IndraLab

Statements

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"The most frequently observed forms of congenital LQTS arise from mutations to KCNQ1 and hERG (alternative nomenclature KCNH2), which respectively contribute to the slow delayed rectifier potassium current (I , LQT1) and the rapid delayed rectifier potassium current (I , LQT2); these account for 44% and 35% of cases, respectively [9]."
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"Some pleiotropic KCNQ1 variants in humans can simultaneously increase insulin secretion in the pancreas, reduce serum potassium upon oral glucose challenge, and cause long QT syndrome, putting individuals at risk of sudden, uncontrollable, arrhythmias which may lead to fainting or sudden death 35."
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"KvLQT1 and HERG mutations (one each) reduced K+ currents in vitro, consistent with the idea that they augment risk for aLQTS."
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"KCNE1 is known to modulate the voltage gated potassium channel alpha subunit KCNQ1 to generate slowly activating potassium currents."
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"In LQT1, the loss-of-function mutation in KCNQ1 affects the slowly activating delayed rectifier potassium current (IKs current), preventing the corrected QT interval from appropriately shortening during exercise, aiding in the diagnosis."
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"KCNE1, also known as MinK, is one of the five members of the KCNE family that modulate the voltage gated potassium channel alpha subunit KCNQ1 to generate slowly activating potassium currents [XREF_BIBR, XREF_BIBR]."
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"LQT1 is caused by mutations in the KCNQ1 gene, which causes dysfunction of slow delayed rectifier potassium current (Iks) [1]."
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"Cardiac repolarization is mainly dependent upon rapid and slow delayed-rectifier potassium currents mediated by human ether-a-go-go-related (hERG) gene and the KCNQ1 gene, respectively."
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"After observing that coexpression of Kv7.1 with KCNE1 attenuated the effect of extracellular potassium, KCNE2 and KCNE3 were also coexpressed with Kv7.1."
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"Kcnq1 impairs insulin secretion by enhancing the beta-cell potassium currents."
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"Genetic defects in KCNQ1 linked to LQTS, known as LQT1, cause a decrease in the slow delayed rectifier potassium current (I Ks), resulting in prolongation of the action potential at the cellular level and clinical prolongation of the QT interval [XREF_BIBR]."
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