Liddle's syndrome: a novel mouse Nedd4 isoform regulates the activity of the epithelial Na(+) channel

Détails

ID Serval
serval:BIB_9A5E04EB4BFC
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Liddle's syndrome: a novel mouse Nedd4 isoform regulates the activity of the epithelial Na(+) channel
Périodique
Kidney International
Auteur⸱e⸱s
Kamynina  E., Debonneville  C., Hirt  R. P., Staub  O.
ISSN
0085-2538 (Print)
Statut éditorial
Publié
Date de publication
08/2001
Volume
60
Numéro
2
Pages
466-71
Notes
Journal Article Research Support, Non-U.S. Gov't Review --- Old month value: Aug
Résumé
The epithelial Na(+) channel (ENaC), which plays an essential role in renal Na(+) handling, is composed of three subunits (alpha beta gamma), each containing a conserved PY motif at the C terminus. In Liddle's syndrome, an inherited form of salt-sensitive hypertension, the PY motifs of either beta or gamma ENaC are deleted or modified. We have recently shown that a ubiquitin-protein ligase Nedd4 binds via its WW domains to these PY motifs on ENaC, that ENaC is regulated by ubiquitination, and that Xenopus laevis Nedd4 (xNedd4) controls the cell surface pool of ENaC when coexpressed in Xenopus oocytes. Interestingly, Na(+) transporting cells, derived from mouse cortical collecting duct, express two different Nedd4 isoforms, which we have termed mNedd4-1 and mNedd4-2. Only mNedd4-2, which is orthologous to xNedd4, but not mNedd4-1, is able to regulate ENaC activity, and this property correlates with the capability to bind to the ENaC complex. Hence, Nedd4-2 may be encoded by a novel susceptibility gene for arterial hypertension.
Mots-clé
Animals Calcium-Binding Proteins/chemistry/*genetics/*metabolism Epithelial Sodium Channel Humans Hypertension/*metabolism Isomerism Kidney/*metabolism Ligases/chemistry/*genetics/*metabolism Mice Sodium Channels/*metabolism *Ubiquitin-Protein Ligases
Pubmed
Web of science
Open Access
Oui
Création de la notice
24/01/2008 13:03
Dernière modification de la notice
20/08/2019 15:01
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