The epithelial sodium channel: activation by membrane-bound serine proteases

Détails

ID Serval
serval:BIB_03038BE4C295
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
Institution
Titre
The epithelial sodium channel: activation by membrane-bound serine proteases
Périodique
Proceedings of the American Thoracic Society
Auteur(s)
Rossier  B. C.
ISSN
1546-3222
Statut éditorial
Publié
Date de publication
2004
Volume
1
Numéro
1
Pages
4-9
Notes
Journal Article
Research Support, Non-U.S. Gov't
Review
Résumé
The epithelial sodium channel (ENaC) was cloned just 10 years ago. Since that time, the study of human monogenic diseases (pseudohypoaldosteronism type 1 [PHA-1] and Liddle syndrome), as well as mouse models mimicking salt-losing syndromes (PHA-1) or salt-sensitive hypertension (Liddle syndrome), have greatly contributed to our understanding of the function of ENaC in vivo. In this brief review, I will first discuss ENaC as a limiting factor in the control of ionic composition of the extracellular fluid and then, more specifically, the activation of ENaC by membrane-bound serine proteases. Recent in vitro and in vivo experiments indicate that membrane-bound serine proteases (channel activating proteases [CAP-1, -2, or-3]) may be of critical importance in the activation of ENaC in different organs, such as the kidney, the lung or the cochlea.
Mots-clé
Animals Cell Membrane/enzymology Cochlea/metabolism Epithelial Sodium Channel Humans Kidney/metabolism Lung/metabolism Membrane Proteins/*metabolism Serine Endopeptidases/*metabolism Signal Transduction/physiology Sodium Channels/*metabolism
Pubmed
Création de la notice
24/01/2008 13:00
Dernière modification de la notice
20/08/2019 12:25
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