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. Author manuscript; available in PMC: 2009 Nov 5.
Published in final edited form as: Channels (Austin). 2009 Jan 7;3(1):16–24. doi: 10.4161/chan.3.1.7387

Figure 4.

Figure 4

KCNQ1 Ser-27 is required for functional response of KCNE2/KCNQ1/Yotiao channels to cAMP. Ser-27 in the KCNQ1 N terminus was mutated to Asp (S27D) and Ala (S27A). CHO cells were transfected with KCNE2, the indicated KCNQ1 construct, and Yotiao. (A) Substitutions of Ser-27 abolish PKA-dependent regulation of KCNE2/KCNQ1/Yotiao channels. Filled bars indicate mean ± SEM current amplitudes 7-min after cAMP application (normalized to amplitude before the application), and are compared with time control (open bars) without application of cpt-cAMP (0.5 mM). Currents were measured, and cpt-cAMP was applied as described in Figure 3A. Data for WT in Figure 3A is re-plotted as indicated above, and then is compared with data for S27D and S27A. The numbers of experiments were as follows: WT, time control, n = 8, and cAMP, n = 16; S27D, time control, n = 8, and cAMP, n = 7; S27A, time control, n = 7, and cAMP, n = 8. *p < 0.05 vs. time control, Student’s t-test. Representative current traces before the cAMP application (control, black) are superimposed with the traces after the cAMP application (red) for each KCNQ1 construct. (Scale bars: 10 pA/pF, 1 s). (B) S27D (SD) abolishes the PKA-dependent regulation over activating pulse voltages. Shown are plots of mean current amplitude ± SEM (Left, n = 7) as well as representative current traces as in Figure 3B for WT KCNQ1 (control; open squares, and cpt-cAMP; filled squares). (C) S27A (SA) abolishes the PKA-dependent regulation over activating pulse voltages. Shown are plots of mean current amplitude ± SEM (Left, n = 8) as well as representative current traces as in Figure 3B for WT KCNQ1 (control; open squares, and cpt-cAMP; filled squares).