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Open AccessJournal ArticleDOI

MiRP1 Forms IKr Potassium Channels with HERG and Is Associated with Cardiac Arrhythmia

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TLDR
A mechanism for acquired arrhythmia is revealed: genetically based reduction in potassium currents that remains clinically silent until combined with additional stressors.
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This article is published in Cell.The article was published on 1999-04-16 and is currently open access. It has received 1320 citations till now. The article focuses on the topics: hERG & KCNE4.

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Citations
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Pharmacogenomics: Translating Functional Genomics into Rational Therapeutics

TL;DR: Pharmacogenomic studies are rapidly elucidating the inherited nature of these differences in drug disposition and effects, thereby enhancing drug discovery and providing a stronger scientific basis for optimizing drug therapy on the basis of each patient's genetic constitution.
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Pharmacogenomics — Drug Disposition, Drug Targets, and Side Effects

TL;DR: The existence of large population differences with small intrapatient variability is consistent with inheritance as a determinant of drug response; it is estimated that genetics can account for 20 to 95 percent of variability in drug disposition and effects.
Journal ArticleDOI

hERG potassium channels and cardiac arrhythmia

TL;DR: Insights gained from the crystal structures of other potassium channels have helped understanding of the block of hERG channels and the mechanisms of gating.
References
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Journal ArticleDOI

A mechanistic link between an inherited and an acquird cardiac arrthytmia: HERG encodes the IKr potassium channel

TL;DR: The finding that HERG encodes IKr channels provides a mechanistic link between certain forms of inherited and acquired LQT, and that an additional subunit may be required for drug sensitivity.
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A molecular basis for cardiac arrhythmia: HERG mutations cause long QT syndrome

TL;DR: In this article, the authors investigated patients with long QT syndrome (LQT), an inherited disorder causing sudden death from a ventricular tachyarrythmia, torsade de pointes.
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Coassembly of K(V)LQT1 and minK (IsK) proteins to form cardiac I(Ks) potassium channel.

TL;DR: KVLQT1 is the subunit that coassembles with minK to form IKS channels and IKS dysfunction is a cause of cardiac arrhythmia, and is shown to encode a K+ channel with biophysical properties unlike other known cardiac currents.
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HERG, a Human Inward Rectifier in the Voltage-Gated Potassium Channel Family

TL;DR: The properties of HERG channels are consistent with the gating properties of Eag-related and other outwardly rectifying, S4-containing potassium channels, but with the addition of an inactivation mechanism that attenuates potassium efflux during depolarization.
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Female gender as a risk factor for torsades de pointes associated with cardiovascular drugs

TL;DR: It is suggested that women are more prone than men to develop torsades de pointes during administration of cardiovascular drugs that prolong cardiac repolarization and the pathophysiological basis for, and therapeutic implications of, this gender disparity should be further investigated.
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