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Altered ?-adrenergic response in mice lacking myotonic dystrophy protein kinase.

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 ?-adrenergic function. Our data demonstrate that DMPK knockout mice present altered ?-agonist-induced responses and suggest that this is due, at least in part, to a reduced density of ?(1)-adrenergic receptors in cardiac plasma membranes.

SUBMITTER: Llagostera E

PROVIDER: S-EPMC3422658 | biostudies-literature | 2012 Jan

REPOSITORIES: biostudies-literature

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Altered β-adrenergic response in mice lacking myotonic dystrophy protein kinase.

Llagostera Esther E Álvarez López María Jesús MJ Scimia Cecilia C Catalucci Daniele D Párrizas Marcelina M Ruiz-Lozano Pilar P Kaliman Perla P

Muscle & nerve 20120101 1

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 memb ...[more]

PMID: 22190319

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