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• W2051237605 abstract "Inheritable long-QT syndrome (LQTS) is a disease in which delayed ventricular repolarization leads to cardiac arrhythmias and the possibility of sudden death. In the chromosome 3-linked disease, one mutation of the cardiac Na+ channel gene results in a deletion of residues 1505 to 1507 (Delta KPQ), and two mutation result in substitutions (N1325S and R1644H). We compared all three mutant-channel phenotypes by heterologous expression in Xenopus oocytes. Each produced a late phase of inactivation-resistant, mexiletine- and tetrodotoxin-sensitive whole-cell currents, but the underlying mechanisms were different at the single-channel level. N1325S and R1644H showed dispersed reopenings after the initial transient, whereas Delta KPQ showed both dispersed reopenings and long-lasting bursts. Thus, two distinct biophysical defects underlie the in vitro phenotype of persistent current in Na+ channel-linked LQTS, and the additive effects of both are responsible for making the Delta KPQ phenotype the most severe." @default.
• W2051237605 created "2016-06-24" @default.
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• W2051237605 date "1996-05-01" @default.
• W2051237605 modified "2023-10-16" @default.
• W2051237605 title "Multiple Mechanisms of Na ⁺ Channel– Linked Long-QT Syndrome" @default.
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• W2051237605 doi "https://doi.org/10.1161/01.res.78.5.916" @default.
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