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MeSH Review

DNA Tumor Viruses

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Disease relevance of DNA Tumor Viruses


High impact information on DNA Tumor Viruses

  • Binding depended upon the minimal regions of Rb necessary for its growth-suppressive activity, as well as upon the D-type cyclin sequence motif shared with Rb-binding DNA tumor virus oncoproteins [6].
  • Wild-type p53 gene has tumor suppressor properties, and is a target for several of the oncoproteins encoded by DNA tumor viruses [7].
  • The disruption of this E2F-Rb interaction, as well as a complex involving E2F in association with the cell cycle-regulated cyclin A-cdk2 kinase complex, may be a common mechanism of action for the oncoproteins encoded by the DNA tumor viruses [8].
  • Inhibiting CDK inhibitors: new lessons from DNA tumor viruses [9].
  • Cells altered by DNA tumor viruses responded to CB with numerous nuclear divisions resulting in highly multinucleated cells [10].

Chemical compound and disease context of DNA Tumor Viruses


Biological context of DNA Tumor Viruses


Gene context of DNA Tumor Viruses

  • p107 and p130 were originally identified as targets of the transforming domains of viral oncoproteins encoded by small DNA tumor viruses [20].
  • This is the first report of STAT activation by a DNA tumor virus protein [21].
  • Unlike serum growth factors, E7 induces S-phase entry without activating cyclin D1 gene expression, in keeping with the finding that cyclin D1 function is not required in cells transformed by DNA tumor viruses [22].
  • Significantly, we have obtained karyotypically stable tumors without the need to use DNA tumor virus oncoproteins and without deliberate ablation of p53 [23].
  • DNA tumor virus oncoproteins bind and inactivate Rb by interfering with the Rb/HDAC1 interaction [24].


  1. Epstein-Barr virus LMP1 blocks p16INK4a-RB pathway by promoting nuclear export of E2F4/5. Ohtani, N., Brennan, P., Gaubatz, S., Sanij, E., Hertzog, P., Wolvetang, E., Ghysdael, J., Rowe, M., Hara, E. J. Cell Biol. (2003) [Pubmed]
  2. Protein domains connect cell cycle stimulation directly to initiation of DNA replication. Gjørup, O.V., Rose, P.E., Holman, P.S., Bockus, B.J., Schaffhausen, B.S. Proc. Natl. Acad. Sci. U.S.A. (1994) [Pubmed]
  3. The three transforming regions of SV40 T antigen are required for immortalization of primary mouse embryo fibroblasts. Conzen, S.D., Cole, C.N. Oncogene (1995) [Pubmed]
  4. ORF73 of herpesvirus saimiri, a viral homolog of Kaposi's sarcoma-associated herpesvirus, modulates the two cellular tumor suppressor proteins p53 and pRb. Borah, S., Verma, S.C., Robertson, E.S. J. Virol. (2004) [Pubmed]
  5. Myristylated polyomavirus VP2: role in the life cycle of the virus. Krauzewicz, N., Streuli, C.H., Stuart-Smith, N., Jones, M.D., Wallace, S., Griffin, B.E. J. Virol. (1990) [Pubmed]
  6. Functional interactions of the retinoblastoma protein with mammalian D-type cyclins. Ewen, M.E., Sluss, H.K., Sherr, C.J., Matsushime, H., Kato, J., Livingston, D.M. Cell (1993) [Pubmed]
  7. The E6 oncoprotein encoded by human papillomavirus types 16 and 18 promotes the degradation of p53. Scheffner, M., Werness, B.A., Huibregtse, J.M., Levine, A.J., Howley, P.M. Cell (1990) [Pubmed]
  8. E2F: a link between the Rb tumor suppressor protein and viral oncoproteins. Nevins, J.R. Science (1992) [Pubmed]
  9. Inhibiting CDK inhibitors: new lessons from DNA tumor viruses. Funk, J.O., Galloway, D.A. Trends Biochem. Sci. (1998) [Pubmed]
  10. Differential response to cytochalasin B among cells transformed by DNA and RNA tumor viruses. O'Neill, F.J., Miller, T.H., Hoen, J., Stradley, B., Devlahovich, V. J. Natl. Cancer Inst. (1975) [Pubmed]
  11. Density-dependent growth inhibition of fibroblasts ectopically expressing p27(kip1). Zhang, X., Wharton, W., Donovan, M., Coppola, D., Croxton, R., Cress, W.D., Pledger, W.J. Mol. Biol. Cell (2000) [Pubmed]
  12. DNA tumor viruses and Src family tyrosine kinases, an intimate relationship. Messerschmitt, A.S., Dunant, N., Ballmer-Hofer, K. Virology (1997) [Pubmed]
  13. Protein phosphatases and DNA tumor viruses: transformation through the back door? Mumby, M.C., Walter, G. Cell Regul. (1991) [Pubmed]
  14. Inhibition of activities of DNA polymerase alpha, beta, gamma, and reverse transcriptase of L1210 cells by phosphonoacetic acid. Allaudeen, H.S., Bertino, J.R. Biochim. Biophys. Acta (1978) [Pubmed]
  15. DNA tumor virus transforming proteins and the cell cycle. Moran, E. Curr. Opin. Genet. Dev. (1993) [Pubmed]
  16. The Rb family contains a conserved cyclin-dependent-kinase-regulated transcriptional repressor motif. Chow, K.N., Starostik, P., Dean, D.C. Mol. Cell. Biol. (1996) [Pubmed]
  17. The promoter of the human proliferating cell nuclear antigen gene is not sufficient for cell cycle-dependent regulation in organotypic cultures of keratinocytes. Noya, F., Chien, W.M., Wu, X., Banerjee, N.S., Kappes, J.C., Broker, T.R., Chow, L.T. J. Biol. Chem. (2002) [Pubmed]
  18. The domain of p53 required for binding HPV 16 E6 is separable from the degradation domain. Mansur, C.P., Marcus, B., Dalal, S., Androphy, E.J. Oncogene (1995) [Pubmed]
  19. Apoptosis induced by ectopic expression of cyclin D1 but not cyclin E. Sofer-Levi, Y., Resnitzky, D. Oncogene (1996) [Pubmed]
  20. p107 and p130: versatile proteins with interesting pockets. Classon, M., Dyson, N. Exp. Cell Res. (2001) [Pubmed]
  21. Activation of STAT transcription factors by herpesvirus Saimiri Tip-484 requires p56lck. Lund, T.C., Garcia, R., Medveczky, M.M., Jove, R., Medveczky, P.G. J. Virol. (1997) [Pubmed]
  22. Sequential activation of cyclin E and cyclin A gene expression by human papillomavirus type 16 E7 through sequences necessary for transformation. Zerfass, K., Schulze, A., Spitkovsky, D., Friedman, V., Henglein, B., Jansen-Dürr, P. J. Virol. (1995) [Pubmed]
  23. The significance of p16INK4a in cell defenses against transformation. Drayton, S., Brookes, S., Rowe, J., Peters, G. Cell Cycle (2004) [Pubmed]
  24. Che-1 affects cell growth by interfering with the recruitment of HDAC1 by Rb. Bruno, T., De Angelis, R., De Nicola, F., Barbato, C., Di Padova, M., Corbi, N., Libri, V., Benassi, B., Mattei, E., Chersi, A., Soddu, S., Floridi, A., Passananti, C., Fanciulli, M. Cancer Cell (2002) [Pubmed]
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