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Kir2.3 is an inwardly rectifying potassium channel subunit encoded by the gene KCNJ4, predominantly expressed in cardiac atrial tissue (also present in ventricle and other excitable cells). As part of the Kir2 subfamily, it forms homo- or heterotetrameric complexes that conduct potassium ions more readily into than out of the cell, crucial for stabilizing the resting membrane potential and facilitating terminal repolarization of cardiac action potentials[6][7]. Kir2.3 differs from Kir2.1 and Kir2.2 in single-channel conductance (lower, about 10–14 pS) and has unique sensitivity to pH, with intracellular and extracellular alkalization enhancing its activity (with pKa ~6.76–7.4)[6][7]. Mutations or altered expression of Kir2.3 can modulate the risk of cardiac arrhythmias and sudden death syndromes. Select drugs can block Kir2.3 and its family members, but pharmacological selectivity for Kir2.3 is limited; common blockers like barium ions, amiodarone, and chloroquine target multiple Kir2 subunits[6]. Kir2.3 serves as a key component in both electrophysiological research and cardiac safety assessment screens.
Channel blockers inhibit potassium efflux, modifying cellular excitability Drug binding to pore or regulatory domains modulates current amplitude and rectification
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