Fig. 7. Schematic representation of the Δ133p53β activity regulation through aggregation.

Increased expression of Δ133p53β in cancer cells leads to its accumulation and creation of the aggregates. Δ133p53β can form stable aggregates mostly due to its unfolded conformation. Δ133p53β sequestration in aggregates would store isoform in inactive form. When this isoform activity is required, recruiting partners release it from aggregates. Recruiting partners are chaperones like CCT complex or p53 family members like p63 isoforms. The presence of recruiting partners increases cancer cell invasion. Interaction with CCT complex activates Δ133p53β driven invasiveness. The binding of Δ133p53β to p63 isoforms further leads to positive effects on invasion, either by synergizing the pro-invasive ∆Np63 isoforms activity or inhibiting the anti-invasive effect of TAp63 isoforms.