Inactivation of sodium-transporting proteins in the kidney

Détails

ID Serval
serval:BIB_015851474B45
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
Inactivation of sodium-transporting proteins in the kidney
Périodique
Pflügers Archiv (European Journal of Physiology)
Auteur(s)
Rubera I., Rossier B. C., Hummler E.
ISSN
0031-6768
Statut éditorial
Publié
Date de publication
01/2003
Peer-reviewed
Oui
Volume
445
Numéro
4
Pages
463-69
Notes
Journal Article Research Support, Non-U.S. Gov't Review --- Old month value: Jan
Résumé
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.
Mots-clé
Animals Biological Transport Disease Models, Animal Humans Kidney/*metabolism Kidney Diseases/*metabolism Mice Mice, Knockout Sodium/*metabolism
Pubmed
Web of science
Création de la notice
24/01/2008 14:00
Dernière modification de la notice
20/08/2019 13:23
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