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J Am Soc Nephrol 11:S129-S134, 2000
© 2000 American Society of Nephrology

Scnn1 Sodium Channel Gene Family in Genetically Engineered Mice

EDITH HUMMLER* and FRIEDRICH BEERMANN{dagger}

* Institut de Pharmacologie et de Toxicologie, Université de Lausanne, Lausanne, Switzerland.
{dagger} Swiss Institute for Experimental Cancer Research, Epalinges, Switzerland.

Correspondence to Dr. Edith Hummler, Institut 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: ehummler{at}pop-server.unil.ch

Abstract. The amiloride-sensitive epithelial sodium channel is the limiting step in salt absorption. In mice, this channel is composed of three subunits ({alpha}, {beta}, and {gamma}), which are encoded by different genes (Scnn1a, Scnn1b, and Scnn1c, respectively). The functions of these genes were recently investigated in transgenic (knockout) experiments, and the absence of any subunit led to perinatal lethality. More defined phenotypes have been obtained by introducing specific mutations or using transgenic rescue experiments. In this report, these approaches are summarized and a current gene-targeting strategy to obtain conditional inactivation of the channel is illustrated. This latter approach will be indispensable for the investigation of channel function in a wide variety of organ systems.






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