Johannes Loffing

A Golgi-associated PDZ domain protein modulates cystic fibrosis transmembrane regulator plasma membrane expression.

Cell-surface expression of the channel activating protease xCAP-1 is required for activation of ENaC in the Xenopus oocyte.

Human cortical distal nephron: distribution of electrolyte and water transport pathways.

Impaired renal Na(+) retention in the sgk1-knockout mouse.

Sodium and calcium transport pathways along the mammalian distal nephron: from rabbit to human.

SGK1: aldosterone-induced relay of Na+ transport regulation in distal kidney nephron cells.

Thiazide-induced hypocalciuria is accompanied by a decreased expression of Ca2+ transport proteins in kidney.

Collecting duct-specific gene inactivation of alphaENaC in the mouse kidney does not impair sodium and potassium balance.

Dysfunction of the epithelial sodium channel expressed in the kidney of a mouse model for Liddle syndrome.

Impaired regulation of renal K+ elimination in the sgk1-knockout mouse.

A naturally occurring human Nedd4-2 variant displays impaired ENaC regulation in Xenopus laevis oocytes.

Loss-of-function mutations of the K(+) channel gene KCNJ2 constitute a rare cause of long QT syndrome.

Altered renal distal tubule structure and renal Na(+) and Ca(2+) handling in a mouse model for Gitelman's syndrome.

Sodium and potassium handling by the aldosterone-sensitive distal nephron: the pivotal role of the distal and connecting tubule.

Paradoxical antidiuretic effect of thiazides in diabetes insipidus: another piece in the puzzle.

Role of Sgk1 in salt and potassium homeostasis.

Mineralocorticoid versus glucocorticoid receptor occupancy mediating aldosterone-stimulated sodium transport in a novel renal cell line.

Characterization of renal interstitial fibroblast-specific protein 1/S100A4-positive cells in healthy and inflamed rodent kidneys.

Enhanced passive Ca2+ reabsorption and reduced Mg2+ channel abundance explains thiazide-induced hypocalciuria and hypomagnesemia.

Sodium retention in rats with liver cirrhosis is associated with increased renal abundance of NaCl cotransporter (NCC).

Aldosterone-induced serum and glucocorticoid-induced kinase 1 expression is accompanied by Nedd4-2 phosphorylation and increased Na+ transport in cortical collecting duct cells.

Progesterone down-regulates the open probability of the amiloride-sensitive epithelial sodium channel via a Nedd4-2-dependent mechanism.

Luminal kidney and intestine SLC6 amino acid transporters of B0AT-cluster and their tissue distribution in Mus musculus.

Functional domains of the epithelial sodium channel.

Tissue kallikrein-deficient mice display a defect in renal tubular calcium absorption.

Hyperaldosteronemia and activation of the epithelial sodium channel are not required for sodium retention in puromycin-induced nephrosis.

Sgk kinases and their role in epithelial transport.

Dietary sodium intake regulates the ubiquitin-protein ligase nedd4-2 in the renal collecting system.

Pendrin regulation in mouse kidney primarily is chloride-dependent.

Replication of segment-specific and intercalated cells in the mouse renal collecting system.

Impairment of sodium balance in mice deficient in renal principal cell mineralocorticoid receptor.

Renal expression of parvalbumin is critical for NaCl handling and response to diuretics.

Mouse model of type II Bartter's syndrome. II. Altered expression of renal sodium- and water-transporting proteins.

Upregulation of apical sodium-chloride cotransporter and basolateral chloride channels is responsible for the maintenance of salt-sensitive hypertension.

Regulated sodium transport in the renal connecting tubule (CNT) via the epithelial sodium channel (ENaC).

Thiazide effects and adverse effects: insights from molecular genetics.

In vivo nuclear translocation of mineralocorticoid and glucocorticoid receptors in rat kidney: differential effect of corticosteroids along the distal tubule.

Decreased ENaC expression compensates the increased NCC activity following inactivation of the kidney-specific isoform of WNK1 and prevents hypertension.

alphaENaC-mediated lithium absorption promotes nephrogenic diabetes insipidus.

Vasopressin-dependent coupling between sodium transport and water flow in a mouse cortical collecting duct cell line.

Inducible renal principal cell-specific mineralocorticoid receptor gene inactivation in mice.

Immunofluorescent localization of the Rab-GAP protein TBC1D4 (AS160) in mouse kidney.

A primary culture of distal convoluted tubules expressing functional thiazide-sensitive NaCl transport.

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

Aldosterone deficiency adversely affects pregnancy outcome in mice.

Low-dose oral sirolimus and the risk of menstrual-cycle disturbances and ovarian cysts: analysis of the randomized controlled SUISSE ADPKD trial.

Parvalbumin: calcium and magnesium buffering in the distal nephron.

Renal tubular NEDD4-2 deficiency causes NCC-mediated salt-dependent hypertension.

Rapid dephosphorylation of the renal sodium chloride cotransporter in response to oral potassium intake in mice.

Mice carrying ubiquitin-specific protease 2 (Usp2) gene inactivation maintain normal sodium balance and blood pressure.

Common noncoding UMOD gene variants induce salt-sensitive hypertension and kidney damage by increasing uromodulin expression.

Protein phosphatase 1 inhibitor-1 deficiency reduces phosphorylation of renal NaCl cotransporter and causes arterial hypotension.

The sodium chloride cotransporter SLC12A3: new roles in sodium, potassium, and blood pressure regulation.

Hydrochlorothiazide attenuates lithium-induced nephrogenic diabetes insipidus independently of the sodium-chloride cotransporter.

Common variants in UMOD associate with urinary uromodulin levels: a meta-analysis.

Sympathetic stimulation of thiazide-sensitive sodium chloride cotransport in the generation of salt-sensitive hypertension.

Mechanisms of renal control of potassium homeostasis in complete aldosterone deficiency.

Gitelman syndrome and glomerular proteinuria: a link between loss of sodium-chloride cotransporter and podocyte dysfunction?

“Deletion of both Rab-GTPase–activating proteins TBC1D1 and TBC1D4 in mice eliminates insulin- and AICAR-stimulated glucose transport [corrected].

Dietary potassium and the renal control of salt balance and blood pressure.

Akt Substrate of 160 kD Regulates Na+,K+-ATPase Trafficking in Response to Energy Depletion and Renal Ischemia.

Deletion of both Rab-GTPase-activating proteins TBC14KO and TBC1D4 in mice eliminates insulin- and AICAR-stimulated glucose transport. Diabetes 2015;64:746-759.

ENaC activity in collecting ducts modulates NCC in cirrhotic mice.

The Rho-GTPase binding protein IQGAP2 is required for the glomerular filtration barrier.

Rab-GAP TBC1D4 (AS160) is dispensable for the renal control of sodium and water homeostasis but regulates GLUT4 in mouse kidney.

An Integrated View of Potassium Homeostasis.

Acetazolamide Attenuates Lithium-Induced Nephrogenic Diabetes Insipidus.

Severe Salt-Losing Syndrome and Hyperkalemia Induced by Adult Nephron-Specific Knockout of the Epithelial Sodium Channel α-Subunit.

Adult nephron-specific MR-deficient mice develop a severe renal PHA-1 phenotype.

The mineralocorticoid receptor (MR) regulates ENaC but not NCC in mice with random MR deletion.

Renal tubular SGK1 deficiency causes impaired K+ excretion via loss of regulation of NEDD4-2/WNK1 and ENaC.

The Authors Reply.

TRPV4 is associated with central rather than nephrogenic osmoregulation.

Extracellular K(+) rapidly controls NaCl cotransporter phosphorylation in the native distal convoluted tubule by Cl(-) -dependent and independent mechanisms.