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

Details

Serval ID
serval:BIB_93E6BF51F72E
Type
Article: article from journal or magazin.
Collection
Publications
Title
Feedback inhibition of epithelial Na(+) channels in Xenopus oocytes does not require G(0) or G(i2) proteins.
Journal
Febs Letters
Author(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
Publication state
Published
Issued date
1999
Peer-reviewed
Oui
Volume
459
Number
3
Pages
443-447
Language
english
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't Publication Status: ppublish
Abstract
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.
Keywords
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
Create date
05/08/2012 12:24
Last modification date
20/08/2019 15:56
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