Feedback inhibition of epithelial Na(+) channels in Xenopus oocytes does not require G(0) or G(i2) proteins.

Détails

ID Serval
serval:BIB_93E6BF51F72E
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Feedback inhibition of epithelial Na(+) channels in Xenopus oocytes does not require G(0) or G(i2) proteins.
Périodique
Febs Letters
Auteur(s)
Hübner M., Schreiber R., Boucherot A., Sanchez-Perez A., Poronnik P., Cook D.I., Kunzelmann K.
ISSN
0014-5793 (Print)
ISSN-L
0014-5793
Statut éditorial
Publié
Date de publication
1999
Peer-reviewed
Oui
Volume
459
Numéro
3
Pages
443-447
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't Publication Status: ppublish
Résumé
Regulation of amiloride-sensitive epithelial Na(+) channels (ENaC) is a prerequisite for coordination of electrolyte transport in epithelia. Downregulation of Na(+) conductance occurs when the intracellular Na(+) concentration is increased during reabsorption of electrolytes, known as feedback inhibition. Recent studies have demonstrated the involvement of alphaG(0) and alphaG(i2) proteins in the feedback control of ENaC in mouse salivary duct cells. In this report, we demonstrate that Na(+) feedback inhibition is also present in Xenopus oocytes after expression of rat alpha,beta, gamma-ENaC. Interfering with intracellular alphaG(0) or alphaG(i2) signaling by coexpression of either constitutively active alphaG(0)/alphaG(i2) or dominant negative alphaG(0)/alphaG(i2) and by coinjecting sense or antisense oligonucleotides for alphaG(0) had no impact on Na(+) feedback. Moreover, no evidence for involvement of the intracellular G protein cascade was found in experiments in which a regulator of G protein signaling (RGS3) or beta-adrenergic receptor kinase (betaARK) was coexpressed together with alpha,beta, gamma-ENaC. Although some experiments suggest the presence of an intracellular Na(+) receptor, we may conclude that Na(+) feedback in Xenopus oocytes is different from that described for salivary duct cells in that it does not require G protein signaling.
Mots-clé
Animals, Epithelium/metabolism, Feedback, GTP-Binding Protein alpha Subunit, Gi2, GTP-Binding Protein alpha Subunits, Gi-Go, Heterotrimeric GTP-Binding Proteins/metabolism, Mice, Oocytes/metabolism, Proto-Oncogene Proteins/metabolism, Rats, Sodium/metabolism, Sodium Channels/metabolism, Xenopus laevis
Pubmed
Web of science
Création de la notice
05/08/2012 12:24
Dernière modification de la notice
03/03/2018 19:36
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