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dc.contributor.authorStewart, Alan J.
dc.contributor.authorPitt, Samantha Jane
dc.identifier.citationStewart , A J & Pitt , S J 2015 , ' Zinc controls RyR2 activity during excitation-contraction coupling ' , Channels , vol. 9 , no. 5 , pp. 223-225 .
dc.identifier.otherPURE: 204377371
dc.identifier.otherPURE UUID: 2230979b-2c36-4464-afa5-4c6b252edbf9
dc.identifier.otherScopus: 84957790770
dc.identifier.otherORCID: /0000-0003-4580-1840/work/60195815
dc.identifier.otherORCID: /0000-0003-2257-1595/work/60196238
dc.identifier.otherWOS: 000364325100005
dc.description.abstractCardiac excitation-contraction (EC) coupling is a process which governs contractility of the heart through the controlled release of Ca2+ from the sarcoplasmic reticulum (SR). The type-2 ryanodine receptor (RyR2) is the route through which Ca2+ is released from the SR providing the necessary driving force for cellular contraction. In heart failure, RyR2-channels become abnormally active, or ‘leaky’, and are unable to remain closed during diastole resulting in unwanted irregular contractile and electrical activity1. Defective Zn2+ handling has been shown to contribute to the cellular pathology of certain cardiomyopathies which give rise to impaired contractility including heart failure 2. This is likely a consequence of altered EC coupling as a result of modified RyR2 function. How zinc impacts upon the contractile force and the release of calcium from intracellular stores in heart is not fully understood.
dc.rightsThis is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The moral rights of the named author(s) have been asserted.en
dc.subjectRyanodine receptoren
dc.subjectExcitation-contraction couplingen
dc.subjectR Medicineen
dc.titleZinc controls RyR2 activity during excitation-contraction couplingen
dc.typeJournal articleen
dc.description.versionPublisher PDFen
dc.contributor.institutionUniversity of St Andrews.School of Medicineen
dc.contributor.institutionUniversity of St Andrews.Biomedical Sciences Research Complexen
dc.contributor.institutionUniversity of St Andrews.Institute of Behavioural and Neural Sciencesen
dc.description.statusPeer revieweden

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