n?=?6/group. vehicle-treated MI hearts, p?Rabbit Polyclonal to C-RAF the %EF post-MI (39.71??2.3%, p?Pim1/AKK1-IN-1 (Fig.?2a). This hypertrophy was accompanied by the activation of cardiac mTOR (Fig.?2c), and an increased phosphorylation of P70S6KThr389, a downstream effector of mTOR (Fig.?2d). mAb A treatment limited cardiac hypertrophy, an effect which was associated with abrogating mTOR/P70S6K signalling (Fig.?2bCd). In addition, a decrease in cardiac SERCA2A expression was observed in the post-MI.