Carboxyl‐terminal modulator protein (CTMP) inhibits the activation of protein kinase B (AKT) signaling in hypertrophic hearts and myocytes. A, Western blot analysis and quantitative results of total (T) and phosphorylated (P) levels of AKT, mammalian target of rapamycin (mTOR), glycogen synthase kinase 3β (GSK3β), and ribosomal protein S6 kinase β‐1 (P70S6K) in the left ventricular tissues of CTMPloxP/loxP (CTMP‐Flox) and cardiac‐specific knockout of CTMP (CTMP‐CKO) mice 4 weeks after sham or aortic banding (AB) surgery (n=4 mice per group; **P<0.01 vs CTMP‐Flox sham; ##
P<0.01 vs CTMP‐Flox AB). B, Western blot analysis and quantitative results of T and P levels of AKT, mTOR, GSK3β, and P70S6K in left ventricular tissues from transgenic (TG) and nontransgenic (NTG) mice 4 weeks after sham or AB surgery (n=4 mice per group; **P<0.01 vs NTG sham; ##
P<0.01 vs NTG AB). C, Western blot analysis and quantitative results of the T and P levels of AKT, mTOR, GSK3β, and P70S6K in neonatal rat cardiomyocytes (NRCMs) infected with adenoviral short‐hairpin RNA (AdshRNA) and adenoviral short‐hairpin CTMP (AdshCTMP) and treated with PBS or angiotensin II (AngII; n=3 independent experiments; **P<0.01 vs AdshRNA+PBS; ##
P<0.01 vs AdshRNA+AngII). D, Western blot analysis and quantitative results of the T and P levels of AKT, mTOR, GSK3β, and P70S6K in NRCMs infected with adenoviral green fluorescent protein (AdGFP) and adenoviral CTMP (AdCTMP) and treated with PBS or AngII (n=3 independent experiments; **P<0.01 vs AdGFP+PBS; ##
P<0.01 vs AdGFP+AngII) by Bonferroni post hoc analysis (A [P‐AKT and P‐mTOR], C [P‐mTOR], and D [P‐mTOR and P‐P70S6K]) or Tamhane's T2 analysis (A [P‐GSK3β and P‐P70S6K], B, C [P‐AKT, P‐GSK3β, and P‐P70S6K], and D [P‐AKT and P‐GSK3β]).