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. Author manuscript; available in PMC: 2016 Apr 7.
Published in final edited form as: Cell Rep. 2015 Apr 2;11(1):125–136. doi: 10.1016/j.celrep.2015.03.010

Figure 4. Rictor/mTORC2 disruption promotes cardiac dysfunction and dilation through MST1 activation.

Figure 4

A–B. Phosphorylated, total and cleaved levels of MST1 were evaluated in the hearts of CT and R-cKO mice at baseline and after pressure overload. Representative immunoblots are shown, and densitometric analyses are shown in Figure S4. C. Six-month-old CT, R-cKO, DN-MST1 and R-cKO+DN-MST1 mice underwent echocardiographic analysis. Fractional shortening (FS) was measured. N=3–7. D–F. CT, R-cKO, DN-MST1 and R-cKO+DN-MST1 mice around 10 weeks of age were subjected to 4 weeks of TAC and then underwent echocardiographic analysis. Left ventricular end-diastolic diameter (LVEDD) and fractional shortening (FS) were measured. N=3–7. All data are expressed as mean ± SEM * p<0.05.