Interactions of the human papillomavirus E7 protein with cell cycle regulators

被引:80
|
作者
Jones, DL [1 ]
Munger, K [1 ]
机构
[1] HARVARD UNIV,SCH MED,PROGRAM BIOL & BIOMED SCI,BOSTON,MA 02115
关键词
cell division cycle; human papillomavirus; keratinocyte differentiation; protein degradation; tumor suppressor protein; viral oncoprotein;
D O I
10.1006/scbi.1996.0042
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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.
引用
收藏
页码:327 / 337
页数:11
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