Human Connexin40 Mutations Slow Conduction and Increase Propensity for Atrial Fibrillation

Background Patch clamping studies using non-cardiomyocytes revealed that the human connexin40 mutations P88S, G38D, and A96S are associated with reduced gap junction conductances compared to wild type connexin40 (wtCx40). Their effects within myocytes however are unclear. We aimed to characterise P8...

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Veröffentlicht in:	Heart, lung & circulation lung & circulation, 2018-01, Vol.27 (1), p.114-121
Hauptverfasser:	Kanthan, Ajita, PhD, MBBS, BMedSc, FRACP, Fahmy, Peter, PhD, MBBS, FRACP, Rao, Renuka, PhD, Pouliopoulos, Jim, PhD, MSc(Med), Alexander, Ian E., PhD, MBBS, FRACP, Thomas, Stuart P., PhD, MBBS, FRACP, Kizana, Eddy, PhD, MBBS, FRACP
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Atrial fibrillation Atrial Fibrillation - genetics Atrial Fibrillation - metabolism Atrial Fibrillation - pathology Blotting, Western Cardiac electrophysiology Cardiovascular Connexin40 Connexins - genetics Connexins - metabolism Disease Models, Animal DNA - genetics DNA Mutational Analysis Gap Junction alpha-5 Protein Gap Junctions Gene mutation Humans Mutation Myocytes, Cardiac - metabolism Myocytes, Cardiac - pathology Rats Rats, Sprague-Dawley
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