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| Content Provider | PubMed Central |
|---|---|
| Author | Wells, Susanne I. Francis, Delicia A. Karpova, Alla Y. Dowhanick, Jennifer J. Benson, John D. Howley, Peter M. |
| Copyright Year | 2000 |
| Abstract | A hallmark of human papillomavirus (HPV) associated carcinogenesis is the integration of the viral DNA into the cellular genome, usually accompanied by the loss of expression of the viral E2 gene. E2 binds to and represses the viral promoter directing expression of the E6 and E7 oncogenes. The re-introduction and expression of exogenous E2 in HPV-positive cancer cells results in cellular growth arrest, while growth in the context of exogenous E2 can be restored through the expression of exogenous E6 and E7. Here we examine the individual contributions of the viral E6 and E7 genes to this phenotype. E6 alone displays moderate activity, whereas both E7 and adenovirus E1A display high activity in reversing E2-mediated cellular growth suppression. Using defined mutants of E7 and E1A, we show that an intact retinoblastoma interaction domain is required for this function. In addition, we show that the E2-mediated growth arrest of HPV-positive cells results in cellular senescence, and implicate the cyclin/cdk inhibitor p21 CIP as a downstream E2 effector in this phenotype. |
| Related Links | http://dx.doi.org/10.1093/emboj/19.21.5762 |
| Ending Page | 5771 |
| Page Count | 10 |
| Starting Page | 5762 |
| File Format | |
| ISSN | 14602075 |
| e-ISSN | 14602075 |
| Journal | The EMBO Journal |
| Issue Number | 21 |
| Volume Number | 19 |
| Language | English |
| Publisher | Oxford University Press |
| Publisher Date | 2000-11-01 |
| Access Restriction | Open |
| Rights Holder | Oxford University Press |
| Subject Keyword | Biochemistry, Genetics and Molecular Biology(all) Immunology and Microbiology(all) Neuroscience(all) Molecular Biology Research in Higher Education |
| Content Type | Text |
| Resource Type | Article |
| Subject | Neuroscience Immunology and Microbiology Medicine Molecular Biology |
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