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Zinc controls RyR2 activity during excitation-contraction coupling
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dc.contributor.author | Stewart, Alan J. | |
dc.contributor.author | Pitt, Samantha Jane | |
dc.date.accessioned | 2015-11-10T11:10:02Z | |
dc.date.available | 2015-11-10T11:10:02Z | |
dc.date.issued | 2015-09 | |
dc.identifier.citation | Stewart , A J & Pitt , S J 2015 , ' Zinc controls RyR2 activity during excitation-contraction coupling ' , Channels , vol. 9 , no. 5 , pp. 223-225 . https://doi.org/10.1080/19336950.2015.1075784 | en |
dc.identifier.issn | 1933-6950 | |
dc.identifier.other | PURE: 204377371 | |
dc.identifier.other | PURE UUID: 2230979b-2c36-4464-afa5-4c6b252edbf9 | |
dc.identifier.other | Scopus: 84957790770 | |
dc.identifier.other | ORCID: /0000-0003-4580-1840/work/60195815 | |
dc.identifier.other | ORCID: /0000-0003-2257-1595/work/60196238 | |
dc.identifier.other | WOS: 000364325100005 | |
dc.identifier.uri | https://hdl.handle.net/10023/7761 | |
dc.description.abstract | Cardiac 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.language.iso | eng | |
dc.relation.ispartof | Channels | en |
dc.rights | This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/), 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.subject | Ryanodine receptor | en |
dc.subject | Excitation-contraction coupling | en |
dc.subject | Ca2+-release | en |
dc.subject | Zn2+-signalling | en |
dc.subject | Cardiomyocyte | en |
dc.subject | R Medicine | en |
dc.subject | NDAS | en |
dc.subject.lcc | R | en |
dc.title | Zinc controls RyR2 activity during excitation-contraction coupling | en |
dc.type | Journal article | en |
dc.contributor.sponsor | The Royal Society of Edinburgh | en |
dc.description.version | Publisher PDF | en |
dc.contributor.institution | University of St Andrews. School of Medicine | en |
dc.contributor.institution | University of St Andrews. Biomedical Sciences Research Complex | en |
dc.contributor.institution | University of St Andrews. Institute of Behavioural and Neural Sciences | en |
dc.identifier.doi | https://doi.org/10.1080/19336950.2015.1075784 | |
dc.description.status | Peer reviewed | en |
dc.identifier.grantnumber | en |
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