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Subunit-specific inhibition of inward-rectifier K+ channels by quinidine

Distinct inward-rectifier K+ channel subunits were expressed in Xenopus oocytes and tested for their sensitivity to the channel blocker quinidine. The ‘strong’ inward-rectifier K+ channel IRK1 was inhibited by quinidine with an EC50 of 0.7 mM, while the ‘weak’ reactifier channel ROMK1 was only moder...

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Main Authors: Doi, Tadashi (Author) , Fakler, B. (Author) , Schultz, Jobst-Hendrik (Author) , Ehmke, Heimo (Author) , Brändle, U. (Author) , Zenner, H.-P. (Author) , Süßbrich, H. (Author) , Lang, F. (Author) , Ruppersberg, J.P. (Author) , Busch, A.E. (Author)
Format: Article (Journal)
Language:English
Published: November 20, 1995
In: FEBS letters
Year: 1995, Volume: 375, Issue: 3, Pages: 193-196
ISSN:1873-3468
DOI:10.1016/0014-5793(95)01182-E
Online Access:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1016/0014-5793(95)01182-E
Verlag, lizenzpflichtig, Volltext: https://onlinelibrary.wiley.com/doi/abs/10.1016/0014-5793%2895%2901182-E
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Author Notes:T. Doi, B. Fakler, J.-H. Schultz, H. Ehmke, U. Brändle, H.-P. Zenner, H. Süßbrich, F. Lang, J.P. Ruppersberg, A.E. Busch
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Summary:Distinct inward-rectifier K+ channel subunits were expressed in Xenopus oocytes and tested for their sensitivity to the channel blocker quinidine. The ‘strong’ inward-rectifier K+ channel IRK1 was inhibited by quinidine with an EC50 of 0.7 mM, while the ‘weak’ reactifier channel ROMK1 was only moderately inhibited. ROMK1(N171D)-IRKIC-term chimeric channels, which carry both sites for strong rectification of IRK1 channels (the negatively charged D171 in the second transmembrane domain and the IRK1-C-terminus including E224), displayed strong rectification like IRK1, but showed weak sensitivity to quinidine-like ROMK1, suggesting independence of quinidine binding and rectification mechanisms. Moreover, BIR10 and BIR11, two strong rectifier subunits originally cloned from rat brain, exerted subunit-specific sensitivity to quinidine, being much higher for BIR11. Quinidine blockade of IRK1 was not voltage-dependent, but strongly dependent on the pH in the superfusate. These results strongly suggest a subunit-specific interaction of inward-rectifier K+ channels with neutral quinidine within membrane lipid bilayers.
Item Description:Elektronische Reproduktion der Druck-Ausgabe 9. März 2000
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Physical Description:Online Resource
ISSN:1873-3468
DOI:10.1016/0014-5793(95)01182-E

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