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Andersen,
Diabetic nephropathy is associated with increased urine excretion of proteases plasmin, prostasin and urokinase and activation of amiloride-sensitive current in collecting duct cells.
2015, Pubmed
Andersen,
Diabetic nephropathy is associated with increased urine excretion of proteases plasmin, prostasin and urokinase and activation of amiloride-sensitive current in collecting duct cells.
2015,
Pubmed
Bockenhauer,
Over- or underfill: not all nephrotic states are created equal.
2013,
Pubmed
Buhl,
Urinary plasmin activates collecting duct ENaC current in preeclampsia.
2012,
Pubmed
Buhl,
Plasmin in urine from patients with type 2 diabetes and treatment-resistant hypertension activates ENaC in vitro.
2014,
Pubmed
Carattino,
Prostasin interacts with the epithelial Na+ channel and facilitates cleavage of the γ-subunit by a second protease.
2014,
Pubmed
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Xenbase
Chamney,
A whole-body model to distinguish excess fluid from the hydration of major body tissues.
2007,
Pubmed
Diakov,
Cleavage in the {gamma}-subunit of the epithelial sodium channel (ENaC) plays an important role in the proteolytic activation of near-silent channels.
2008,
Pubmed
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Xenbase
Frindt,
Acute effects of aldosterone on the epithelial Na channel in rat kidney.
2015,
Pubmed
Haerteis,
Plasmin and chymotrypsin have distinct preferences for channel activating cleavage sites in the γ subunit of the human epithelial sodium channel.
2012,
Pubmed
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Xenbase
Haerteis,
An inhibitory peptide derived from the α-subunit of the epithelial sodium channel (ENaC) shows a helical conformation.
2012,
Pubmed
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Xenbase
Haerteis,
Proteolytic activation of the human epithelial sodium channel by trypsin IV and trypsin I involves distinct cleavage sites.
2014,
Pubmed
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Xenbase
Jacquillet,
Protease stimulation of renal sodium reabsorption in vivo by activation of the collecting duct epithelial sodium channel (ENaC).
2013,
Pubmed
Kashlan,
Inhibitory tract traps the epithelial Na+ channel in a low activity conformation.
2012,
Pubmed
Kleyman,
ENaC at the cutting edge: regulation of epithelial sodium channels by proteases.
2009,
Pubmed
Luchner,
Improvement of the cardiac marker N-terminal-pro brain natriuretic peptide through adjustment for renal function: a stratified multicenter trial.
2010,
Pubmed
Moissl,
Body fluid volume determination via body composition spectroscopy in health and disease.
2006,
Pubmed
Narikiyo,
Regulation of prostasin by aldosterone in the kidney.
2002,
Pubmed
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Xenbase
Navarrete,
Proteomic characterization of serine hydrolase activity and composition in normal urine.
2013,
Pubmed
Oxlund,
Amiloride lowers blood pressure and attenuates urine plasminogen activation in patients with treatment-resistant hypertension.
2014,
Pubmed
Passero,
Plasmin activates epithelial Na+ channels by cleaving the gamma subunit.
2008,
Pubmed
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Xenbase
Patel,
Tissue kallikrein activation of the epithelial Na channel.
2012,
Pubmed
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Xenbase
Rossier,
Activation of the epithelial sodium channel (ENaC) by serine proteases.
2009,
Pubmed
Rossier,
Epithelial sodium channel (ENaC) and the control of blood pressure.
2014,
Pubmed
Svenningsen,
Prostasin-dependent activation of epithelial Na+ channels by low plasmin concentrations.
2009,
Pubmed
Svenningsen,
Plasmin in nephrotic urine activates the epithelial sodium channel.
2009,
Pubmed
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Xenbase
Svenningsen,
Physiological regulation of epithelial sodium channel by proteolysis.
2011,
Pubmed
Svenningsen,
Urinary serine proteases and activation of ENaC in kidney--implications for physiological renal salt handling and hypertensive disorders with albuminuria.
2015,
Pubmed
Vallet,
An epithelial serine protease activates the amiloride-sensitive sodium channel.
1997,
Pubmed
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Xenbase
Vaziri,
Plasma levels and urinary excretion of fibrinolytic and protease inhibitory proteins in nephrotic syndrome.
1994,
Pubmed
Zachar,
The epithelial sodium channel γ-subunit is processed proteolytically in human kidney.
2015,
Pubmed
