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Altered β‐adrenergic response in mice lacking myotonic dystrophy protein kinase
Author(s) -
Llagostera Esther,
Jesús Álvarez López María,
Scimia Cecilia,
Catalucci Daniele,
Párrizas Marcelina,
RuizLozano Pilar,
Kaliman Perla
Publication year - 2012
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.22256
Subject(s) - myotonic dystrophy , knockout mouse , context (archaeology) , endocrinology , medicine , protein kinase a , adrenergic , agonist , gene knockout , pathophysiology , kinase , biology , gene product , myotonia , muscular dystrophy , gene , receptor , gene expression , microbiology and biotechnology , genetics , paleontology
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. Muscle Nerve 45: 128–130, 2012