Source:http://linkedlifedata.com/resource/pubmed/id/18473122
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1-2
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pubmed:dateCreated |
2008-6-13
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pubmed:abstractText |
Overexpression of the Galphaq-protein has been shown to result in hypertrophic and dilated cardiomyopathy. This study investigated Ca(2+ )sensitivity of tension and myosin-ATPase activity in skinned fiber preparations of male and female wildtype (WT; n = 12) and transgenic mice with a cardiac specific overexpression of the Galphaq-protein (Galphaq-OE; n = 11). In addition, the phosphorylation status of troponin I was measured. Ca(2+) sensitivity of tension was increased in Galphaq-OE with a significant reduction in the half-maximum Ca(2+) concentration (EC(50)) compared to WT. Similarly, Ca(2+) sensitivity of myosin ATPase activity was increased in Galphaq-OE when comparing Galphaq-OE to WT. Maximum Ca(2+)-dependent tension and ATPase activity were both enhanced in Galphaq-OE compared to WT littermates. Phosphorylation of troponin I was significantly reduced in Galphaq-OE compared to WT. In the above experiments, no gender specific differences were observed in either Gaq-OE or in WT. We conclude that, in mice, increased expression of the Galphaq-protein induces alterations of myofibrillar function and energy consumption, which are also characteristics of human heart failure. This may result from a decreased phosphorylation of troponin I in Galphaq-OE.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adenosine Triphosphate,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/GTP-Binding Protein alpha...,
http://linkedlifedata.com/resource/pubmed/chemical/Keratolytic Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Octoxynol,
http://linkedlifedata.com/resource/pubmed/chemical/Troponin I
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0300-8177
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
314
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
133-41
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:18473122-Adenosine Triphosphate,
pubmed-meshheading:18473122-Animals,
pubmed-meshheading:18473122-Calcium,
pubmed-meshheading:18473122-Calcium Signaling,
pubmed-meshheading:18473122-Female,
pubmed-meshheading:18473122-GTP-Binding Protein alpha Subunits, Gq-G11,
pubmed-meshheading:18473122-Keratolytic Agents,
pubmed-meshheading:18473122-Male,
pubmed-meshheading:18473122-Mice,
pubmed-meshheading:18473122-Mice, Transgenic,
pubmed-meshheading:18473122-Muscle Contraction,
pubmed-meshheading:18473122-Muscle Fibers, Skeletal,
pubmed-meshheading:18473122-Octoxynol,
pubmed-meshheading:18473122-Phosphorylation,
pubmed-meshheading:18473122-Troponin I,
pubmed-meshheading:18473122-Up-Regulation
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pubmed:year |
2008
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pubmed:articleTitle |
Reduced troponin I phosphorylation and increased Ca(2+)-dependent ATP-consumption in triton X-skinned fiber preparations from Galphaq overexpressor mice.
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pubmed:affiliation |
Department of Cardiology and Angiology, Hospital of the University of Münster, Munster, Germany.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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