AI Article Synopsis
- Previous research highlighted that the HPV-16 E6 protein disrupts the function of the transcriptional co-activator p300/CBP, but its biological effects and specificity among HPV types were unclear.
- Recent studies revealed that both high-risk (HPV-16, HPV-18) and low-risk (HPV-11) E6 proteins can interact with p300.
- The findings indicate that the E6-p300 interaction is crucial for HPV E6 proteins to promote cell transformation, as a modified HPV-16 E6 that does not bind p300 was unable to support cell transformation in experiments.
Article Abstract
Previous studies have shown that the human papillomavirus type 16 (HPV-16) E6 protein binds to p300/CBP and abrogates its transcriptional co-activator function. However, there is little information on the biological consequences of this interaction and discrepancy as to whether the interaction is high-risk E6 specific or not. We performed a series of studies to compare the interactions of HPV-18 and HPV-11 E6 with p300, and showed that both high- and low- risk E6 proteins bind p300. In addition, using a transformation-deficient mutant of adenovirus E1a, which cannot interact with p300, we demonstrated that HPV-16, HPV-18 and, to a lesser extent, HPV-11 E6, can complement this mutant in cell transformation assays. In contrast, a mutant of HPV-16 E6 which does not bind p300 failed to rescue the E1a mutant. These results suggest that the E6-p300 interaction may be important for the ability of HPV E6 to contribute towards cell transformation.
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| http://dx.doi.org/10.1099/0022-1317-83-4-829 | DOI Listing |
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