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. Author manuscript; available in PMC: 2019 Jul 10.
Published in final edited form as: Oncogene. 2019 Jan 10;38(17):3274–3287. doi: 10.1038/s41388-018-0633-1

Figure 5.

Figure 5.

TopBP1 activation of E2F1 and p73 expression is dependent upon AKT. A). Western blot analysis of p-AKT, AKT and GAPDH levels in HFK, HFK-16, HFK-18, and HFK-31 grown in monolayer cultures. B). Western blot analysis for p-AKT, AKT and GAPDH levels in HFK cells stably infected with LXSN vector control, HPV31E6, HPV31E7, and HPV31E6E7. C). Western blot analysis of p-AKT, AKT, p-TopBP1, TopBP1, E2F1, p73, p-CHK1, CHK1 and GAPDH protein levels in 31E7-expressing cells upon differentiation in high-calcium media for 72 hours in the presence of the AKT inhibitor MK2206. D). Western blot analysis of p-AKT, AKT, p-TopBP1, TopBP1, E2F1, p73, p-CHK1, CHK1 and GAPDH protein levels in HPV31 cells upon differentiation in high-calcium media for 72 hours in the presence of the AKT inhibitor MK2206. E) Southern blot analysis for HPV31 episomes in CIN612 cells with MK2206 treatment following differentiation in high calcium media for indicated times (hrs). F) Southern blot analysis for HPV31 episomes in CIN612 cells treated with LY294002 following differentiation in high calcium media for indicated times (hrs). All results are representative of observations from 3 independent experiments.