scholarly journals A helical segment makes potassium channels go-go

2017 ◽  
Vol 292 (18) ◽  
pp. 7706-7707
Author(s):  
Lucie Parent
Keyword(s):  
Nmr Spectroscopy ◽  
Sudden Cardiac Death ◽  
Potassium Channels ◽  
Ion Channel ◽  
Functional Properties ◽  
Cardiac Death ◽  
Channel Function ◽  
Helical Segment

More than 500 variants in the KCNH2 gene, which encodes the cardiac human ether-a-go-go (hERG) ion channel, have been associated with sudden cardiac death, but only a subset of these variants have been investigated. Matthew D. Perry and colleagues now combine NMR spectroscopy and electrophysiological experiments to explore the functional properties of mutations within an overlooked hERG helix, finding important contributions to channel function.

Non-cardiovascular drugs that inhibit hERG-encoded potassium channels and risk of sudden cardiac death

Heart ◽  
2010 ◽  
Vol 97 (3) ◽  
pp. 215-220 ◽  
Author(s):  
C. van Noord ◽  
M. C. J. M. Sturkenboom ◽  
S. M. J. M. Straus ◽  
J. C. M. Witteman ◽  
B. H. C. Stricker
Keyword(s):  
Sudden Cardiac Death ◽  
Potassium Channels ◽  
Cardiac Death ◽  
Cardiovascular Drugs

scholarly journals Common Variants in Cardiac Ion Channel Genes Are Associated With Sudden Cardiac Death

2010 ◽  
Vol 3 (3) ◽  
pp. 222-229 ◽  
Author(s):  
Christine M. Albert ◽  
Calum A. MacRae ◽  
Daniel I. Chasman ◽  
Martin VanDenburgh ◽  
Julie E. Buring ◽  
...  
Keyword(s):  
Sudden Cardiac Death ◽  
Ion Channel ◽  
Cardiac Death ◽  
Common Variants

scholarly journals Ion Channel Disorders and Sudden Cardiac Death

2018 ◽  
Vol 19 (3) ◽  
pp. 692 ◽  
Author(s):  
Anna Garcia-Elias ◽  
Begoña Benito
Keyword(s):  
Sudden Cardiac Death ◽  
Ion Channel ◽  
Cardiac Death

scholarly journals Sudden cardiac death and inherited channelopathy: the basic electrophysiology of the myocyte and myocardium in ion channel disease

Heart ◽  
2012 ◽  
Vol 98 (7) ◽  
pp. 536-543 ◽  
Author(s):  
Claire A Martin ◽  
Gareth D K Matthews ◽  
Christopher L-H Huang
Keyword(s):  
Sudden Cardiac Death ◽  
Ion Channel ◽  
Cardiac Death ◽  
Ion Channel Disease

New Roles for Old Holes: Ion Channel Function in Aquaporin-1

Physiology ◽  
2002 ◽  
Vol 17 (2) ◽  
pp. 68-72 ◽  
Author(s):  
Andrea J. Yool ◽  
Alan M. Weinstein
Keyword(s):  
Ion Channels ◽  
Ion Channel ◽  
Functional Properties ◽  
Major Intrinsic Protein ◽  
Aquaporin 1 ◽  
Intrinsic Protein ◽  
Channel Proteins ◽  
Channel Function ◽  
Transmembrane Channel ◽  
Structural And Functional Properties

Mammalian aquaporins are part of the diverse major intrinsic protein family of water and solute channels. Intriguing links exist in structural and functional properties between aquaporins and ion channels. A novel role for aquaporin-1 as a gated ion channel reshapes our current views of this ancient family of transmembrane channel proteins.

Abstract MP114: Cardiotropic Adenovirus Increases Arrhythmia Susceptibility During Acute Infection

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Rachel L Padget ◽  
D. Ryan King ◽  
Michael D North ◽  
Mira N Tanenbaum ◽  
Patrick J Calhoun ◽  
...  
Keyword(s):  
Sudden Cardiac Death ◽  
Electrical Activity ◽  
Ion Channel ◽  
Gap Junction ◽  
Cardiac Death ◽  
Optical Mapping ◽  
Acute Infection ◽  
Intercellular Coupling ◽  
Viral Genomes ◽  
Arrhythmogenic Substrate

Myocarditis is responsible for up to 42% of sudden cardiac death in young adults yet mechanisms underlying virally-induced arrhythmia remain elusive. Adenovirus is a leading etiological agent of myocarditis but due to species-specificity, in vivo models are limited. Altered cardiac gap junction function underlies sudden cardiac death and given that gap junctions also propagate antiviral immune responses, we hypothesized adenovirus would target intercellular coupling, leading to arrhythmogenesis. Employing a recently described strain of mouse adenovirus, MAdV-3, we investigated cardiotropism, arrhythmia susceptibility, and molecular mechanisms of a virally-induced arrhythmogenic substrate. Adult C57BL/6 mice were inoculated with MAdV-3 and infection allowed to progress for one week. Viral genomes were detected by qPCR to measure tissue tropism together with whole animal histopathology. Echo- and electrocardiography were used to measure cardiac function and electrical activity. Viral effects on transcription and junctional protein/ion channel expression and localization were quantified using RT-qPCR, confocal microscopy, and western blotting. Finally, ex vivo optical mapping was employed to test conduction defects and susceptibility to arrhythmia. We find MAdV-3 viral genomes specifically enriched in heart tissue, confirming cardiotropism. Immune cell infiltration was not detected in the heart and no cardiomyopathy was apparent by echocardiography. RR interval widening, however, does occur in MAdV-3 infected mice with reductions in cardiac ion channel and gap junction mRNA transcripts. Optical mapping experiments show that conduction velocity is altered in acutely infected hearts and norepinephrine challenge uncovered electrical impairment presenting as atrioventricular dissociation with increased premature ventricular contraction burden. Our data demonstrate that MAdV-3 is cardiotropic and acute infection result in changes in cardiac electrical activity prior to development of cardiomyopathy or a detectable immune response. MAdV-3 infection is a novel model for adenoviral myocarditis, providing insights into viral subversion of cardiac intercellular coupling and mechanisms of arrhythmogenesis.

Genomic imbalances in key ion channel genes and telomere shortening in sudden cardiac death victims

2008 ◽  
Vol 122 (3-4) ◽  
pp. 350-355 ◽  
Author(s):  
B. Banerjee ◽  
D.N. Peiris ◽  
S.H. Koo ◽  
P. Chui ◽  
E.J.D. Lee ◽  
...  
Keyword(s):  
Sudden Cardiac Death ◽  
Ion Channel ◽  
Cardiac Death ◽  
Telomere Shortening ◽  
Genomic Imbalances
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