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.
| Original language | English |
|---|---|
| Pages (from-to) | 128-130 |
| Number of pages | 3 |
| Journal | Muscle and Nerve |
| Volume | 45 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - Jan 2012 |
Keywords
- β-adrenergic
- DMPK
- Heart
- Isoproterenol
- Myotonic dystrophy
- Receptor trafficking
ASJC Scopus subject areas
- Clinical Neurology
- Cellular and Molecular Neuroscience
- Physiology (medical)
- Physiology
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Llagostera, E., López, M. J. Á., Scimia, C., Catalucci, D., Párrizas, M., Ruiz-Lozano, P., & Kaliman, P. (2012). Altered β-adrenergic response in mice lacking myotonic dystrophy protein kinase. Muscle and Nerve, 45(1), 128-130. https://doi.org/10.1002/mus.22256