaC)‐mediated sodium retention in experimental nephrotic syndrome

Acta Physiologica, 2019-12, Vol.227 (4), p.e13286-n/a

2019

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A polycystin-2 protein with modified channel properties leads to an increased diameter of renal tubules and to renal cysts

Journal of cell science, 2021-08, Vol.134 (16)

2021

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The degenerin region of the human bile acid-sensitive ion channel (BASIC) is involved in channel inhibition by calcium and activation by bile acids

Pflügers Archiv, 2018-07, Vol.470 (7), p.1087-1102

2018

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Bile acids potentiate proton‐activated currents in Xenopus laevis oocytes expressing human acid‐sensing ion channel (ASIC1a)

Physiological reports, 2017-02, Vol.5 (3), p.np-n/a

2017

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Lipophilic Methanethiosulfonate (MTS) Reagents Inhibit Ion Channel Function of Polycystin-2 With a Gain-of-Function Mutation (F604P): FR-PO266

Journal of the American Society of Nephrology, 2022-11, Vol.33 (11S), p.398-398

2022

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Electrophysiological Characterization of Polycystin-2 Mutants With Disease-Associated Missense Mutations in the Channel's Pore Loop: FR-PO265

Journal of the American Society of Nephrology, 2022-11, Vol.33 (11S), p.398-398

2022

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Activation of the Human Epithelial Sodium Channel (ENaC) by the Peptidomimetic S3969 Involves a Specific Binding Pocket in the Channel’s β-Subunit

Physiology (Bethesda, Md.), 2024-05, Vol.39 (S1)

2024

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Electrophysiological Analysis of a Gain-of-Function Polycystin-1/Polycystin-2 Ion Channel: FR-OR13

Journal of the American Society of Nephrology, 2024-10, Vol.35 (10S)

2024

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Epithelialer Natriumkanal (ENaC) im distalen Nephron: Zentrale Rolle von ENaC für die Na+- und K+-Homöostase

Der Nephrologe, 2022-02, Vol.17 (2), p.119-124

2022

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Application of Mathematical Modeling for Analysis of Experimental Data on Cell Water-Electrolyte Balance

Biophysical journal, 2013-01, Vol.104 (2), p.287a-287a

2013

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Inhibition of the epithelial sodium channel (ENaC) by connexin 30 involves stimulation of clathrin-mediated endocytosis

Contributions of bile acids to gastrointestinal physiology as receptor agonists and modifiers of ion channels

Disease-associated missense mutations in the pore loop of polycystin-2 alter its ion channel function in a heterologous expression system

The small molecule activator S3969 stimulates the epithelial sodium channel by interacting with a specific binding pocket in the channel's β-subunit

Bile acids inhibit human purinergic receptor P2X4 in a heterologous expression system

Transmembrane serine protease 2 (TMPRSS2) proteolytically activates the epithelial sodium channel (ENaC) by cleaving the channel’s γ-subunit

Activation of the Human Epithelial Sodium Channel (ENaC) by Bile Acids Involves the Degenerin Site

Transmembrane Serine Protease 2 and Proteolytic Activation of the Epithelial Sodium Channel in Mouse Kidney

Zymogen‐locked mutant prostasin (Prss8) leads to incomplete proteolytic activation of the epithelial sodium channel (ENaC) and severely compromises triamterene tolerance in mice

Proteolytic activation of the epithelial sodium channel (ENaC) by factor VII activating protease (FSAP) and its relevance for sodium retention in nephrotic mice

Urokinase‐type plasminogen activator (uPA) is not essential for epithelial sodium channel (ENaC)‐mediated sodium retention in experimental nephrotic syndrome

A polycystin-2 protein with modified channel properties leads to an increased diameter of renal tubules and to renal cysts

The degenerin region of the human bile acid-sensitive ion channel (BASIC) is involved in channel inhibition by calcium and activation by bile acids

Bile acids potentiate proton‐activated currents in Xenopus laevis oocytes expressing human acid‐sensing ion channel (ASIC1a)

Lipophilic Methanethiosulfonate (MTS) Reagents Inhibit Ion Channel Function of Polycystin-2 With a Gain-of-Function Mutation (F604P): FR-PO266

Electrophysiological Characterization of Polycystin-2 Mutants With Disease-Associated Missense Mutations in the Channel's Pore Loop: FR-PO265

Activation of the Human Epithelial Sodium Channel (ENaC) by the Peptidomimetic S3969 Involves a Specific Binding Pocket in the Channel’s β-Subunit

Electrophysiological Analysis of a Gain-of-Function Polycystin-1/Polycystin-2 Ion Channel: FR-OR13

Epithelialer Natriumkanal (ENaC) im distalen Nephron: Zentrale Rolle von ENaC für die Na+- und K+-Homöostase

Application of Mathematical Modeling for Analysis of Experimental Data on Cell Water-Electrolyte Balance

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