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Human papillomavirus-induced carcinogenesis and the ubiquitin-proteasome system.

机译:人乳头瘤病毒引起的癌变和泛素-蛋白酶体系统。

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摘要

Certain types of human papillomaviruses have been etiologically associated with malignant lesions, most notably with cervical cancer. The major oncoproteins of these cancer-associated viruses are encoded by the viral E6 and E7 genes. Thorough characterization of these oncoproteins and their interaction with cellular proteins has shown that both E6 and E7 exploit the ubiquitin-proteasome system to degrade and, thus, to functionally inactivate negative cell-regulatory proteins including members of the p110(RB) family and p53. This act of piracy is assumed to contribute to both the efficient propagation of HPVs and HPV-induced carcinogenesis.
机译:某些类型的人乳头瘤病毒在病因上与恶性病变有关,最明显的是与宫颈癌有关。这些与癌症相关的病毒的主要癌蛋白由病毒E6和E7基因编码。这些癌蛋白及其与细胞蛋白相互作用的全面表征表明,E6和E7都利用泛素-蛋白酶体系统降解,从而使包括p110(RB)家族和p53在内的负性细胞调节蛋白功能失活。认为这种盗版行为有助于HPV的有效繁殖和HPV诱导的致癌作用。

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