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. 2008 May;131(5):421–429. doi: 10.1085/jgp.200709948

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© 2008 Lundbæk

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.jgp.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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Figure 4. — Relation between amphiphile-induced shifts in the potential causing 50% inactivation of VDSCs in HEK293 cells (V_in − V_{in, contr}) and change in gA channel lifetime in dioleoylphosphatidylcholine/n-decane bilayers (ln{τ/τ_contr}). β-Octyl glucoside (βOG), capsaicin, Genapol X-100 (GX100), Triton X-100 (TX100), and reduced Triton X-100 (rTX100) were used at concentrations of 0.3, 1 mM; 30 μM; 4.5 μM; 10, 30 μM; 10, 30 μM. Cells were depolarized to +20 mV from 300-ms prepulses to potentials varying from −130 to +50 mV. The insert shows the relation between the effects on VDSCs and on gA channels including higher amphiphile concentrations at which the correlation between the effects on the two channel types breaks down. Modified from Lundbæk et al. (2005).