The cardiac I Ks channel is composed of the Kv7.1 α‐subunit and the auxiliary β‐subunit KCNE1. This study investigates the properties of the PUFA tail with the goal of determining what features of the PUFA tail are important for the activating effects of PUFAs on the cardiac I Ks channel. 12, 13 However, the features of these PUFAs that are necessary for the effects on the I Ks channel are not fully understood. 10, 11 Polyunsaturated fatty acids (PUFAs) have been shown to reverse the loss‐of‐function of some LQT1 mutants in I Ks channels expressed in Xenopus laevis oocytes and also to reverse drug‐induced arrhythmia in cultured cardiomyocytes and a drug‐induced prolongation of the QT interval in guinea pig hearts. LQTS predisposes individuals to Torsades de Pointes, which can degenerate into ventricular fibrillation and lead to sudden cardiac death. 9 The most common form of LQTS, LQT1 is due to mutations of the cardiac I Ks channel that reduce outward K + current.
Loss‐of‐function mutations in the I Ks channel result in a prolongation of the QT interval (the interval between ventricular depolarization and repolarization) in the electrocardiogram - a characteristic of Long QT Syndrome (LQTS). 2, 3, 4, 5, 6, 7, 8 The Kv7.1/KCNE1 macromolecular complex, here forward referred to as the I Ks channel (a slow delayed rectifier Kv channel) is important for the repolarization of the cardiac ventricular action potential. 1 Voltage‐gated K + channels (Kv channels) comprise an important family of channels that are involved in the repolarization phase of the cardiac action potential. Excitable tissues, such as brain, heart, and muscle, express a wide variety of voltage‐gated ion channels that play a critical role in the firing and the shaping of action potentials.
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