XB-IMG-136568
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FIG. 4. ATP modulation of gliclazide block of wild-type KATP channels and mutant channels with impaired ATP binding to Kir6.2. A–C: Gliclazide concentration-inhibition relations for wild-type and mutant channels in the absence (○) and presence (●) of MgATP. Currents are expressed relative to those in the absence of gliclazide. The MgATP concentration was 15 μmol/L for Kir6.2/SUR1, 1 mmol/L for Kir6.2-G334D/SUR1, and 100 μmol/L for Kir6.2-R201C/SUR1, respectively. The lines are the best fit of Eq. 1 to the mean data with the following parameters: Kir6.2/SUR1 (A): IC50 = 67 nmol/L, h = 1.3, a = 0.45 (○) and IC50 = 71 nmol/L, h = 1.0, a = 0.20 (●); Kir6.2-G334D/SUR1 (B): IC50 = 67 nmol/L, h = 1.1, a = 0.39 (○) and IC50 = 213 nmol/L, h = 1.0, a = 0.21 (●); and Kir6.2-R201C/SUR1 (C): IC50 = 49 nmol/L, h = 1.2, a = 0.48 (○) and IC50 = 190 nmol/L, h = 1.2, a = 0.27 (●). n = 6 in all experiments. Image published in: Proks P et al. (2013) © 2013 by the American Diabetes Association. This image is reproduced with permission of the journal and the copyright holder. This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives license Larger Image Printer Friendly View |