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Spectrum of HERG K+-channel dysfunction in an inherited cardiac arrhythmia.

Abstract：

:Long QT syndrome (LQT) is an autosomal dominant disorder that can cause sudden death from cardiac arrhythmias. We recently discovered that mutations in HERG, a K+-channel gene, cause chromosome 7-linked LQT. Heterologous expression of HERG in Xenopus oocytes revealed that HERG current was similar to a well-characterized cardiac delayed rectifier K+ current, IKr, and led to the hypothesis that mutations in HERG reduced IKr, causing prolonged myocellular action potentials. To define the mechanism of LQT, we injected oocytes with mutant HERG complementary RNAs, either singly or in combination with wild-type complementary RNA. Some mutations caused loss of function, whereas others caused dominant negative suppression of HERG function. These mutations are predicted to cause a spectrum of diminished IKr and delayed ventricular repolarization, consistent with the prolonged QT interval observed in individuals with LQT.

journal_name

Proc Natl Acad Sci U S A

journal_title

Proceedings of the National Academy of Sciences of the United States of America

authors

Sanguinetti MC,Curran ME,Spector PS,Keating MT

doi

10.1073/pnas.93.5.2208

subject

Has Abstract

pub_date

1996-03-05 00:00:00

pages

2208-12

issue

5

eissn

0027-8424

issn

1091-6490

journal_volume

93

pub_type

杂志文章

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