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. 2023 May 9;24(10):8493. doi: 10.3390/ijms24108493

Figure 8.

Figure 8

Pivotal role of E2 protein and the mechanisms of viral oncogenesis. (A). Transcription repression mechanism of E2. The promoter p105 of the oncoproteins E6 and E7 lies adjacent to the E2 protein binding sites 1 and 2. When the E2 protein dimer binds at its binding sites, it displaces several transcription factors, such as Sp1 and TFIID, thus preventing transcription of E6/E7. (B). HPV E6 and E7 targeted degradation of p53 and pRb tumor suppressor genes. E6 protein binds to the cellular ubiquitin-ligase, E6AP, and causes the ubiquitinylated degradation of the p53 protein. This forces the cells through uncontrolled cellular division, evading the preventive checkpoints. (C). HPV E7 protein binds to the pRB-E2F complex. An essential checkpoint for the cells to travel through the G1-S phase transition. E7 binds to this complex, leading to the ubiquitinylated degradation of the pRb tumor suppressor protein. Degradation of pRb sets the E2F transcription factor free, leading to the unregulated transcription of S-phase cyclin genes and, ultimately, to an unregulated cell cycle.