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. 2014 Aug 8;9(8):e104444. doi: 10.1371/journal.pone.0104444

Figure 5. Proposed model: MDM2-ALT1 and MDMX-ALT2 antagonize their full-length counterparts and lead to p53 stabilization.

Figure 5

A. Under normal conditions, MDM2 and MDMX function to maintain low levels of p53 (via ubiquitination and subsequent degradation) and curb its transcriptional activity by binding p53. This helps maintain homeostasis and normal cellular functions including cell cycle progression. B. Under genotoxic stress, alternative splice forms MDM2-ALT1 and MDMX-ALT2 interact with the full-length MDM proteins and interfere in their p53-regulatory functions. This leads to the stabilization and upregulation of p53 levels and also the activation of p53 transcriptional targets leading to changes in cell cycle progression.