Source:http://linkedlifedata.com/resource/pubmed/id/12491770
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2002-12-20
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pubmed:abstractText |
Contraction of skeletal and cardiac muscles is regulated by Ca2+ through specific Ca(2+)-regulatory proteins, troponin and tropomyosin, located in the thin filament. Troponin is a Ca2+ receptive protein consisting of three differet components, troponins C, I, and T. The essential mechanisms of Ca(2+)-regulation are the inhibition of contractile interaction between myosin and actin by the inhibitory action of troponin I and the reversal of the inhibition by troponin I through the Ca(2+)-binding to troponin C. All three components of troponin are required for the Ca(2+)-regulation of contraction. This article reviews following aspects of troponin researches: 1) early studies on the structure and function of troponin, 2) molecular mechanisms of Ca(2+)-regulation, 3) principles of troponin-exchange in skinned fibers and properties of troponin isoforms thereafter clarified under physiological conditions, 4) recent studies on the functional consequences of the mutations in human cardiac troponins T and I that cause genetic disorders, familial hypertrophic cardiomyopathy (HCM), and familial dilated cardiomyopathy (DCM).
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pubmed:language |
jpn
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0015-5691
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
120
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
20P-23P
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pubmed:dateRevised |
2011-7-27
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pubmed:meshHeading |
pubmed-meshheading:12491770-Calcium,
pubmed-meshheading:12491770-Cardiomyopathy, Dilated,
pubmed-meshheading:12491770-Cardiomyopathy, Hypertrophic, Familial,
pubmed-meshheading:12491770-Humans,
pubmed-meshheading:12491770-Muscle Contraction,
pubmed-meshheading:12491770-Mutation,
pubmed-meshheading:12491770-Troponin
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pubmed:year |
2002
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pubmed:articleTitle |
[Calcium regulation by troponin and its genetic disorder in striated muscle contraction].
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pubmed:affiliation |
Department of Physiology, Jikei University Medical School, Tokyo, Japan.
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pubmed:publicationType |
Journal Article,
English Abstract,
Review,
Research Support, Non-U.S. Gov't
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