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. 2016 Jul 22;8(35):58021–58036. doi: 10.18632/oncotarget.10770

Figure 2. Effect of BRAFi, MEKi and AKTi treatment on ERK and AKT phosphorylation of CM cells.

Figure 2

A. Basal protein level of p-ERK, p-AKT and PARP signalling in untreated cell lines. B-D. Cropped western blots of CRMM1, CRMM2 and CM2005.1 treated with increasing doses of Vemurafenib, Dabrafenib, MEK162 and MK2206 at 24 hrs, showing changes in p-ERK and p-AKT. E. To confirm the efficacy of MK2206 at the molecular level, the downstream substrate of AKT, p-PRAS40, was detected after 24 hrs of exposure to MK2206. All experiments were repeated three times, and representative graphs are shown.