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. 1999 Aug 1;114(2):203–213. doi: 10.1085/jgp.114.2.203

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© 1999 The Rockefeller University Press

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).

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Pip₂ abolishes high-affinity tolbutamide inhibition of Kir6.2+SUR1 channels. (A) Representative currents from inside-out patches containing wild-type (Kir6.2+SUR1) or Kir6.2 [ΔN2-30]+SUR1 channels. The patches were exposed to [tolbutamide], [ATP], or [Pip₂] as indicated. The dashed line indicates zero current (determined in 5 mM ATP). (B) Percent tolbutamide inhibition versus time in Pip₂ for four individual patches containing wild-type K_ATP channels. (C) Percent inhibition by ATP or tolbutamide before (Precontrol) or after (Post Pip₂) application of Pip₂ (2–4 min) from patches in B. (D) Plot of the change in percent tolbutamide inhibition versus change in K _1/2,ATP after application of Pip₂ for patches from B.