{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1362544420735001088.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1093/oxfordjournals.jbchem.a022615"}},{"identifier":{"@type":"URI","@value":"http://academic.oup.com/jb/article-pdf/127/3/355/2651036/127-3-355.pdf"}},{"identifier":{"@type":"PMID","@value":"10731705"}}],"dc:title":[{"@value":"Effect of Arg145Gly Mutation in Human Cardiac Troponin I on the ATPase Activity of Cardiac Myofibrils"}],"description":[{"notation":[{"@value":"In order to determine the functional consequences of the Arg145Gly mutation in troponin I found in familial hypertrophic cardiomyopathy, human cardiac troponin I and its mutant were expressed in Escherichia coli and purified, and then their effects on the ATPase activity of porcine cardiac myofibrillar preparations from which both troponins C and I had been depleted were examined. Both the wild-type and mutant troponin Is suppressed the ATPase activity of the troponin C.I-depleted myofibrils, but the maximum inhibition caused by mutant troponin I was weaker than that by wild-type troponin I. In the Ca(2)(+)-activation profile of the myofibrillar ATPase activity after reconstitution with both troponins I and C, the Ca(2)(+)-sensitivity with mutant troponin I was higher than that with wild-type troponin I, whereas the maximum level of the ATPase activity with mutant troponin I was lower than that with wild-type troponin I. These findings strongly suggest that the Arg145Gly mutation in human cardiac troponin I modulates the Ca(2)(+)-regulation of contraction by impairing the interaction of troponin I with both actin-tropomyosin and troponin C."}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1380569646352048385","@type":"Researcher","foaf:name":[{"@value":"F. Takahashi-Yanaga"}]},{"@id":"https://cir.nii.ac.jp/crid/1382544420735001088","@type":"Researcher","foaf:name":[{"@value":"S. Morimoto"}]},{"@id":"https://cir.nii.ac.jp/crid/1382544420735001089","@type":"Researcher","foaf:name":[{"@value":"I. Ohtsuki"}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"0021924X"},{"@type":"PISSN","@value":"http://id.crossref.org/issn/0021924X"}],"prism:publicationName":[{"@value":"Journal of Biochemistry"}],"dc:publisher":[{"@value":"Oxford University Press (OUP)"}],"prism:publicationDate":"2000-03-01","prism:volume":"127","prism:number":"3","prism:startingPage":"355","prism:endingPage":"357"},"reviewed":"false","url":[{"@id":"http://academic.oup.com/jb/article-pdf/127/3/355/2651036/127-3-355.pdf"}],"createdAt":"2012-04-19","modifiedAt":"2017-08-23","foaf:topic":[{"@id":"https://cir.nii.ac.jp/all?q=Adenosine%20Triphosphatases","dc:title":"Adenosine Triphosphatases"},{"@id":"https://cir.nii.ac.jp/all?q=DNA,%20Complementary","dc:title":"DNA, Complementary"},{"@id":"https://cir.nii.ac.jp/all?q=Dose-Response%20Relationship,%20Drug","dc:title":"Dose-Response Relationship, Drug"},{"@id":"https://cir.nii.ac.jp/all?q=Myocardium","dc:title":"Myocardium"},{"@id":"https://cir.nii.ac.jp/all?q=Troponin%20I","dc:title":"Troponin I"},{"@id":"https://cir.nii.ac.jp/all?q=Glycine","dc:title":"Glycine"},{"@id":"https://cir.nii.ac.jp/all?q=Cardiomyopathy,%20Hypertrophic","dc:title":"Cardiomyopathy, Hypertrophic"},{"@id":"https://cir.nii.ac.jp/all?q=Arginine","dc:title":"Arginine"},{"@id":"https://cir.nii.ac.jp/all?q=Recombinant%20Proteins","dc:title":"Recombinant Proteins"},{"@id":"https://cir.nii.ac.jp/all?q=Myofibrils","dc:title":"Myofibrils"},{"@id":"https://cir.nii.ac.jp/all?q=Mutagenesis","dc:title":"Mutagenesis"},{"@id":"https://cir.nii.ac.jp/all?q=Mutation","dc:title":"Mutation"},{"@id":"https://cir.nii.ac.jp/all?q=Escherichia%20coli","dc:title":"Escherichia coli"},{"@id":"https://cir.nii.ac.jp/all?q=Animals","dc:title":"Animals"},{"@id":"https://cir.nii.ac.jp/all?q=Humans","dc:title":"Humans"},{"@id":"https://cir.nii.ac.jp/all?q=Rabbits","dc:title":"Rabbits"}],"relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1390282679249293568","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Towards Understanding Mechanisms of Drug Action and Functions of the Body on the Molecular Level. Molecular mechanisms of calcium regulation of striated muscle contraction and its genetic disorder."},{"@language":"ja","@value":"薬の作用機序と生体機能の分子的理解に向けて　　筋収縮カルシウム受容調節の分子機構と遺伝性機能障害"},{"@value":"筋収縮カルシウム受容調節の分子機構と遺伝性機能障害"},{"@language":"ja-Kana","@value":"キンシュウシュク カルシウム ジュヨウ チョウセツ ノ ブンシ キコウ ト イデンセイ キノウ ショウガイ"}]},{"@id":"https://cir.nii.ac.jp/crid/1390282680019813888","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Inherited Cardiomyopathies as a Troponin Disease"}]}],"dataSourceIdentifier":[{"@type":"CROSSREF","@value":"10.1093/oxfordjournals.jbchem.a022615"},{"@type":"OPENAIRE","@value":"doi_dedup___::98a611bbd0928d168bbf9629fdfc34fb"},{"@type":"CROSSREF","@value":"10.1254/fpj.118.147_references_DOI_5Ajgsyj1B9V6rLgyj6SHMAO3dAb"},{"@type":"CROSSREF","@value":"10.2170/jjphysiol.54.307_references_DOI_5Ajgsyj1B9V6rLgyj6SHMAO3dAb"}]}