Heart-Specific Ablation of Prkar1a Causes Failure of Heart Development and Myxomagenesis | Zendy

Zhirong Yin | Zendy; Georgette N. Jones | Zendy; William H. Towns | Zendy; Xiaoli Zhang | Zendy; E. Dale Abel | Zendy; Philip F. Binkley | Zendy; David Jarjoura | Zendy; Lawrence S. Kirschner | Zendy

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Heart-Specific Ablation of Prkar1a Causes Failure of Heart Development and Myxomagenesis

Author(s) -

Zhirong Yin,

Georgette N. Jones,

William H. Towns,

Xiaoli Zhang,

E. Dale Abel,

Philip F. Binkley,

David Jarjoura,

Lawrence S. Kirschner

Publication year - 2008

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.107.759233

Subject(s) - medicine , transcription factor , heart development , protein kinase a , heart failure , knockout mouse , heterozygote advantage , carney complex , phenotype , downregulation and upregulation , gata4 , endocrinology , microbiology and biotechnology , kinase , biology , cancer research , embryonic stem cell , gene , genetics , receptor , allele

Protein kinase A signaling has long been known to play an important role in cardiac function. Dysregulation of the protein kinase A system, caused by mutation of the protein kinase A regulatory subunit gene PRKAR1A, causes the inherited tumor syndrome Carney complex, which includes cardiac myxomas as one of its cardinal features. Mouse models of this genetic defect have been unsatisfactory because homozygote null animals die early in development and heterozygotes do not exhibit a cardiac phenotype.

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