Skip to main content
. Author manuscript; available in PMC: 2015 Aug 5.
Published in final edited form as: Cell Metab. 2014 Jul 3;20(2):306–319. doi: 10.1016/j.cmet.2014.06.004

Figure 4. Oncogenic Kras enhances histone acetylation in vitro in an Akt- and ACL-dependent manner.

Figure 4

(A) Mouse pancreatic primary cells derived from KPCY mouse PanIN lesions were treated with indicated inhibitors for 24 hours. Acetylation of histones and phosphorylation of signaling proteins were assessed by Western Blot in acid extracts and RIPA lysates, respectively. Ponceau staining is shown as loading control for histones. (B) Glucose consumption and Lactate production were measured in PanIN-derived primary mouse cells treated as in (A), mean +/− SD of triplicates (*, p<0.05). (C) Acetyl-CoA and CoASH levels were measured in PanIN cells, +/− Akt inhibitor, mean +/− SD of triplicates (***, p<0.001). (D) PanIN-derived primary cells were transduced with control (shCtrl) or ACL-targeting (shACL) short hairpin RNA. Cells were cultivated under indicated glucose concentrations, +/− Akt inhibitor, +/− 5 mM acetate for 24 hours. Histones were acid-extracted and analyzed by Western Blot. Ponceau staining is shown as loading control for histones.