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KCNH2 inhibits IKr. 7 / 7
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"Heterologous expression of HERG in Xenopus oocytes revealed that HERG current was similar to a well characterized cardiac delayed rectifier K+ current, IKr, and led to the hypothesis that mutations in HERG reduced IKr, causing prolonged myocellular action potentials."

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"We investigated the effects of DHA in wild type (WT) and transgenic long QT Type 1 (LQT1; loss of IKs), LQT2 (loss of IKr), LQT5 (reduction of IKs), and LQT2-5 (loss of IKr and reduction of IKs) rabbits."

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"First, hypoglycemia itself inhibits the rapid component of the cardiac delayed rectifier K current (IKr), which is one of the main repolarizing K channels in human myocytes and encoded by human ether-a-go-go-related gene (HERG)[74]."

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"A lesser number of membrane hERG channels reduce IKr, prolonging the QT interval."

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"Loperamide's inhibition of the I Na channel and hERG-mediated IKr are the most likely basis for this cardiac electrophysiological toxicity at overdose exposures."

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"Vandetanib inhibits hERG/KCNH2 channels decreasing IKr current amplitude, leading to a long QT."

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"KCNH2 gene mutations and drugs targeting hERG channel can partially or completely reduce IKr, which mainly function in the third phase of cardiac action potentials, resulting in prolonged action potential duration (APD), shown on the ECG as a prolonged QT interval.FIGURE 2: Single alpha subunit of the previous hERG structure (A), new hERGT structure (B), 3D side view of full hERGT(C), obtained from PDB: 5VA2; hERGT) and single subunit of the hERGT on the cell membrane (D)."