Up-regulation of miR-31 in human atrial fibrillation begets the arrhythmia by depleting dystrophin and neuronal nitric oxide synthase
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Title
Up-regulation of miR-31 in human atrial fibrillation begets the arrhythmia by depleting dystrophin and neuronal nitric oxide synthase
Authors
Keywords
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Journal
Science Translational Medicine
Volume 8, Issue 340, Pages 340ra74-340ra74
Publisher
American Association for the Advancement of Science (AAAS)
Online
2016-05-26
DOI
10.1126/scitranslmed.aac4296
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- MicroRNAs and atrial fibrillation: mechanisms and translational potential
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- Mechanochemotransduction During Cardiomyocyte Contraction Is Mediated by Localized Nitric Oxide Signaling
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- miR-31 modulates dystrophin expression: new implications for Duchenne muscular dystrophy therapy
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- MicroRNAs Involved in Molecular Circuitries Relevant for the Duchenne Muscular Dystrophy Pathogenesis Are Controlled by the Dystrophin/nNOS Pathway
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- New antiarrhythmic drugs for treatment of atrial fibrillation
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- Effects of Neuronal Nitric Oxide Synthase on Human Coronary Artery Diameter and Blood Flow In Vivo
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- Nitric Oxide Increases Cardiac I K1 by Nitrosylation of Cysteine 76 of Kir2.1 Channels
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- Nitric oxide inhibits Kv4.3 and human cardiac transient outward potassium current (Ito1)
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