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pubmed-article:20448214pubmed:abstractTextFamilial sick sinus syndrome (SSS) has been linked to loss-of-function mutations of the SCN5A gene, which result in decreased inward Na(+) current, I(Na). However, the functional role of I(Na) in cardiac pacemaking is controversial, and mechanistic links between mutations and sinus node dysfunction in SSS are unclear. Objective: To determine mechanisms by which the SCN5A mutations impair cardiac pacemaking.lld:pubmed
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pubmed-article:20448214pubmed:articleTitleMechanistic links between Na+ channel (SCN5A) mutations and impaired cardiac pacemaking in sick sinus syndrome.lld:pubmed
pubmed-article:20448214pubmed:affiliationBiological Physics Group, School of Physics and Astronomy, University of Manchester, Manchester M13 9PL, United Kingdom.lld:pubmed
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