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Interaction between the HPV E7 oncoprotein and the transcriptional coactivator p300

机译：HPV E7癌蛋白与转录共激活因子p300之间的相互作用

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Infection with high-risk human papillomaviruses (HPV) can lead to the development of cervical cancer. This process depends on the interaction of the virus-encoded oncoproteins, E6 and E7, with a variety of host regulatory proteins. As E7 shares both functional and structural similarities with the Adenovirus E1a (Ad E1a) protein, we were interested in investigating the possible interactions between E7 and the transcriptional coactivator p300, since it was originally identified as a target of Ad E1a. Using a variety of assays, we show that E7s from both high- and low-risk HPV types interact with p300. Mutational analysis of E7 maps the site of the interaction to a region spanning the pRb-binding domain and the CKII phosphorylation site. We also map the site of interaction on p300 largely to the CH1 domain. In addition, we demonstrate that the binding between 16E7 and p300 is direct, and can be detected in vivo by coimmunoprecipitation and mammalian two-hybrid assays. Finally, we show that E7 can abolish the p300-mediated E2 transactivation function, suggesting that complex formation between E7 and p300 may contribute to the regulation of E2 transcriptional activity.
机译：高危人类乳头瘤病毒（HPV）感染可导致宫颈癌的发展。这个过程取决于病毒编码的癌蛋白E6和E7与多种宿主调节蛋白的相互作用。由于E7与腺病毒E1a（Ad E1a）蛋白共享功能和结构上的相似性，因此我们有兴趣研究E7与转录共激活因子p300之间的可能相互作用，因为它最初被确定为Ad E1a的靶标。使用多种分析方法，我们显示来自高风险和低风险HPV类型的E7与p300相互作用。 E7的突变分析将相互作用的位点映射到跨pRb结合域和CKII磷酸化位点的区域。我们还将p300上的相互作用位点主要映射到CH1域。此外，我们证明了16E7和p300之间的结合是直接的，并且可以通过共免疫沉淀和哺乳动物两杂交试验在体内进行检测。最后，我们表明E7可以废除p300介导的E2反式激活功能，这表明E7和p300之间的复合物形成可能有助于E2转录活性的调节。

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