Source:http://linkedlifedata.com/resource/pubmed/id/10385411
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
7
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| pubmed:dateCreated |
1999-7-15
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| pubmed:abstractText |
Thyroid hormone affects the contractile and electrophysiological properties of the cardiac myocyte that result in part from changes in the expression of thyroid hormone-responsive cardiac genes, including those that regulate membrane ion currents. To determine the molecular mechanisms underlying this effect, expression of a voltage-gated K+ channel, Kv1.5, was measured in response to thyroid hormone. Using quantitative RT-PCR methodology, the content of Kv1.5 messenger RNA (mRNA) in left ventricles of euthyroid rats was 4.25+/-0.6x10(-20) mol/microg total RNA and was decreased by 70% in the hypothyroid rat ventricle to 1.27+/-0.80x10(-20) mol/microg RNA (P<0.01). Administration of T3 to hypothyroid animals restored ventricular Kv1.5 mRNA to control levels within 1 h of treatment, making this the most rapid T3-responsive cardiac gene reported to date. The half-life of Kv1.5 mRNA was 1.9 h and 2.0 h in euthyroid and hypothyroid ventricles, respectively, and T3 treatment of the rats did not alter its half-life. In atrial myocardium, expression of Kv1.5 mRNA (6.10+/-0.37x10(-20) mol/microg RNA) was unaltered by thyroid hormone status. The myocyte-specific and chamber-selective expression of Kv1.5 mRNA was confirmed in primary cultures of rat atrial and ventricular myocytes.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Kcna5 protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Kv1.5 Potassium Channel,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels, Voltage-Gated,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Triiodothyronine
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| pubmed:status |
MEDLINE
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| pubmed:month |
Jul
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| pubmed:issn |
0013-7227
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
140
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
3170-6
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| pubmed:dateRevised |
2007-11-14
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| pubmed:meshHeading |
pubmed-meshheading:10385411-Animals,
pubmed-meshheading:10385411-Gene Expression,
pubmed-meshheading:10385411-Half-Life,
pubmed-meshheading:10385411-Heart,
pubmed-meshheading:10385411-Hyperthyroidism,
pubmed-meshheading:10385411-Hypothyroidism,
pubmed-meshheading:10385411-Kv1.5 Potassium Channel,
pubmed-meshheading:10385411-Myocardium,
pubmed-meshheading:10385411-Organ Size,
pubmed-meshheading:10385411-Potassium Channels,
pubmed-meshheading:10385411-Potassium Channels, Voltage-Gated,
pubmed-meshheading:10385411-RNA, Messenger,
pubmed-meshheading:10385411-Rats,
pubmed-meshheading:10385411-Rats, Sprague-Dawley,
pubmed-meshheading:10385411-Reference Values,
pubmed-meshheading:10385411-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:10385411-Time Factors,
pubmed-meshheading:10385411-Triiodothyronine
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| pubmed:year |
1999
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| pubmed:articleTitle |
Regulation of rat cardiac Kv1.5 gene expression by thyroid hormone is rapid and chamber specific.
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| pubmed:affiliation |
Department of Medicine, North Shore University Hospital/New York University School of Medicine, Manhasset 11030, USA. kojamaa@nshs.edu
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| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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