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

Details

Serval ID
serval:BIB_03038BE4C295
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
The epithelial sodium channel: activation by membrane-bound serine proteases
Journal
Proceedings of the American Thoracic Society
Author(s)
Rossier  B. C.
ISSN
1546-3222
Publication state
Published
Issued date
2004
Volume
1
Number
1
Pages
4-9
Notes
Journal Article
Research Support, Non-U.S. Gov't
Review
Abstract
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.
Keywords
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
Create date
24/01/2008 14:00
Last modification date
20/08/2019 13:25
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