Figure 3. Depletion of endogenous β-TRCP results in elevated Mdm2 levels, which subsequently suppress the amplitude of the p53 pulse in response to DNA damage.

This further suggests that disruption of the CKI/SCF^β-TRCP signaling pathway, which governs Mdm2 ubiquitination and degradation, might lead to misregulation of the p53 activity that contributes to cancer development.