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pubmed-article:15897344pubmed:abstractTextDesensitization and downregulation of myocardial beta-adrenergic receptors (betaARs) are initiated by the increase in betaAR kinase 1 (betaARK1) levels. By interacting with betaARK1 through the phosphoinositide kinase (PIK) domain, phosphoinositide 3-kinase (PI3K) is targeted to agonist-stimulated betaARs, where it regulates endocytosis. We tested the hypothesis that inhibition of receptor-targeted PI3K activity would alter receptor trafficking and ameliorate betaAR signaling, ultimately improving contractility of failing cardiomyocytes.lld:pubmed
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pubmed-article:15897344pubmed:articleTitleRestoration of beta-adrenergic receptor signaling and contractile function in heart failure by disruption of the betaARK1/phosphoinositide 3-kinase complex.lld:pubmed
pubmed-article:15897344pubmed:affiliationDepartment of Medicine, Cell Biology and Molecular Genetics, Duke University Medical Center, Durham, NC 27710, USA.lld:pubmed
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pubmed-article:15897344pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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