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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2003-6-9
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pubmed:abstractText |
Mutations in cardiac voltage-gated K+ channels cause long QT syndrome (LQTS) and sudden death. We created a transgenic mouse with a long QT phenotype (Kv1DN) by overexpression of a truncated K+ channel in the heart and investigated whether the dominant negative effect of the transgene would be overcome by the direct injection of adenoviral vectors expressing wild-type Kv1.5 (AV-Kv1.5) into the myocardium. End points at 3-10 days included electrophysiology in isolated cardiomyocytes, surface ECG, programmed stimulation of the right ventricle, and in vivo optical mapping of action potentials and repolarization gradients in Langendorff-perfused hearts. Overexpression of Kv1.5 reconstituted a 4-aminopyridine-sensitive outward K+ current, shortened the action potential duration, eliminated early afterdepolarizations, shortened the QT interval, decreased dispersion of repolarization, and increased the heart rate. Each of these changes is consistent with a physiologically significant primary effect of adenoviral expression of Kv1.5 on ventricular repolarization of Kv1DN mice.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0363-6135
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pubmed:author |
pubmed-author:BakerLindaL,
pubmed-author:BrunnerMichaelM,
pubmed-author:BuckettPeter DPD,
pubmed-author:ChanDanny PDP,
pubmed-author:FolcoEduardo JEJ,
pubmed-author:KodirovSodikdjon ASA,
pubmed-author:KorenGideonG,
pubmed-author:MitchellGary FGF,
pubmed-author:SalamaGuyG,
pubmed-author:ShibataKatsushiK,
pubmed-author:ZhouJunJ
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pubmed:issnType |
Print
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pubmed:volume |
285
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
H194-203
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:12793978-4-Aminopyridine,
pubmed-meshheading:12793978-Action Potentials,
pubmed-meshheading:12793978-Adenoviridae,
pubmed-meshheading:12793978-Animals,
pubmed-meshheading:12793978-Blotting, Western,
pubmed-meshheading:12793978-Cells, Cultured,
pubmed-meshheading:12793978-Cloning, Molecular,
pubmed-meshheading:12793978-Electrocardiography,
pubmed-meshheading:12793978-Electrophysiology,
pubmed-meshheading:12793978-Gene Transfer Techniques,
pubmed-meshheading:12793978-Kv1.5 Potassium Channel,
pubmed-meshheading:12793978-Long QT Syndrome,
pubmed-meshheading:12793978-Mice,
pubmed-meshheading:12793978-Muscle Cells,
pubmed-meshheading:12793978-Myocardium,
pubmed-meshheading:12793978-Patch-Clamp Techniques,
pubmed-meshheading:12793978-Phenotype,
pubmed-meshheading:12793978-Potassium Channel Blockers,
pubmed-meshheading:12793978-Potassium Channels,
pubmed-meshheading:12793978-Potassium Channels, Voltage-Gated
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pubmed:year |
2003
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pubmed:articleTitle |
In vivo gene transfer of Kv1.5 normalizes action potential duration and shortens QT interval in mice with long QT phenotype.
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pubmed:affiliation |
Bioelectricity Laboratory, Cardiovascular Division, Brigham and Women's Hospital, Boston, MA 02115, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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