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Human Papilloma Virus (HPV) and Host Cellular Interactions

机译:人乳头瘤病毒(HPV)与宿主细胞的相互作用

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Viral-induced carcinogenesis has been attributed to the ability of viral oncoproteins to target and interact with the host cellular proteins. It is generally accepted that Human papilloma virus (HPV) E6 and E7 function as the dominant oncoproteins of ‘high-risk’ HPVs by altering the function of critical cellular proteins. Initially it was shown that HPV E6 enhances the degradation of p53, while HPV E7 inactivates the function of the retinoblastoma tumor suppressor protein Rb. However, recent studies during the last decade have identified a number of additional host cellular targets of both HPV E6 and E7 that may also play an important role in malignant cellular transformation. In this review we present the interactions of HPV E6 and E7 with the host cellular target proteins. We also present the role of DNA integration in the malignant transformation of the epithelial cell.
机译:病毒诱导的癌变已归因于病毒癌蛋白靶向宿主细胞蛋白并与宿主细胞蛋白相互作用的能力。人们普遍认为,人乳头瘤病毒(HPV)E6和E7通过改变关键细胞蛋白的功能,成为“高危” HPV的主要癌蛋白。最初显示,HPV E6增强p53的降解,而HPV E7灭活视网膜母细胞瘤抑癌蛋白Rb的功能。但是,最近十年来的最新研究已经确定了HPV E6和E7的许多其他宿主细胞靶标,它们在恶性细胞转化中也可能起重要作用。在这篇综述中,我们介绍了HPV E6和E7与宿主细胞靶蛋白的相互作用。我们还介绍了DNA整合在上皮细胞恶性转化中的作用。

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