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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
6
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pubmed:dateCreated |
2009-6-24
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pubmed:abstractText |
Clinical studies have revealed that the D166V mutation in the ventricular myosin regulatory light chain (RLC) can cause a malignant phenotype of familial hypertrophic cardiomyopathy (FHC). It has been proposed that RLC induced FHC in the heart originates at the level of the myosin cross-bridge due to alterations in the rates of cross-bridge cycling. In this report, we examine whether the environment of an active cross-bridge in cardiac myofibrils from transgenic (Tg) mice is altered by the D166V mutation in RLC. The cross-bridge environment was monitored by tracking the fluorescence lifetime (tau) of Alexa488-phalloidin-labeled actin. The fluorescence lifetime is the average rate of decay of a fluorescent species from the excited state, which strongly depends on various environmental factors. We observed that the lifetime was high when cross-bridges were bound to actin and low when they were dissociated from it. The lifetime was measured every 50 ms from the center half of the I-band during 60 s of rigor, relaxation and contraction of muscle. We found no differences between lifetimes of Tg-WT and Tg-D166V muscle during rigor, relaxation and contraction. The duty ratio expressed as a fraction of time that cross-bridges spend attached to the thin filaments during isometric contraction was similar in Tg-WT and Tg-D166V muscles. Since independent measurements showed a large decrease in the cross-bridge turnover rate in Tg-D166V muscle compared to Tg-WT, the fact that the duty cycle remains constant suggests that the D166V mutation of RLC causes a decrease in the rate of cross-bridge attachment to actin.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/19159226-10952953,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19159226-11017871,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19159226-11984027,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19159226-12707239,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19159226-12714020,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19159226-12769642,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19159226-13485191,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19159226-14594949,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19159226-14609025,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19159226-15041669,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19159226-15647159,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19159226-15647167,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19159226-15711885,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19159226-16076902,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19159226-16936699,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19159226-17278378,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19159226-17343488,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19159226-17496049,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19159226-17916152,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19159226-18315381,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19159226-18426224,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19159226-3801396,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19159226-6417144,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19159226-7981198,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19159226-8126219,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19159226-8155632,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19159226-8343514,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19159226-8586652,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19159226-8814556
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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 |
Feb
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pubmed:issn |
1520-4995
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
17
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pubmed:volume |
48
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1264-71
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:19159226-Actin Cytoskeleton,
pubmed-meshheading:19159226-Actins,
pubmed-meshheading:19159226-Animals,
pubmed-meshheading:19159226-Cardiomyopathy, Hypertrophic, Familial,
pubmed-meshheading:19159226-Fluorescence,
pubmed-meshheading:19159226-Heart,
pubmed-meshheading:19159226-Mice,
pubmed-meshheading:19159226-Mice, Transgenic,
pubmed-meshheading:19159226-Myocardial Contraction,
pubmed-meshheading:19159226-Myofibrils,
pubmed-meshheading:19159226-Phalloidine,
pubmed-meshheading:19159226-Rigor Mortis,
pubmed-meshheading:19159226-Time Factors
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pubmed:year |
2009
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pubmed:articleTitle |
Fluorescence lifetime of actin in the familial hypertrophic cardiomyopathy transgenic heart.
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pubmed:affiliation |
Department of Molecular Biology & Immunology and Center for Commercialization of Fluorescence Technologies, University of North Texas, 3500 Camp Bowie Blvd., Fort Worth, Texas 76107, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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