Interactions of the human papillomavirus E7 protein with cell cycle regulators.
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.
Jones
D L
DL
Department of Pathology, Harvard Medical School, Boston, MA, USA.
Münger
K
K
D000595:Amino Acid Sequence; D018797:Cell Cycle Proteins / Q000502:physiology*; D016193:G1 Phase / Q000502:physiology; D006801:Humans; D008969:Molecular Sequence Data; D009856:Oncogene Proteins, Viral / Q000502:physiology*; D027383:Papillomaviridae; D050725:Papillomavirus E7 Proteins; D016160:Retinoblastoma Protein / Q000502:physiology; D016159:Tumor Suppressor Protein p53 / Q000502:physiology; D014779:Virus Replication / Q000502:physiology
D018797:Cell Cycle Proteins; D009856:Oncogene Proteins, Viral; D050725:Papillomavirus E7 Proteins; D016160:Retinoblastoma Protein; D016159:Tumor Suppressor Protein p53; C059731:oncogene protein E7, Human papillomavirus type 16