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. Author manuscript; available in PMC: 2017 Jun 14.
Published in final edited form as: Cell Metab. 2016 Jun 14;23(6):1013–1021. doi: 10.1016/j.cmet.2016.05.010

Figure 1. Energy status regulates the senescence growth arrest.

Figure 1

Senescent cells have increased AMP:ATP and ADP:ATP ratios, which activate AMP-activated protein kinase (AMPK). AMP kinase in turn activates p53, which increases p21 transcription. AMPK also inactivates HuR, which increases the stability of the p21 and p16INK4a mRNAs. p21 and p16INK4a are cyclin-dependent kinase inhibitors that impose the senescence proliferative arrest by increasing activity of the pRB tumor suppressor. p53 and pRB might counterbalance each other in regulating glycolysis in senescent cells.