Regular ArticleEffects of External Acidosis on HERG Current Expressed in Xenopus Oocytes
References (33)
- et al.
A mechanistic link between an inherited and an acquired cardiac arrhythmia: HERG encodes the IKrpotassium channel
Cell
(1995) - et al.
A molecular basis for cardiac arrhythmia: HERG mutations cause long QT syndrome
Cell
(1995) - et al.
Sensitivity to H Li and Mg ions of the slow inward sodium current in frog atrial fibres
J Mol Cell Cardiol
(1975) - et al.
External pH regulates the slowly activating potassium current IsKexpressed in Xenopus oocytes
FEBS Letters
(1993) - et al.
The inactivation gate of the Shaker K+channel behaves like an open-channel blocker
Neuron
(1991) - et al.
ElectroÍphysiologic and extracellular ionic changes during acute ischemia in failing and normal rabbit myocardium
J Mol Cell Cardiol
(1996) - et al.
HERG, a human inward rectifier in the voltage-gated potassium channel family
Science
(1995) - et al.
Isoproterenol antagonizes prolongation of refractory period by the class III antiarrhythmic agent E-4031 in guinea pig myocytes. Mechanism of action
Circ Res
(1991) - et al.
Two components of cardiac delayed rectifier K+current. Differential sensitivity to block by class III antiarrhythmic agents
J Gen Physiol
(1990) - et al.
Effects of a combination of acidosis, lactate, and lysoÍphosphatidylcholine on action potentials and ionic currents in guinea pig ventricular myocytes
J Cardiovasc Pharmacol
(1992)
KVLQT1 and IsK(minK) proteins associate to form the IKscardiac potassium current
Nature
Coassembly of KVLQT1 and minK (IsK) proteins to form cardiac IKspotassium channel
Nature
The min K channel underlies the cardiac potassium current IKsand mediates species-specific responses to protein kinase C
Proc Natl Acad Sci USA
Blockade of HERG current expressed in Xenopus oocytes by external H+(Abstract)
Biophys J
Involvement of N terminus in the extracellular proton-accelerated HERG tail current deactivation (Abstract)
Biophys J
Novel mechanism of HERG current suppression in LQT2: shift in voltage dependence of HERG inactivation
Circ Res
Cited by (16)
hERG1 channel subunit composition mediates proton inhibition of rapid delayed rectifier potassium current (I<inf>Kr</inf>) in cardiomyocytes derived from hiPSCs
2023, Journal of Biological ChemistryCitation Excerpt :The data presented herein demonstrate that increased hERG1a and reduced hERG1b in matured hiPSC-CMs diminish IKr sensitivity to extracellular protons compared to IKr recorded from immature hiPSC-CMs. Protons decrease hERG1 current amplitude and accelerate the time course of hERG1 deactivation (27,31,33,34,37,52). However, the specific effects of extracellular acidosis can vary across expression systems.
Enhanced inhibitory effect of acidosis on hERG potassium channels that incorporate the hERG1b isoform
2011, Biochemical and Biophysical Research CommunicationsCitation Excerpt :Extracellular acidosis occurs in the heart under a number of pathological conditions including myocardial ischemia and reperfusion [18]; it can alter the function of ion channels and predispose the heart to dangerous arrhythmias [19]. The effects of acidosis on hERG1a channels have been investigated, with decreases in current amplitude and accelerated deactivation both reported [20–28]. However, despite the emerging evidence for a physiological role for hERG1b in native cardiac IKr, to our knowledge no study has hitherto investigated the effects of acidosis on K+ current mediated by hERG1b.
Modulation of hERG K<sup>+</sup> Channel Deactivation by Voltage Sensor Relaxation
2020, Frontiers in PharmacologyExtracellular protons accelerate hERG channel deactivation by destabilizing voltage sensor relaxation
2019, Journal of General PhysiologyExternal protons destabilize the activated voltage sensor in hERG channels
2014, European Biophysics Journal
- f1
Please address all correspondence to: Masayasu Hiraoka, MD, PhD, Department of Cardiovascular Disease, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, Tokyo-113-8510, Japan.