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Science 17 February 1989:
Vol. 243. no. 4893, pp. 934 - 937
DOI: 10.1126/science.2537532

Articles

Science, Vol 243, Issue 4893, 934-937
Copyright © 1989 by American Association for the Advancement of Science


articles

The human papilloma virus-16 E7 oncoprotein is able to bind to the retinoblastoma gene product

N Dyson, PM Howley, K Munger, and E Harlow

Cold Spring Harbor Laboratory, NY 11724.

Deletions or mutations of the retinoblastoma gene, RB1, are common features of many tumors and tumor cell lines. Recently, the RB1 gene product, p105-RB, has been shown to form stable protein/protein complexes with the oncoproteins of two DNA tumor viruses, the adenovirus E1A proteins and the simian virus 40 (SV40) large T antigen. Neither of these viruses is thought to be associated with human cancer, but they can cause tumors in rodents. Binding between the RB anti-oncoprotein and the adenovirus or SV40 oncoprotein can be recapitulated in vitro with coimmunoprecipitation mixing assays. These assays have been used to demonstrate that the E7 oncoprotein of the human papilloma virus type-16 can form similar complexes with p105-RB. Human papilloma virus-16 is found associated with approximately 50 percent of cervical carcinomas. These results suggest that these three DNA viruses may utilize similar mechanisms in transformation and implicate RB binding as a possible step in human papilloma virus-associated carcinogenesis.


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J. Virol. 78, 2620-2626
   Abstract »    Full Text »    PDF »
Epstein-Barr Virus Nuclear Antigen 3C Regulates Cyclin A/p27 Complexes and Enhances Cyclin A-Dependent Kinase Activity.
J. S. Knight and E. S. Robertson (2004)
J. Virol. 78, 1981-1991
   Abstract »    Full Text »    PDF »
Recapitulation of the Effects of the Human Papillomavirus Type 16 E7 Oncogene on Mouse Epithelium by Somatic Rb Deletion and Detection of pRb-Independent Effects of E7 In Vivo.
S. J. Balsitis, J. Sage, S. Duensing, K. Munger, T. Jacks, and P. F. Lambert (2003)
Mol. Cell. Biol. 23, 9094-9103
   Abstract »    Full Text »    PDF »
Signals That Dictate Nuclear Localization of Human Papillomavirus Type 16 Oncoprotein E6 in Living Cells.
M. Tao, M. Kruhlak, S. Xia, E. Androphy, and Z.-M. Zheng (2003)
J. Virol. 77, 13232-13247
   Abstract »    Full Text »    PDF »
Notch1 Can Contribute to Viral-Induced Transformation of Primary Human Keratinocytes.
S. Lathion, J. Schaper, P. Beard, and K. Raj (2003)
Cancer Res. 63, 8687-8694
   Abstract »    Full Text »    PDF »
A promoter within the E6 ORF of human papillomavirus type 16 contributes to the expression of the E7 oncoprotein from a monocistronic mRNA.
J. A. Glahder, C. N. Hansen, J. Vinther, B. S. Madsen, and B. Norrild (2003)
J. Gen. Virol. 84, 3429-3441
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Human Papillomavirus Type 16 E7 Oncoprotein Can Induce Abnormal Centrosome Duplication through a Mechanism Independent of Inactivation of Retinoblastoma Protein Family Members.
S. Duensing and K. Munger (2003)
J. Virol. 77, 12331-12335
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Keratinocyte Growth Conditions Modulate Telomerase Expression, Senescence, and Immortalization by Human Papillomavirus Type 16 E6 and E7 Oncogenes.
B. Fu, J. Quintero, and C. C. Baker (2003)
Cancer Res. 63, 7815-7824
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The HBZ Factor of Human T-cell Leukemia Virus Type I Dimerizes with Transcription Factors JunB and c-Jun and Modulates Their Transcriptional Activity.
J. Basbous, C. Arpin, G. Gaudray, M. Piechaczyk, C. Devaux, and J.-M. Mesnard (2003)
J. Biol. Chem. 278, 43620-43627
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Direct Activation of Cyclin-Dependent Kinase 2 by Human Papillomavirus E7.
W. He, D. Staples, C. Smith, and C. Fisher (2003)
J. Virol. 77, 10566-10574
   Abstract »    Full Text »    PDF »
Study of viral integration of HPV-16 in young patients with LSIL.
G Gallo, M Bibbo, L Bagella, A Zamparelli, F Sanseverino, M R Giovagnoli, A Vecchione, and A Giordano (2003)
J. Clin. Pathol. 56, 532-536
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Inactivation of RAS Association Domain Family 1A Gene in Cervical Carcinomas and the Role of Human Papillomavirus Infection.
I. Kuzmin, L. Liu, R. Dammann, L. Geil, E. J. Stanbridge, S. P. Wilczynski, M. I. Lerman, and G. P. Pfeifer (2003)
Cancer Res. 63, 1888-1893
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