Interactions of the human papillomavirus E7 protein with cell cycle regulators
Interactions of the human papillomavirus E7 protein with cell cycle regulators
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DOI：
10.1006/scbi.1996.0042
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发表时间：
1996-12-01
影响因子：
14.5
通讯作者：
Munger, K
中科院分区：
文献类型：
--
作者：
Jones, DL;Munger, K
人乳头瘤病毒（HPV）严重依赖于细胞机器复制其基因组。病毒复制仅限于正常生长停滞的皮肤的分化层。因此，HPV已经开发出破坏细胞生长调节途径的策略，并且能够解偶联细胞增殖和分化。HPV E7蛋白能克服某些细胞周期蛋白依赖性激酶抑制剂的活性，与细胞周期蛋白/细胞周期蛋白依赖性激酶复合物结合，并使视网膜母细胞瘤肿瘤抑制蛋白不稳定。这些生物活性有助于高危HPV E7蛋白的致癌潜力，这些蛋白在HPV阳性宫颈癌中持续表达。(C)1997年出版社有限公司。
Human papillomaviruses (HPVs) critically depend on the cellular machinery for the replication of their genome. Viral replication is restricted to the differentiated strata of the skin that are normally growth arrested. Hence, the HPVs have developed strategics to subvert cellular growth regulatory pathways and are able to uncouple cellular proliferation and differentiation. The HPV E7 protein can overcome the activity of some cyclin-dependent kinase inhibitors, associate with cyclin/cyclin dependent Kinase complexes and Bind to and destabilize the retinoblastoma tumor suppressor protein. These biological activities contribute to the carcinogenic potential of the high risk HPV E7 proteins which are consistently expressed in HPV-positive cervical carcinomas. (C) 1997 Academic Press Ltd.