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Impact of Nedd4 Proteins and Serum and Glucocorticoid-Induced Kinases on Epithelial Na⁺ Transport in the Distal Nephron

Olivier Staub^* and François Verrey

^* Department of Pharmacology and Toxicology, University of Lausanne, Lausanne, Switzerland; and Institute of Physiology, University of Zurich, Zurich, Switzerland

Address correspondence to: Dr. Olivier Staub, Department of Pharmacology & Toxicology, University of Lausanne, Rue du Bugnon 27, 1005 Lausanne, Switzerland. Phone: +41-21-692-5407; Fax: +41-21-692-5355; E-mail: olivier.staub{at}unil.ch or Dr. François Verrey, Institute of Physiology, University of Zurich, Winterthurerstrasse 190, 8057 Zürich, Switzerland. Phone: +41-1-635-50-44/46/11; Fax: +41-1-635-68-14; E-mail: verrey@access.unizh.ch

The precise control of BP occurs via Na⁺ homeostasis and involves the precise regulation of the epithelial Na⁺ channel (ENaC) in the aldosterone-sensitive distal nephron. This has been corroborated by the linkage of mutations in the genes encoding ENaC subunits and Liddle’s syndrome, a heritable form of human hypertension. Mapping of these mutations on ENaC indicated that inactivation of PY motifs is responsible and leads to the proposition that the channel interacts via its PY motifs with the WW domains of the Nedd4/Nedd4-like ubiquitin-protein ligase family. It is now well established that the cell surface expression of ENaC is controlled via ubiquitylation by this protein family and that this ubiquitylation is regulated by the aldosterone-induced protein serum and glucocorticoid induced kinase 1.

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