Figure 5.

Targeting PP2A dysregulation using molecular disruptors.A, the synthetic peptide, SHAP, competes with STRN3 for binding to the PP2A A/C dimer, thus preventing the formation of the STRN3-PP2A holoenzyme. By extension, SHAP could theoretically prevent the formation and function of the oncogenic STRIPAK complex by displacing STRN3 from the heterodimer, and even if assembled, the SHAP peptide could render the PP2A complex inert (143). B, CS-11 is a PP2A molecular disruptor aimed at dissociating β-catenin from the B55α-PP2A heterotrimer, ultimately promoting the degradation of β-catenin by preventing its dephosphorylation (182).