Nedd4-2 and the regulation of epithelial sodium transport.

Détails

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Etat: Serval
Version: de l'auteur
ID Serval
serval:BIB_CBB290F20218
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
Nedd4-2 and the regulation of epithelial sodium transport.
Périodique
Frontiers In Physiology
Auteur(s)
Rotin D., Staub O.
ISSN
1664-042X (Electronic)
ISSN-L
1664-042X
Statut éditorial
Publié
Date de publication
2012
Peer-reviewed
Oui
Volume
3
Pages
212
Langue
anglais
Résumé
Nedd4-2 is a ubiquitin ligase previously demonstrated to regulate endocytosis and lysosomal degradation of the epithelial Na(+) channel (ENaC) and other ion channels and transporters. Recent studies using Nedd4-2 knockout mice specifically in kidney or lung epithelia has revealed a critical role for this E3 ubiquitin ligase in regulating salt and fluid transport in these tissues/organs and in maintaining homeostasis of body blood pressure. Interestingly, the primary targets for Nedd4-2 may differ in these two organs: in the lung Nedd4-2 targets ENaC, and loss of Nedd4-2 leads to excessive ENaC function and to cystic fibrosis - like lung disease, whereas in the kidney, Nedd4-2 targets the Na(+)/Cl(-) cotransporter (NCC) in addition to targeting ENaC. In accord, loss of Nedd4-2 in the distal nephron leads to increased NCC abundance and function. The aldosterone-responsive kinase, Sgk1, appears to be involved in the regulation of NCC by Nedd4-2 in the kidney, similar to its regulation of ENaC. Collectively, these new findings underscore the physiological importance of Nedd4-2 in regulating epithelial salt and fluid transport and balance.
Pubmed
Open Access
Oui
Création de la notice
19/01/2013 13:02
Dernière modification de la notice
09/05/2019 1:18
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