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. 2020 Nov 3;13(6):e003133. doi: 10.1161/CIRCGEN.120.003133

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© 2020 The Authors.

Circulation: Genomic and Precision Medicine is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDerivs License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.

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Figure 5. — KCNQ1 T224M loss of IKs function.A and B, IKs recorded in Chinese hamster ovary (CHO) cells in which wild-type (WT) KCNQ1 or T224M were co-expressed with KCNE1 (the I_Ks accessory subunit). C and D, Summarize activating and deactivating I_Ks in the 2 groups of cells. The mutant T224M channel had significantly reduced total activating and deactivating currents, with a marked positive shift in the voltage dependence of activation, by ≈26 mV (P<0.01). Current densities were expressed in pA/pF after normalization of current amplitude to cell capacitance. The voltage clamp protocol is shown in the inset.