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. Author manuscript; available in PMC: 2017 Feb 1.
Published in final edited form as: Int J Biochem Cell Biol. 2015 Dec 21;71:72–80. doi: 10.1016/j.biocel.2015.12.010

Fig. 2.

Fig. 2

Transcriptional upregulation of p16 in AMPKα2−/− MEFs. (A) (Upper) AMPKα2 deletion significantly upregulated p16. (Bottom) Quantification of Western blot data. n=8, *p< 0.001 vs WT. (B) (Upper) AMPKα2 deletion significantly down-regulated E2F1. (Bottom) Quantification of Western blot data. n=6, *p< 0.001 vs WT. (C) Proteasome inhibitor, MG132 (20 μM, 8 h) did not further increase p16 in AMPKα2−/− MEFs. n=4, *p< 0.001 vs WT. (D) Quantitative RT-PCR analysis of p16 expression in MEFs. β-actin was used as endogenous loading control. Values are mean ± SEM of four independent experiments, *p< 0.001 vs WT.