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. 2014 Mar 4;5:30. doi: 10.3389/fphar.2014.00030

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Copyright © 2014 Heijman, Voigt, Wehrens and Dobrev.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Putative substrates for CaMKII-dependent phosphorylation in atrial cardiomyocytes and their consequences for atrial cellular electrophysiology and Ca²⁺-handling. CaMKII can phosphorylate the transient-outward K⁺-current (I_to), inward-rectifier K⁺-current (I_K1) and ultra-rapid delayed-rectifier K⁺-current (I_Kur), augmenting their functions and shortening action potential duration (APD). Phosphorylation of L-type Ca²⁺-current (I_Ca,L) and Na⁺-current (I_Na; resulting in an increased late component: I_Na,late) by CaMKII increases intracellular Ca²⁺ levels and prolongs APD. CaMKII-dependent phosphorylation of phospholamban (PLB) and sarcolipin (SLN) increases sarcoplasmic reticulum (SR) Ca²⁺-uptake, whereas phosphorylation of type-2 ryanodine-receptor channels (RyR2) promotes diastolic SR Ca²⁺-leak. CaMKII-dependent increases in expression of Na⁺/Ca²⁺-exchanger type-1 (NCX1) augment NCX-current (I_NCX), promoting the occurrence of delayed afterdepolarizations (DADs). In addition, Ca²⁺-handling abnormalities can activate small-conductance Ca²⁺-activated K⁺-currents (I_SK) and agonist-independent “constitutive” I_K,ACh, shortening APD, and promote altered gene expression via the Ca²⁺-dependent phosphatase calcineurin (Cn).