Abstract: Recent experiments demonstrated that three E6 single-site mutants (F47R, R102A, and L50E) can inhibit the E6/E6AP/p53 heterotrimer formation and rescue p53 from the degradation pathway.
Anti-tumor effects of genetic vaccines against HPV major oncogenes.
PMID: 25483514
2015
Human vaccines & immunotherapeutics
Abstract: These E7 and E6 vaccines were made with mutated oncogenes, the E7GGG mutant that does not bind pRb and the E6F47R mutant that is less effective in inhibiting p53, respectively.
Introduction: Our previous data have demonstrated the induction of antitumor activity in a safe setting by vaccines based on two mutated, non-transforming forms of HPV16 E7 (E7GGG) and E6 (E6F47R) (De Giuli Morghen, Personal Communication).
Result: As shown in Figure 7A, tumor appearance was delayed to day 13 post challenge (p.c.) in 75% of the pcDNA3-E7GGG-CP treated animals, in 60% of mice vaccinated with pcDNA3-E6F47R-CP and pCI-
A prime/boost strategy using DNA/fowlpox recombinants expressing the genetically attenuated E6 protein as a putative vaccine against HPV-16-associated cancers.
PMID: 25763880
2015
Journal of translational medicine
Method: The recombinant FP virus expressing the E6F47R protein (FPE6F47R) was obtained by in-vitro homologous recombination.
Method: To detect the expression of the E6F47R protein, immunofluorescence was also carried out on CEFs and Vero and MRC-5 cells infected with 5 PFU/cell, as described previously.
Method: To determine whether the E6F47R protein was expressed correctly, CEFs and Vero and MRC-5
Discussion: When expressed in HPV-positive cervical cancer cells, E6F47R acts as a dominant-negative mutant by counteracting the p53 degradation activity of the endogenous E6, and thus restores high p53 protein levels.
A single-codon mutation converts HPV16 E6 oncoprotein into a potential tumor suppressor, which induces p53-dependent senescence of HPV-positive HeLa cervical cancer cells.
Abstract: Finally, small interfering RNAs directed against p53 counteract the effect of E6 F47R expression, indicating that E6 F47R-induced cellular senescence is strongly dependent on p53 signaling pathway.
Abstract: Here, we show that a single-point mutation, F47R, is sufficient to convert the HPV16 E6 oncoprotein into a suppressor of HPV-positive HeLa cervical cancer cells proliferation.
Abstract: Moreover, the prolonged expression of E6 F47R leads to suppression of HeLa cells proliferation through the induction of premature senescence.
HPV mutation literature information.
PMID: 
2022
Biophysical journal
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