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Calcium/calmodulin-dependent protein kinase II (CaMKII) inhibition ameliorates arrhythmias elicited by junctin ablation under stress conditions

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dc.bibliographiccitation.firstpage1599
dc.bibliographiccitation.issue7
dc.bibliographiccitation.journalHeart Rhythm
dc.bibliographiccitation.lastpage1610
dc.bibliographiccitation.volume12
dc.contributor.authorTzimas, Christos
dc.contributor.authorTerrovitis, John
dc.contributor.authorLehnart, Stephan Elmar
dc.contributor.authorKranias, Evangelia G.
dc.contributor.authorSanoudou, Despina
dc.date.accessioned2018-05-07T12:04:20Z
dc.date.available2018-05-07T12:04:20Z
dc.date.issued2015
dc.description.abstractAberrant calcium signaling is considered one of the key mechanisms contributing to arrhythmias, especially in the context of heart failure. In human heart failure, there is significant down-regulation of the sarcoplasmic reticulum (SR) protein junctin, and junctin deficiency in mice is associated with stress-induced arrhythmias.
dc.identifier.doi10.1016/j.hrthm.2015.03.043
dc.identifier.pmid25814413
dc.identifier.urihttps://resolver.sub.uni-goettingen.de/purl?gro-2/14624
dc.language.isoen
dc.notes.statusfinal
dc.relation.doi10.1016/j.hrthm.2015.03.043
dc.relation.eissn1556-3871
dc.relation.issn1556-3871
dc.titleCalcium/calmodulin-dependent protein kinase II (CaMKII) inhibition ameliorates arrhythmias elicited by junctin ablation under stress conditions
dc.typejournal_article
dc.type.internalPublicationunknown
dspace.entity.typePublication

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