| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 8475352 | Journal of Molecular and Cellular Cardiology | 2013 | 9 Pages |
Abstract
⺠F764L and S532P point mutations were engineered into mouse cardiac myosin. ⺠Dilated cardiomyopathy developed in heterozygous F764L/+ and S532P/+ mice. ⺠Myocardial strips exhibited higher rates of force development and MgATP binding. ⺠These alterations in myofilament function preceded development of DCM.
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Authors
Bradley M. Palmer, Joachim P. Schmitt, Christine E. Seidman, J.G. Seidman, Yuan Wang, Stephen P. Bell, Martin M. LeWinter, David W. Maughan,