Figure 4
From: GILZ inhibits the mTORC2/AKT pathway in BCR-ABL+ cells
GILZ deregulates AKT (Ser473) phosphorylation in imatinib-resistant BCR-ABL+ cells. (a) WB analysis of BCR-ABL, CRKL and STAT5 phosphorylation in GILZ- or Void-transfected M1 cells. (b) WB analysis of FoxO3a, AKT (Ser473) and Erk44/42 phosphorylation in transfected M1 and DA1 cells. (c) WB analysis of MDM2, AKT (Thr308), Bad and S6 phosphorylation in transfected M1 cells. (d) WB analysis of FoxO3a and AKT (Ser473) phosphorylation in transfected K562-r cells. (e) WB analysis of S6 phosphorylation in transfected K562-r cells. (f) WB analysis of PKCα (Ser657), SGK (Ser422) and 4E-BP1 phosphorylation in M1 (Void and GILZ) and K562-r (Void and GILZ) cells. The loading controls were actin and unphosphorylated PKCα, SGK and 4E-BP1. (g) ELISA analysis of P-AKT1 (Ser473) and total AKT in Void- versus GILZ-transfected M1 cells. **P<0.01, Kruskal–Wallis test. The error bars represent mean±s.d. of three separate experiments performed in triplicate.
