IndraLab

Statements



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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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"Kcnq1 impairs insulin secretion by enhancing the beta-cell potassium currents."

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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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"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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"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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"Long QT syndrome type 1 (LQT1) is caused by mutations in the KCNQ1 gene resulting in a decrease in the repolarizing potassium current slow delayed rectifier current (I Ks)."

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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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"Clinical Perspectives Long QT syndrome type 1 (LQT1) is caused by mutations in the KCNQ1 gene resulting in a decrease in the repolarizing potassium current I Ks."

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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."