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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
