TEAD-1 induced changes in cardiac myosin heavy chain protein and LV power output of isolated working hearts. High resolution glycerol gel electrophoresis of protein extract (0.75 μg) isolated from the left ventricle of 5-month-old WT and Tg lines 4, 12, and 14 revealed that a sustained increase in TEAD-1 protein leads to an αMyHC to βMyHC transition in TEAD-1 transgenic mice (A). LV power output of isolated TEAD-1 transgenic hearts of 5-month-old mice confirm a contractile dysfunction (B). High resolution glycerol gel electrophoresis of protein extract (0.75 μg) isolated from LV, right ventricle (RV), and septum of 10-month-old WT and TEAD-1 Tg line 12 mice (C) display a significant induction of βMyHC protein (n = 3). *, p < 0.05.