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pubmed-article:11044432pubmed:abstractTextIn the pathogenesis of cardiac dysfunction in heart failure, a decrease in the activity of the sarcoplasmic reticulum (SR) Ca(2+)-ATPase is believed to be a major determinant. Here, we report a novel mechanism of cardiac dysfunction revealed by assessing the functional interaction of FK506-binding protein (FKBP12.6) with the cardiac ryanodine receptor (RyR) in a canine model of pacing-induced heart failure.lld:pubmed
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pubmed-article:11044432pubmed:articleTitleAltered stoichiometry of FKBP12.6 versus ryanodine receptor as a cause of abnormal Ca(2+) leak through ryanodine receptor in heart failure.lld:pubmed
pubmed-article:11044432pubmed:affiliationSecond Department of Internal Medicine, Yamaguchi University School of Medicine, Yamaguchi, Japan. yanoma@po.cc.yamaguchi-u.ac.jplld:pubmed
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