Reversibility of PRKAG2 Glycogen-Storage Cardiomyopathy and Electrophysiological Manifestations | Zendy

Cordula M. Wolf | Zendy; Michael Arad | Zendy; Ferhaan Ahmad | Zendy; Atsushi Sanbe | Zendy; Scott Bernstein | Zendy; Okan Toka | Zendy; Tetsuo Konno | Zendy; Gregory E. Morley | Zendy; Jeffrey Robbins | Zendy; J.G. Seidman | Zendy; Christine E. Seidman | Zendy; Charles I. Berul | Zendy

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Reversibility of PRKAG2 Glycogen-Storage Cardiomyopathy and Electrophysiological Manifestations

Author(s) -

Cordula M. Wolf,

Michael Arad,

Ferhaan Ahmad,

Atsushi Sanbe,

Scott Bernstein,

Okan Toka,

Tetsuo Konno,

Gregory E. Morley,

Jeffrey Robbins,

J.G. Seidman,

Christine E. Seidman,

Charles I. Berul

Publication year - 2007

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.107.726752

Subject(s) - medicine , cardiomyopathy , glycogen , transgene , glycogen storage disease , cardiology , genetically modified mouse , electrical conduction system of the heart , endocrinology , heart failure , biology , electrocardiography , biochemistry , gene

PRKAG2 mutations cause glycogen-storage cardiomyopathy, ventricular preexcitation, and conduction system degeneration. A genetic approach that utilizes a binary inducible transgenic system was used to investigate the disease mechanism and to assess preventability and reversibility of disease features in a mouse model of glycogen-storage cardiomyopathy.

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