Nedd4-2 and the regulation of epithelial sodium transport.

Details

Ressource 1Download: BIB_CBB290F20218.P001.pdf (1084.12 [Ko])
State: Public
Version: author
Serval ID
serval:BIB_CBB290F20218
Type
Article: article from journal or magazin.
Publication sub-type
Review (review): journal as complete as possible of one specific subject, written based on exhaustive analyses from published work.
Collection
Publications
Institution
Title
Nedd4-2 and the regulation of epithelial sodium transport.
Journal
Frontiers In Physiology
Author(s)
Rotin D., Staub O.
ISSN
1664-042X (Electronic)
ISSN-L
1664-042X
Publication state
Published
Issued date
2012
Peer-reviewed
Oui
Volume
3
Pages
212
Language
english
Abstract
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
Yes
Create date
19/01/2013 12:02
Last modification date
20/10/2020 10:12
Usage data