Fig. 5: Suggested model.
From: Deacetylation of CHK2 by SIRT1 protects cells from oxidative stress-dependent DNA damage response
Under normal conditions, SIRT1 binds to CHK2 and inhibits its activity through deacetylation. Oxidative stress initiates DDR pathways, which leads to dissociation of SIRT1 from CHK2, and this in turn increases the acetylation and the activity of CHK2. The phosphorylation and acetylation of CHK2 potentiates p53 activity, which results in cell death upon oxidative stress
