Abstract
The protein kinase product of the gene mutated in myotonic dystrophy 1 (DMPK) is reported to play a role in cardiac pathophysiology. To gain insight into the molecular mechanisms modulated by DMPK, we characterize the impact of DMPK ablation in the context of cardiac β-adrenergic function. Our data demonstrate that DMPK knockout mice present altered β-agonist-induced responses and suggest that this is due, at least in part, to a reduced density of β(1)-adrenergic receptors in cardiac plasma membranes.
Copyright © 2011 Wiley Periodicals, Inc.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Adrenergic beta-Agonists / pharmacology
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Animals
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Cell Membrane / drug effects
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Disease Models, Animal
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Dose-Response Relationship, Drug
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Echocardiography
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Isoproterenol / pharmacology
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Mice
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Mice, Knockout
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Myocardium / cytology
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Myotonic Dystrophy / genetics
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Myotonic Dystrophy / pathology
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Myotonic Dystrophy / physiopathology
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Myotonin-Protein Kinase
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Phosphorylation / drug effects
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Protein Serine-Threonine Kinases / deficiency*
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Receptors, Adrenergic, beta / blood
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Receptors, Adrenergic, beta / metabolism*
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Serine / metabolism
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Sodium-Potassium-Exchanging ATPase / metabolism
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Vesicular Transport Proteins / metabolism
Substances
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Adrenergic beta-Agonists
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DMPK protein, mouse
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Receptors, Adrenergic, beta
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Vesicular Transport Proteins
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early endosome antigen 1
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Serine
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Myotonin-Protein Kinase
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Protein Serine-Threonine Kinases
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Sodium-Potassium-Exchanging ATPase
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Isoproterenol