Fig. 7
From: MRE11A: a novel negative regulator of human DNA mismatch repair
Schematic summary of the study. In naïve cells, a proportion of MRE11A may interact with MLH1 but does not interfere with the proper interaction between intrinsic PMS2 and MLH1. In MRE11A-overexpressing cells, excess MRE11A occupied the binding site of PMS2 to MLH1, leading to the degradation of unbound PMS2 and decreased MLH1·PMS2 heterodimer on chromatin, consequently compromising MMR activity. In MRE11A-deficient cells, more intrinsic PMS2 binds to MLH1, leading to increased MMR activity and thus increased sensitivity to MNNG treatment