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Lessons from Mouse Mutants of Epithelial Sodium Channel and Its Regulatory Proteins

Edith Hummler^* and Volker Vallon

^* Département de Pharmacologie et de Toxicologie, Université de Lausanne, Lausanne, Switzerland; and Departments of Medicine and Pharmacology, University of California San Diego and Veterans Administration Medical Center, San Diego, California

Address correspondence to: Dr. Edith Hummler, Département de Pharmacologie et de Toxicologie, Rue du Bugnon 27, CH-1005 Lausanne, Switzerland. Phone: +41-21-692-5357; Fax: +41-21-692-5355; E-mail: edith.hummler{at}unil.ch; or Dr. Volker Vallon, Division of Nephrology/Hypertension, Departments of Medicine and Pharmacology, University of California, San Diego, 3350 La Jolla Village Drive (9151), San Diego, CA 92161. Phone: 858-552-8585; Fax: 858-642-1438; E-mail: vvallon{at}ucsd.edu

The use of gene-modified mouse models allows the experimental in vivo analysis of specific gene defects at the level of target cells. With respect to the epithelial sodium channel and some of its regulatory proteins, gene-modified models that control gene defects in a time- and tissue-dependent conditional or constitutive manner have been generated. The combination of molecular and physiologic approaches in these mouse models increases the understanding of the complex regulation and the cell signaling cascades involved in Na⁺ transport in target cells and may ultimately provide new insights into the pathophysiology of renal Na⁺ retention and BP regulation. This review summarizes and discusses the gene-targeting approaches that have been applied to the epithelial sodium channel and its regulatory proteins.

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Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673