ArticleThe Journal of physiology2010
Cysteine 723 in the C-linker segment confers oxidative inhibition of hERG1 potassium channels.
Article in The Journal of physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 44 citations in OpenAlex.
- Recurrent Constellations of Embryonic Malformations (RCEM): Teratogenicity Linked to Transient Hypoxia and Hormone Pregnancy Tests Agrees With RCEM and Suggest a Reactive Oxygen Species Pathogenesis.Birth defects research · 2026Review
- Protective function of the voltage-gated potassium channel Kv11.3 in a mouse model of cardiac ischemia/reperfusion injury.PloS one · 2025Article
- Redox Regulation of KAntioxidants & redox signaling · 2024Review
- hERG1 channel subunit composition mediates proton inhibition of rapid delayed rectifier potassium current (IThe Journal of biological chemistry · 2023Article
- Role of mitochondrial reactive oxygen species in homeostasis regulation.Redox report : communications in free radical research · 2022Review
- COVID-19: Electrophysiological mechanisms underlying sudden cardiac death during exercise with facemasks.Medical hypotheses · 2020Article
- Suppression of hERG KRedox biology · 2018Article
- CO-independent modification of KEuropean journal of pharmacology · 2017Article
- A key role for peroxynitrite-mediated inhibition of cardiac ERG (Kv11.1) KFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- Diesel Exhaust Worsens Cardiac Conduction Instability in Dobutamine-Challenged Wistar-Kyoto and Spontaneously Hypertensive Rats.Cardiovascular toxicology · 2017Article
- Increased serum gamma-glutamyltransferase levels are associated with ventricular instability in type 2 diabetes.Endocrine · 2016Article
- Interactions between the N-terminal tail and the gating machinery of hERG K⁺ channels both in closed and open/inactive states.Pflugers Archiv : European journal of physiology · 2015Article
- Article
- PyTMs: a useful PyMOL plugin for modeling common post-translational modifications.BMC bioinformatics · 2014Article
- Looking into a conceptual framework of ROS-miRNA-atrial fibrillation.International journal of molecular sciences · 2014Review
- Oxidative modulation of voltage-gated potassium channels.Antioxidants & redox signaling · 2014Review
- Analyzing cell physiology in C. elegans with fluorescent ratiometric reporters.Methods (San Diego, Calif.) · 2014Article
- Aging effects on QT interval: Implications for cardiac safety of antipsychotic drugs.Journal of geriatric cardiology : JGC · 2014Article
- S-glutathionylation of an auxiliary subunit confers redox sensitivity to Kv4 channel inactivation.PloS one · 2014Article
- Class 3 inhibition of hERG K+ channel by caffeic acid phenethyl ester (CAPE) and curcumin.Pflugers Archiv : European journal of physiology · 2013Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excess reactive oxygen species (ROS) play a crucial role under pathophysiological conditions, such as ischaemia/reperfusion and diabetes, potentially contributing to cardiac arrhythmia. hERG1 (KCNH2) potassium channels terminate the cardiac action potential and malfunction can lead to long-QT syndrome and fatal arrhythmia. To investigate the molecular mechanisms of hERG1 channel alteration by ROS, hERG1 and mutants thereof were expressed in HEK293 cells and studied with the whole-cell patch-clamp method. Even mild ROS stress induced by hyperglycaemia markedly decreased channel current. Intracellular H2O2 or cysteine-specific modifiers also strongly inhibited channel activity and accelerated deactivation kinetics. Mutagenesis revealed that cysteine 723 (C723), a conserved residue in a structural element linking the C-terminal domain to the channel's gate, is critical for oxidative functional modification. Moreover, kinetics of channel closure strongly influences ROS-induced modification, where rapid channel deactivation diminishes ROS sensitivity. Because of its fast deactivation kinetics, the N-terminally truncated splice variant hERG1b possesses greater resistance to oxidative modification.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.