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

Esther Llagostera, María Jesúsá Álvarez López, Cecilia Scimia, Daniele Catalucci, Marcelina Párrizas, Pilar Ruiz-Lozano, Perla Kaliman

Research output: Contribution to journalArticlepeer-review


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 languageEnglish
Pages (from-to)128-130
Number of pages3
JournalMuscle and Nerve
Issue number1
Publication statusPublished - Jan 2012


  • 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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