Trafficking and cell surface stability of ENaC

Détails

ID Serval
serval:BIB_84F03E4B90E4
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Titre
Trafficking and cell surface stability of ENaC
Périodique
American Journal of Physiology. Renal Physiology
Auteur(s)
Rotin  D., Kanelis  V., Schild  L.
ISSN
0363-6127 (Print)
Statut éditorial
Publié
Date de publication
09/2001
Volume
281
Numéro
3
Pages
F391-9
Notes
Journal Article
Research Support, Non-U.S. Gov't
Review --- Old month value: Sep
Résumé
The epithelial Na(+) channel (ENaC) plays a key role in the regulation of Na(+) and water absorption in several epithelia, including those of the distal nephron, distal colon, and lung. Accordingly, mutations in ENaC leading to reduced or increased channel activity cause human diseases such as pseudohypoaldosteronism type I or Liddle's syndrome, respectively. The gain of ENaC function in Liddle's syndrome is associated with increased activity and stability of the channel at the plasma membrane. Thus understanding the regulation of channel processing and trafficking to and stability at the cell surface is of fundamental importance. This review describes some of the recent advances in our understanding of ENaC trafficking, including the role of glycosylation, ENaC solubility in nonionic detergent, targeting signal(s) and hormones. It also describes the regulation of ENaC stability at the cell surface and the roles of the ubiquitin ligase Nedd4 (and ubiquitination) and clathrin-mediated endocytosis in that regulation.
Mots-clé
Animals Cell Membrane/*physiology Endocytosis Epithelial Cells/*physiology Epithelial Sodium Channel Humans Hyperaldosteronism/physiopathology Kidney/*physiology/physiopathology Protein Conformation Sodium Channels/chemistry/*physiology Syndrome
Pubmed
Web of science
Création de la notice
24/01/2008 13:55
Dernière modification de la notice
03/03/2018 18:55
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