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Semin Cancer Biol. 1996 Dec;7(6):327-37.

Interactions of the human papillomavirus E7 protein with cell cycle regulators.

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1
Department of Pathology, Harvard Medical School, Boston, MA, USA.

Abstract

Human papillomavirus (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 strategies 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.

PMID:
9284525
DOI:
10.1006/scbi.1996.0042
[Indexed for MEDLINE]
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