Pressure overload-induced cardiac hypertrophy and heart failure involve profound remodeling of the myocardial proteome. To elucidate the role of the E3 adaptor protein SPOP in this process, we performed TMT-based quantitative proteomic analysis on left ventricular tissues collected four weeks after transverse aortic constriction (TAC) from Myh6-Cre control mice (n=5) and cardiac-specific SPOP knockout (cKO) mice (n=5).