ArticleThe Journal of physiology2015
Differential thermosensitivity in mixed syndrome cardiac sodium channel mutants.
Article in The Journal of physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 38 citations in OpenAlex.
- Hyperthermia Augments the H1-Histamine Receptor-Mediated Force in the Human Atrium.International journal of molecular sciences · 2025Article
- Structural basis for the rescue of hyperexcitable cells by the amyotrophic lateral sclerosis drug Riluzole.Nature communications · 2024Article
- Temperature alters the inotropic, chronotropic and proarrhythmic effects of histamine in atrial muscle preparations from humans and HNaunyn-Schmiedeberg's archives of pharmacology · 2023Article
- Brugada Syndrome: More than a Monogenic Channelopathy.Biomedicines · 2023Review
- Spike desensitisation as a mechanism for high-contrast selectivity in retinal ganglion cells.Frontiers in cellular neuroscience · 2023Article
- Development of automated patch clamp assays to overcome the burden of variants of uncertain significance in inheritable arrhythmia syndromes.Frontiers in physiology · 2023Review
- Genomic and Non-Genomic Regulatory Mechanisms of the Cardiac Sodium Channel in Cardiac Arrhythmias.International journal of molecular sciences · 2022Review
- The resting membrane potential of hSC-CM in a syncytium is more hyperpolarised than that of isolated cells.Channels (Austin, Tex.) · 2021Article
- The L1624Q Variant inFrontiers in pharmacology · 2021Article
- Protein Kinases Mediate Anti-Inflammatory Effects of Cannabidiol and Estradiol Against High Glucose in Cardiac Sodium Channels.Frontiers in pharmacology · 2021Article
- E1784K, the most common Brugada syndrome and long-QT syndrome type 3 mutant, disrupts sodium channel inactivation through two separate mechanisms.The Journal of general physiology · 2020Article
- Biophysical Investigation of Sodium Channel Interaction with β-Subunit Variants Associated with Arrhythmias.Bioelectricity · 2020Article
- Brugada Syndrome: Oligogenic or Mendelian Disease?International journal of molecular sciences · 2020Review
- Modifications of sodium channel voltage dependence induce arrhythmia-favouring dynamics of cardiac action potentials.PloS one · 2020Article
- Ranolazine as an Alternative Therapy to Flecainide for SCN5A V411M Long QT Syndrome Type 3 Patients.Frontiers in pharmacology · 2020Article
- Voltage vs. Ligand I: Structural basis of the intrinsic flexibility of S3 segment and its significance in ion channel activation.Channels (Austin, Tex.) · 2019Article
- Article
- "Pill-in-the-Pocket" Treatment of Propafenone Unmasks ECG Brugada Pattern in an Atrial Fibrillation Patient With a Common SCN5A R1193Q Polymorphism.Frontiers in physiology · 2019Article
- The efficacy of Ranolazine on E1784K is altered by temperature and calcium.Scientific reports · 2018Article
- Arrhythmogenic triggers associated with Sudden Cardiac Death.Channels (Austin, Tex.) · 2018Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac arrhythmias are often associated with mutations in SCN5A the gene that encodes the cardiac paralogue of the voltage-gated sodium channel, NaV 1.5. The NaV 1.5 mutants R1193Q and E1784K give rise to both long QT and Brugada syndromes. Various environmental factors, including temperature, may unmask arrhythmia. We sought to determine whether temperature might be an arrhythmogenic trigger in these two mixed syndrome mutants. Whole-cell patch clamp was used to measure the biophysical properties of NaV 1.5 WT, E1784K and R1193Q mutants. Recordings were performed using Chinese hamster ovary (CHOk1) cells transiently transfected with the NaV 1.5 α subunit (WT, E1784K, or R1193Q), β1 subunit, and eGFP. The channels' voltage-dependent and kinetic properties were measured at three different temperatures: 10ºC, 22ºC, and 34ºC. The E1784K mutant is more thermosensitive than either WT or R1193Q channels. When temperature is elevated from 22°C to 34°C, there is a greater increase in late INa and use-dependent inactivation in E1784K than in WT or R1193Q. However, when temperature is lowered to 10°C, the two mutants show a decrease in channel availability. Action potential modelling using Q10 fit values, extrapolated to physiological and febrile temperatures, show a larger transmural voltage gradient in E1784K compared to R1193Q and WT with hyperthermia. The E1784K mutant is more thermosensitive than WT or R1193Q channels. This enhanced thermosensitivity may be a mechanism for arrhythmogenesis in patients with E1784K sodium channels.
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