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. Author manuscript; available in PMC: 2013 Oct 1.
Published in final edited form as: J Mol Cell Cardiol. 2012 Jul 21;53(4):532–541. doi: 10.1016/j.yjmcc.2012.07.004

Figure 5. Administration of triciribine (TCN) in icaPI3Kα animals blocks the hyperphosphorylation of cardiac Akt.

Figure 5

(A) Schematic illustration of the caPI3Kα transgene induction and the pan-Akt inhibitor triciribine (TCN) injection protocol in icaPI3Kα animals. (B) LVW/TL ratios were similar in WT+Vehicle, icaPI3Kα+Vehicle and icaPI3Kα+TCN animals. (C) Representative Western blots of fractionated LV proteins from WT+Vehicle, icaPI3Kα+Vehicle and icaPI3Kα+TCN animals (n=4 in each group) probed with anti-pAkt and anti-total Akt antibodies. The expression level of pAkt in each lane on each blot was measured and normalized to the expression of total-Akt in the same lane on the same blot. Mean pAkt/Akt ratios in the LV from icaPI3Kα animals, vehicle- or TCN-treated, were expressed relative to the mean value in the control (WT+Vehicle) LV samples. (D) The mean ± SEM pAkt/Akt ratio is significantly (*P<0.001) higher in icaPI3Kα+Vehicle (n=4), compared with WT+Vehicle (n=4), LV. In addition, 4 week administration of TCN significantly (*P<0.001) reduced the phosphorylation of Akt in icaPI3Kα LV (see text).