Associated Papers
Exceptionally selective voltage-sensor trapping of NaV1.5 channels by Mg-protoporphyrin impairs cancer cell migration.
Jamili M et al.
Scientific Reports, 2026
Differential regulation of cardiac sodium channels by intracellular fibroblast growth factors.
Angsutararux P et al.
The Journal of General Physiology, 2023
Extracellular hemin is a reverse use-dependent gating modifier of cardiac voltage-gated Na+ channels.
Gessner G et al.
Biological Chemistry, 2022
Biophysical Investigation of Sodium Channel Interaction with β-Subunit Variants Associated with Arrhythmias.
Llongueras JP et al.
Bioelectricity, 2020
pH Modulation of Voltage-Gated Sodium Channels.
Peters CH et al.
Handbook of Experimental Pharmacology, 2018
Regulation of Na+ channel inactivation by the DIII and DIV voltage-sensing domains.
Hsu EJ et al.
The Journal of General Physiology, 2017
Calmodulin limits pathogenic Na+ channel persistent current.
Yan H et al.
The Journal of General Physiology, 2017
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
A novel NaV1.5 voltage sensor mutation associated with severe atrial and ventricular arrhythmias.
Wang HG et al.
Journal of Molecular and Cellular Cardiology, 2016
Direct Measurement of Cardiac Na+ Channel Conformations Reveals Molecular Pathologies of Inherited Mutations.
Varga Z et al.
Circulation. Arrhythmia and Electrophysiology, 2015
Brugada syndrome disease phenotype explained in apparently benign sodium channel mutations.
Hoshi M et al.
Circulation. Cardiovascular Genetics, 2014
Unexpected α-α interactions with NaV1.5 genetic variants in Brugada syndrome.
Abriel H et al.
Circulation. Cardiovascular Genetics, 2014
Outward stabilization of the voltage sensor in domain II but not domain I speeds inactivation of voltage-gated sodium channels.
Sheets MF et al.
American Journal of Physiology. Heart and Circulatory Physiology, 2013
Proton sensors in the pore domain of the cardiac voltage-gated sodium channel.
Jones DK et al.
The Journal of Biological Chemistry, 2013
Ca2+/calmodulin-dependent protein kinase II-based regulation of voltage-gated Na+ channel in cardiac disease.
Koval OM et al.
Circulation, 2012
Lidocaine partially depolarizes the S4 segment in domain IV of the sodium channel.
Sheets MF et al.
Pflugers Archiv : European Journal of Physiology, 2011
Expression of skeletal but not cardiac Na+ channel isoform preserves normal conduction in a depolarized cardiac syncytium.
Protas L et al.
Cardiovascular Research, 2009
Outward stabilization of the S4 segments in domains III and IV enhances lidocaine block of sodium channels.
Sheets MF et al.
The Journal of Physiology, 2007
Charge at the lidocaine binding site residue Phe-1759 affects permeation in human cardiac voltage-gated sodium channels.
McNulty MM et al.
The Journal of Physiology, 2007
Molecular interactions of the gating modifier toxin ProTx-II with NaV 1.5: implied existence of a novel toxin binding site coupled to activation.
Smith JJ et al.
The Journal of Biological Chemistry, 2007
An inner pore residue (Asn406) in the Nav1.5 channel controls slow inactivation and enhances mibefradil block to T-type Ca2+ channel levels.
McNulty MM et al.
Molecular Pharmacology, 2006
Isoform-dependent interaction of voltage-gated sodium channels with protons.
Khan A et al.
The Journal of Physiology, 2006
SCN5A polymorphism restores trafficking of a Brugada syndrome mutation on a separate gene.
Poelzing S et al.
Circulation, 2006
The voltage dependence of recovery from use-dependent block by QX-222 separates mechanisms for drug egress in the cardiac sodium channel.
Lardin HA et al.
Biochemical Pharmacology, 2006
Charge immobilization of the voltage sensor in domain IV is independent of sodium current inactivation.
Sheets MF et al.
The Journal of Physiology, 2005
Molecular action of lidocaine on the voltage sensors of sodium channels.
Sheets MF et al.
The Journal of General Physiology, 2003
The outermost lysine in the S4 of domain III contributes little to the gating charge in sodium channels.
Sheets MF et al.
Biophysical Journal, 2002
Extrapore residues of the S5-S6 loop of domain 2 of the voltage-gated skeletal muscle sodium channel (rSkM1) contribute to the mu-conotoxin GIIIA binding site.
Chahine M et al.
Biophysical Journal, 1998