Interactions of the human papillomavirus E7 protein with cell cycle regulators

DL Jones, K Münger - Seminars in cancer biology, 1996 - Elsevier
DL Jones, K Münger
Seminars in cancer biology, 1996Elsevier
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 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 …
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 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.
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