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Epithelial Sodium Channel/Degenerin Family of Ion Channels: A Variety of Functions for a Shared Structure

Epithelial Sodium Channel/Degenerin Family of Ion Channels: A Variety of Functions for a Shared... Abstract The recently discovered epithelial sodium channel (ENaC)/degenerin (DEG) gene family encodes sodium channels involved in various cell functions in metazoans. Subfamilies found in invertebrates or mammals are functionally distinct. The degenerins in Caenorhabditis elegans participate in mechanotransduction in neuronal cells, FaNaC in snails is a ligand-gated channel activated by neuropeptides, and the Drosophila subfamily is expressed in gonads and neurons. In mammals, ENaC mediates Na + transport in epithelia and is essential for sodium homeostasis. The ASIC genes encode proton-gated cation channels in both the central and peripheral nervous system that could be involved in pain transduction. This review summarizes the physiological roles of the different channels belonging to this family, their biophysical and pharmacological characteristics, and the emerging knowledge of their molecular structure. Although functionally different, the ENaC/DEG family members share functional domains that are involved in the control of channel activity and in the formation of the pore. The functional heterogeneity among the members of the ENaC/DEG channel family provides a unique opportunity to address the molecular basis of basic channel functions such as activation by ligands, mechanotransduction, ionic selectivity, or block by pharmacological ligands. Footnotes Address for reprint requests and other correspondence: L. Schild, Institut de Pharmacologie et de Toxicologie, Bugnon 27, Université de Lausanne, CH-1005 Lausanne, Switzerland (E-mail: Laurent.Schild@ipharm.unil.ch ). Copyright © 2002 The American Physiological Society http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Physiological Reviews The American Physiological Society

Epithelial Sodium Channel/Degenerin Family of Ion Channels: A Variety of Functions for a Shared Structure

Physiological Reviews , Volume 82 (3): 735 – Jan 7, 2002

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Publisher
The American Physiological Society
Copyright
Copyright © 2011 the American Physiological Society
ISSN
0031-9333
eISSN
1522-1210
DOI
10.1152/physrev.00007.2002
pmid
12087134
Publisher site
See Article on Publisher Site

Abstract

Abstract The recently discovered epithelial sodium channel (ENaC)/degenerin (DEG) gene family encodes sodium channels involved in various cell functions in metazoans. Subfamilies found in invertebrates or mammals are functionally distinct. The degenerins in Caenorhabditis elegans participate in mechanotransduction in neuronal cells, FaNaC in snails is a ligand-gated channel activated by neuropeptides, and the Drosophila subfamily is expressed in gonads and neurons. In mammals, ENaC mediates Na + transport in epithelia and is essential for sodium homeostasis. The ASIC genes encode proton-gated cation channels in both the central and peripheral nervous system that could be involved in pain transduction. This review summarizes the physiological roles of the different channels belonging to this family, their biophysical and pharmacological characteristics, and the emerging knowledge of their molecular structure. Although functionally different, the ENaC/DEG family members share functional domains that are involved in the control of channel activity and in the formation of the pore. The functional heterogeneity among the members of the ENaC/DEG channel family provides a unique opportunity to address the molecular basis of basic channel functions such as activation by ligands, mechanotransduction, ionic selectivity, or block by pharmacological ligands. Footnotes Address for reprint requests and other correspondence: L. Schild, Institut de Pharmacologie et de Toxicologie, Bugnon 27, Université de Lausanne, CH-1005 Lausanne, Switzerland (E-mail: Laurent.Schild@ipharm.unil.ch ). Copyright © 2002 The American Physiological Society

Journal

Physiological ReviewsThe American Physiological Society

Published: Jan 7, 2002

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