ArticlePloS one2013
Kinetic model of Nav1.5 channel provides a subtle insight into slow inactivation associated excitability in cardiac cells.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Long-term inactivation mediated by different FGF-A homologues on heterologously expressed NaV1.2 currents.The Journal of general physiology · 2026Article
- COMPUTATIONAL ANALYSIS OF THE NOVEL LQT3 MUTATIONS G1481V AND Q1491H IN MYOCARDIAL AND PURKINJE CELLS.Annual Modeling and Simulation Conference (ANNSIM). Annual Modeling and Simulation Conference (Online) · 2025Article
- Changes in ion channel expression and function associated with cardiac arrhythmogenic remodeling by Sorbs2.Biochimica et biophysica acta. Molecular basis of disease · 2021Article
- Slow recovery from fast inactivation of Nav1.3 channels: a common gating mechanism shared in sweet- and sour-sensing cells.Pflugers Archiv : European journal of physiology · 2021Article
- Fast inactivation of Nav current in rat adrenal chromaffin cells involves two independent inactivation pathways.The Journal of general physiology · 2021Article
- Human neuronal signaling and communication assays to assess functional neurotoxicity.Archives of toxicology · 2021Article
- Phenomenological models of NaScientific reports · 2019Article
- A single Markov-type kinetic model accounting for the macroscopic currents of all human voltage-gated sodium channel isoforms.PLoS computational biology · 2017Article
- Depolarization of the conductance-voltage relationship in the NaV1.5 mutant, E1784K, is due to altered fast inactivation.PloS one · 2017Article
- Molecular Pathophysiology of Congenital Long QT Syndrome.Physiological reviews · 2017Review
- PKA phosphorylation reshapes the pharmacological kinetics of BmK AS, a unique site-4 sodium channel-specific modulator.Scientific reports · 2014Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Voltage-gated sodium channel Nav1.5 has been linked to the cardiac cell excitability and a variety of arrhythmic syndromes including long QT, Brugada, and conduction abnormalities. Nav1.5 exhibits a slow inactivation, corresponding to a duration-dependent bi-exponential recovery, which is often associated with various arrhythmia syndromes. However, the gating mechanism of Nav1.5 and the physiological role of slow inactivation in cardiac cells remain elusive. Here a 12-state two-step inactivation Markov model was successfully developed to depict the gating kinetics of Nav1.5. This model can simulate the Nav1.5 channel in not only steady state processes, but also various transient processes. Compared with the simpler 8-state model, this 12-state model is well-behaved in simulating and explaining the processes of slow inactivation and slow recovery. This model provides a good framework for further studying the gating mechanism and physiological role of sodium channel in excitable cells.
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