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

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 β1‐adrenergic receptors in cardiac plasma membranes. Muscle Nerve 45: 128–130, 2012