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Gating pore currents and the resting state of Nav1.4 voltage sensor domains
TLDR
A structural model rationalizes the activation sequence of the different VSDs of the Nav1.4 channel and shows that the hydrophobic septa that isolate the intracellular and the extracellular media within the DI, DII, and DIII V SDs are ∼2 Å long, similar to those of Kv channels.
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A Proton Leak Current through the Cardiac Sodium Channel Is Linked to Mixed Arrhythmia and the Dilated Cardiomyopathy Phenotype
TLDR
It is proposed that acidification of cardiac myocytes and/or downstream events may cause the DCM phenotype and other electrical problems in affected family members and the identification of this clinically significant H+ leak may lead to the development of more targeted treatments.
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Biophysics, pathophysiology, and pharmacology of ion channel gating pores
TLDR
This focus on the VSD motif opens up a new area of research centered on developing molecules to treat a number of cell excitability disorders such as epilepsy, cardiac arrhythmias, and pain.
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Gating pore currents are defects in common with two Nav1.5 mutations in patients with mixed arrhythmias and dilated cardiomyopathy
Nav1.5 channels bearing voltage-sensor domain mutations associated with atypical cardiac arrhythmias and dilated cardiomyopathy generate gating pore currents.
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Biophysical characterization of the honeybee DSC1 orthologue reveals a novel voltage-dependent Ca2+ channel subfamily: CaV4
Insect DSC1 channels have sequences that are intermediate between voltage-gated Na+ and Ca2+ channels but have hitherto been classified as the former. Gosselin-Badaroudine et al. clone and…
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Gating pore currents, a new pathological mechanism underlying cardiac arrhythmias associated with dilated cardiomyopathy
TLDR
An increasing number of ion channelopathies, including periodic paralysis, dilated cardiomyopathy associated with cardiac arrhythmias, and peripheral nerve hyperexcitability (PNH), have been linked to the appearance of a new pathological mechanism involving the creation of an alternative permeation pathway through the normally non-conductive VSD of VGIC.
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Characterization of the honeybee AmNaV1 channel and tools to assess the toxicity of insecticides
TLDR
The functional expression and the molecular, biophysical, and pharmacological characterization of the western honeybee’s sodium channel are reported and could be used to assess the risks that current and next generation pesticides pose to honeybee populations.
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Biophysical characterization of the Varroa destructor NaV1 sodium channel and its affinity for τ‐fluvalinate insecticide
TLDR
It is shown that the honeybee sodium channel is more sensitive to τ‐fluvalinate than the V. destructor channel, suggesting that care must be taken when treating hives with this chemical, which tends to accumulate in hives.
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Nav 1.5 mutations linked to dilated cardiomyopathy phenotypes: Is the gating pore current the missing link?
TLDR
Nav 1.5 dysfunctions are commonly linked to rhythms disturbances that include type 3 long QT syndrome (LQT3), Brugada syndrome (BrS), sick sinus syndrome (SSS) and conduction defects and are also linked to structural heart diseases such as dilated cardiomyopathy (DCM).
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Mutations in the Voltage Sensors of Domains I and II of Nav1.5 that are Associated with Arrhythmias and Dilated Cardiomyopathy Generate Gating Pore Currents
TLDR
This study confirmed the previously reported gain of function of the alpha pores of the mutant channels, which mainly consisted of increased window currents mostly caused by shifts in the voltage dependence of activation, and observed gating pore currents associated with the R225P and R814W mutations.
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