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A mechanistic link between an inherited and an acquird cardiac arrthytmia: HERG encodes the IKr potassium channel
Two components of cardiac delayed rectifier K+ current. Differential sensitivity to block by class III antiarrhythmic agents
The magnitude of IKr was small relative to fully activated IKs, and the two currents were of similar magnitude when measured during a relatively short pulse protocol at membrane potentials typical of the plateau phase of cardiac action potentials.
CaV1.2 Calcium Channel Dysfunction Causes a Multisystem Disorder Including Arrhythmia and Autism
A structural basis for drug-induced long QT syndrome.
Coassembly of KVLQT1 and minK (IsK) proteins to form cardiac IKS potassium channel
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.
hERG potassium channels and cardiac arrhythmia
Insights gained from the crystal structures of other potassium channels have helped understanding of the block of hERG channels and the mechanisms of gating.
Coassembly of K(V)LQT1 and minK (IsK) proteins to form cardiac I(Ks) potassium channel.
K(V)LQT1 is the subunit that coassembles with minK to form I(Ks) channels and I( Ks) dysfunction is a cause of cardiac arrhythmia.
Severe arrhythmia disorder caused by cardiac L-type calcium channel mutations.
- I. Splawski, K. Timothy, M. Keating
- Biology, MedicineProceedings of the National Academy of Sciences…
- 7 June 2005
Computer modeling showed prolongation of cardiomyocyte action potentials and delayed afterdepolarizations, factors that increase risk of arrhythmia, and data indicate that gain-of-function mutations of CaV1.2 exons 8 and 8A cause distinct forms of TS.
Mutations in the hminK gene cause long QT syndrome and suppress lKs function
- I. Splawski, M. Tristani-Firouzi, M. Lehmann, M. Sanguinetti, M. Keating
- BiologyNature Genetics
- 1 November 1997
This is the first description of KCNE1 as an LQT gene and confirms that hminK is an integral protein of the IKS channel, which reduced IKS by shifting the voltage dependence of activation and accelerating channel deactivation.
Fast inactivation causes rectification of the IKr channel
- P. Spector, M. Curran, A. Zou, M. Keating, M. Sanguinetti
- BiologyThe Journal of general physiology
- 1 May 1996
The mechanism of rectification of HERG, the human cardiac delayed rectifier K+ channel, was studied after heterologous expression in Xenopus oocytes, showing voltage-gated fast inactivation and the resulting rectification are partly responsible for the prolonged plateau phase typical of ventricular action potentials.