Ryanodine Receptor Phosphorylation by Calcium/Calmodulin-Dependent Protein Kinase II Promotes Life-Threatening Ventricular Arrhythmias in Mice With Heart Failure | Zendy

Ralph J. van Oort | Zendy; Mark McCauley | Zendy; Sayali S. Dixit | Zendy; Laëtitia Pereira | Zendy; Yi Yang | Zendy; Jonathan L. Respress | Zendy; Qiongling Wang | Zendy; Angela C. De Almeida | Zendy; Darlene G. Skapura | Zendy; Mark E. Anderson | Zendy; Donald M. Bers | Zendy; Xander H.T. Wehrens | Zendy

Open Access

Ryanodine Receptor Phosphorylation by Calcium/Calmodulin-Dependent Protein Kinase II Promotes Life-Threatening Ventricular Arrhythmias in Mice With Heart Failure

Author(s) -

Ralph J. van Oort,

Mark McCauley,

Sayali S. Dixit,

Laëtitia Pereira,

Yi Yang,

Jonathan L. Respress,

Qiongling Wang,

Angela C. De Almeida,

Darlene G. Skapura,

Mark E. Anderson,

Donald M. Bers,

Xander H.T. Wehrens

Publication year - 2010

Publication title -

circulation

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 7.795

H-Index - 607

eISSN - 1524-4539

pISSN - 0009-7322

DOI - 10.1161/circulationaha.110.982298

Subject(s) - ryanodine receptor , medicine , calcium , calmodulin , heart failure , phosphorylation , protein kinase a , endocrinology , kinase , receptor , microbiology and biotechnology , cardiology , biology

approximately half of patients with heart failure die suddenly as a result of ventricular arrhythmias. Although abnormal Ca(2+) release from the sarcoplasmic reticulum through ryanodine receptors (RyR2) has been linked to arrhythmogenesis, the molecular mechanisms triggering release of arrhythmogenic Ca(2+) remain unknown. We tested the hypothesis that increased RyR2 phosphorylation by Ca(2+)/calmodulin-dependent protein kinase II is both necessary and sufficient to promote lethal ventricular arrhythmias.

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