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Targeting zonulin and intestinal epithelial barrier function to prevent onset of arthritis

Nature communications, 2020-04, Vol.11 (1), p.1995-1995, Article 1995

2020

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

Kidney international, 2018-01, Vol.93 (1), p.159-172

2018

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Aldosterone-dependent and -independent regulation of the epithelial sodium channel (ENaC) in mouse distal nephron

American journal of physiology. Renal physiology, 2012-11, Vol.303 (9), p.F1289-F1299

2012

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Plasmin in Nephrotic Urine Activates the Epithelial Sodium Channel

Journal of the American Society of Nephrology, 2009-02, Vol.20 (2), p.299-310

2009

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mTORC2 critically regulates renal potassium handling

The Journal of clinical investigation, 2016-05, Vol.126 (5), p.1773-1782

2016

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Trypsin can activate the epithelial sodium channel (ENaC) in microdissected mouse distal nephron

American journal of physiology. Renal physiology, 2008-10, Vol.295 (4), p.F1052-F1062

2008

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High baseline ROMK activity in the mouse late distal convoluted and early connecting tubule probably contributes to aldosterone-independent K + secretion

American journal of physiology. Renal physiology, 2022-01, Vol.322 (1), p.F42-F54

2022

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Aldosterone responsiveness of the epithelial sodium channel (ENaC) in colon is increased in a mouse model for Liddle's syndrome

The Journal of physiology, 2008-01, Vol.586 (2), p.459-475

2008

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Additional Disruption of the ClC-2 Cl- Channel Does Not Exacerbate the Cystic Fibrosis Phenotype of Cystic Fibrosis Transmembrane Conductance Regulator Mouse Models

The Journal of biological chemistry, 2004-05, Vol.279 (21), p.22276-22283

2004

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Critical role of the mineralocorticoid receptor in aldosterone-dependent and aldosterone-independent regulation of ENaC in the distal nephron

American journal of physiology. Renal physiology, 2021-09, Vol.321 (3), p.F257-F268

2021

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Ubiquitination of renal ENaC subunits in vivo

American journal of physiology. Renal physiology, 2020-05, Vol.318 (5), p.F1113-F1121

2020

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Inhibitors of the proteasome stimulate the epithelial sodium channel (ENaC) through SGK1 and mimic the effect of aldosterone

Pflügers Archiv, 2018-02, Vol.470 (2), p.295-304

2018

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Activation of the Epithelial Sodium Channel (ENaC) by Aldosterone in mCCD cl1 Mouse Renal Cortical Collecting Duct Cells is Dependent on SGK1 and Can be Prevented by Inhibiting Endogenous Proteases

The FASEB journal, 2017-04, Vol.31 (S1)

2017

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In Liddle Syndrome, Epithelial Sodium Channel Is Hyperactive Mainly in the Early Part of the Aldosterone-Sensitive Distal Nephron

Hypertension (Dallas, Tex. 1979), 2016-06, Vol.67 (6), p.1256-1262

2016

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Basolateral PAR-2 receptors mediate KCl secretion and inhibition of Na+ absorption in the mouse distal colon

The Journal of physiology, 2002-02, Vol.539 (1), p.209-222

2002

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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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In mouse kidney endogenous transmembrane serine protease 2 (TMPRSS2) contributes to proteolytic processing and activation of the epithelial sodium channel (ENaC)

Physiology (Bethesda, Md.), 2023-05, Vol.38 (S1)

2023

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Prostaglandin E2 stimulates the epithelial sodium channel (ENaC) in cultured mouse cortical collecting duct cells in an autocrine manner

The Journal of general physiology, 2020-08, Vol.152 (8)

2020

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Norepinephrine stimulates the epithelial Na+ channel in cortical collecting duct cells via α2-adrenoceptors

American journal of physiology. Renal physiology, 2015-03, Vol.308 (5), p.F450-F458

2015

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Aldosterone synthase knockout mouse as a model for sodium‐induced endothelial sodium channel up‐regulation in vascular endothelium

The FASEB journal, 2016-01, Vol.30 (1), p.45-53

2016

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Association of Plasminuria with Overhydration in Patients with CKD

Clinical journal of the American Society of Nephrology, 2016-05, Vol.11 (5), p.761-769

2016

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Basolateral proteinase-activated receptor (PAR-2) induces chloride secretion in M-1 mouse renal cortical collecting duct cells

The Journal of physiology, 1999-11, Vol.521 (1), p.3-17

1999

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Norepinephrine stimulates the epithelial Na + channel in cortical collecting duct cells via α 2 -adrenoceptors

American journal of physiology. Renal physiology, 2015-03, Vol.308 (5), p.F450-F458

2015

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Norepinephrine stimulates the epithelial Na+ channel in cortical collecting duct cells via [alpha]^sub 2^-adrenoceptors

American journal of physiology. Renal physiology, 2015-03, Vol.308 (5), p.F450

2015

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The early part of the aldosterone sensitive distal nephron is the primary site of increased sodium absorption in a mouse model for Liddle’s syndrome (892.25)

The FASEB journal, 2014-04, Vol.28 (S1), p.n/a

2014

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Targeting zonulin and intestinal epithelial barrier function to prevent onset of arthritis

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

Aldosterone-dependent and -independent regulation of the epithelial sodium channel (ENaC) in mouse distal nephron

Plasmin in Nephrotic Urine Activates the Epithelial Sodium Channel

mTORC2 critically regulates renal potassium handling

Trypsin can activate the epithelial sodium channel (ENaC) in microdissected mouse distal nephron

High baseline ROMK activity in the mouse late distal convoluted and early connecting tubule probably contributes to aldosterone-independent K + secretion

Aldosterone responsiveness of the epithelial sodium channel (ENaC) in colon is increased in a mouse model for Liddle's syndrome

Additional Disruption of the ClC-2 Cl- Channel Does Not Exacerbate the Cystic Fibrosis Phenotype of Cystic Fibrosis Transmembrane Conductance Regulator Mouse Models

Critical role of the mineralocorticoid receptor in aldosterone-dependent and aldosterone-independent regulation of ENaC in the distal nephron

Ubiquitination of renal ENaC subunits in vivo

Inhibitors of the proteasome stimulate the epithelial sodium channel (ENaC) through SGK1 and mimic the effect of aldosterone

Activation of the Epithelial Sodium Channel (ENaC) by Aldosterone in mCCD cl1 Mouse Renal Cortical Collecting Duct Cells is Dependent on SGK1 and Can be Prevented by Inhibiting Endogenous Proteases

In Liddle Syndrome, Epithelial Sodium Channel Is Hyperactive Mainly in the Early Part of the Aldosterone-Sensitive Distal Nephron

Basolateral PAR-2 receptors mediate KCl secretion and inhibition of Na+ absorption in the mouse distal colon

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

In mouse kidney endogenous transmembrane serine protease 2 (TMPRSS2) contributes to proteolytic processing and activation of the epithelial sodium channel (ENaC)

Prostaglandin E2 stimulates the epithelial sodium channel (ENaC) in cultured mouse cortical collecting duct cells in an autocrine manner

Norepinephrine stimulates the epithelial Na+ channel in cortical collecting duct cells via α2-adrenoceptors

Aldosterone synthase knockout mouse as a model for sodium‐induced endothelial sodium channel up‐regulation in vascular endothelium

Association of Plasminuria with Overhydration in Patients with CKD

Basolateral proteinase-activated receptor (PAR-2) induces chloride secretion in M-1 mouse renal cortical collecting duct cells

Norepinephrine stimulates the epithelial Na + channel in cortical collecting duct cells via α 2 -adrenoceptors

Norepinephrine stimulates the epithelial Na+ channel in cortical collecting duct cells via [alpha]^sub 2^-adrenoceptors

The early part of the aldosterone sensitive distal nephron is the primary site of increased sodium absorption in a mouse model for Liddle’s syndrome (892.25)

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