Inactivation of sodium-transporting proteins in the kidney

Details

Serval ID
serval:BIB_015851474B45
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
Inactivation of sodium-transporting proteins in the kidney
Journal
Pflügers Archiv (European Journal of Physiology)
Author(s)
Rubera I., Rossier B. C., Hummler E.
ISSN
0031-6768
Publication state
Published
Issued date
01/2003
Peer-reviewed
Oui
Volume
445
Number
4
Pages
463-69
Notes
Journal Article Research Support, Non-U.S. Gov't Review --- Old month value: Jan
Abstract
The kidney plays a dominant role in maintaining sodium homeostasis. The control of a nearly constant electrolyte composition and osmotic pressure in the extracellular fluids is achieved by well-regulated vectorial salt and water transport processes. Derangement in function of Na(+) transporting proteins is likely to be responsible for a number of clinical disorders of fluid and electrolyte homeostasis. The identification of the genes implicated in sodium reabsorption in the kidney not only allows a detailed analysis of regulation and function of these proteins in vitro but also the generation of genetically engineered mice that constitute valuable mouse models for human diseases. Our review will focus on recent strategies for generating nephron segment-specific knock-outs for the main apical renal Na(+) transporters and channels.
Keywords
Animals Biological Transport Disease Models, Animal Humans Kidney/*metabolism Kidney Diseases/*metabolism Mice Mice, Knockout Sodium/*metabolism
Pubmed
Web of science
Create date
24/01/2008 13:00
Last modification date
20/08/2019 12:23
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