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. 2018 May 2;7(10):e008155. doi: 10.1161/JAHA.117.008155

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© 2018 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

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The effect of CPVT CaM N54I on the rate of Ca dissociation from N‐domain of CaM. A, Ca bound N‐domain of CaM binds RyR2 and keeps it refractory following CICR. Meanwhile, CASQ2 senses luminal (Ca) decrease and contributes to RyR2 refractoriness. B, the time course of the decrease in Trp fluorescence as Ca dissociated from CaM^F20W constructs. The data traces have been staggered and normalized for clarity. C, the time course of the increase in Quin‐2 fluorescence as Ca dissociated from CaM‐pRyR2 complex. The data traces have been staggered and normalized for clarity. Ca indicates, calcium; CaM, calmodulin; CASQ2, calsequestrin; CICR, calcium induced calcium release; CPVT, catecholaminergic polymorphic ventricular tachycardia; RyR2, ryanodine receptor 2; Trp, tryptophan.