Florian Sure

Erlangen, BY, Germany

Last Updated: 09/26/2026

Save publications for later

Sign Up

Not sure about your diagnosis?

Check Your Symptoms

Found 11 publications

Distinct functional roles of the GRIP domains in α-, β-, γ- and δ-ENaC.

Distinct functional roles of the GRIP domains in α-, β-, γ- and δ-ENaC.

Journal: The Journal of biological chemistry

Published: November 30, 2025

Acute activation of human epithelial sodium channel (ENaC) by serum and glucocorticoid inducible kinase 1 (SGK1) requires prior cleavage of the channel's γ-subunit at its proximal cleavage site.

Acute activation of human epithelial sodium channel (ENaC) by serum and glucocorticoid inducible kinase 1 (SGK1) requires prior cleavage of the channel's γ-subunit at its proximal cleavage site.

Journal: Pflugers Archiv : European journal of physiology

Published: March 14, 2025

Automated patch-clamp recordings for detecting activators and inhibitors of the epithelial sodium channel (ENaC).

Automated patch-clamp recordings for detecting activators and inhibitors of the epithelial sodium channel (ENaC).

Journal: Pflugers Archiv : European journal of physiology

Published: January 24, 2025

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

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

Journal: Journal of the American Society of Nephrology : JASN

Published: March 25, 2024

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

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

Journal: The Journal of biological chemistry

Published: February 16, 2024

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

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

Journal: The Journal of biological chemistry

Published: September 25, 2023

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

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

Journal: The Journal of biological chemistry

Published: December 23, 2021

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

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

Journal: Pflugers Archiv : European journal of physiology

Published: August 26, 2021

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

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

Journal: Acta physiologica (Oxford, England)

Published: February 27, 2019

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

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

Journal: The Journal of general physiology

Published: November 16, 2018

Aprotinin prevents proteolytic epithelial sodium channel (ENaC) activation and volume retention in nephrotic syndrome.

Aprotinin prevents proteolytic epithelial sodium channel (ENaC) activation and volume retention in nephrotic syndrome.

Journal: Kidney international

Published: March 11, 2017

Showing 1-11 of 11

Last Updated: 09/26/2026