Associated Papers
E1784K, the most common Brugada syndrome and long-QT syndrome type 3 mutant, disrupts sodium channel inactivation through two separate mechanisms.
Peters CH et al.
The Journal of General Physiology, 2020
pH Modulation of Voltage-Gated Sodium Channels.
Peters CH et al.
Handbook of Experimental Pharmacology, 2018
Depolarization of the conductance-voltage relationship in the NaV1.5 mutant, E1784K, is due to altered fast inactivation.
Peters CH et al.
Plos One, 2017
The multi-faceted aspects of the complex cardiac Nav1.5 protein in membrane function and pathophysiology.
Detta N et al.
Biochimica Et Biophysica Acta, 2015
ClinLabGeneticist: a tool for clinical management of genetic variants from whole exome sequencing in clinical genetic laboratories.
Wang J et al.
Genome Medicine, 2015
26338694 (PubMed )
Supplement: 13073_2015_207_MOESM1_ESM.xlsx › S5
Proton modulation of cardiac I Na: a potential arrhythmogenic trigger.
Jones DK et al.
Handbook of Experimental Pharmacology, 2014
Proton sensors in the pore domain of the cardiac voltage-gated sodium channel.
Jones DK et al.
The Journal of Biological Chemistry, 2013
A proton leak current through the cardiac sodium channel is linked to mixed arrhythmia and the dilated cardiomyopathy phenotype.
Gosselin-Badaroudine P et al.
Plos One, 2012
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