New Concepts on the Role of Human Papillomavirus in Cell Cycle Regulation

References

• International Agency for Research on Cancer (IARC). Papillomaviruses. Monographs on the evaluation of carcinogenic risks to humans. IARC, Lyon 1995; Vol 64
   Google Scholar
• Zur Hausen H. Viruses in human tumors – reminiscences and perspectives. Adv Cancer Res 1996; 68: 1–22
   Google Scholar
• Zur Hausen H. Papillomavirus infections - a major cause of human cancers. Biochitn Biophys Acta 1996; 1288: F55–78
   PubMed Web of Science ®Google Scholar
• Zur Hausen H. Roots and perspectives of contemporary papillomavirus research. J Cancer Res Clin Oncol 1996; 122: 3–13
   PubMedGoogle Scholar
• Syrjänen K, Syrjänen S. Papillomavirus Infections in Human Pathology. Wiley, New York, (in press)
   Google Scholar
• Stern P L, Stanley M A. Human Papillomaviruses and Cervical Cancer. Biology and Immunology. Oxford University Press, Oxford 1994
   Google Scholar
• Zur Hausen H. Human pathogenic papillomaviruses. Curr Top Microbiol Immunol 1994; 186: 1–266
   Google Scholar
• Zur Hausen H, de Villiers E M. Human papillomaviruses. Annu Rev Microbiol 1994; 48: 427–47
   PubMed Web of Science ®Google Scholar
• Myers G, Lu H, Calef C, Leitner T. Heterogeneity of papillomaviruses. Semin Cancer Biol 1996; 7: 349–58
   PubMed Web of Science ®Google Scholar
• Arndt O, Johannes A, Zeise K, Brock J. “High risk” HPV types in oral and laryngeal papillomas and in laryngeal leukoplakia. Laryngol Rhinol Otol 1997; 76: 142–9
   Google Scholar
• deVilliers E M. Papillomavirus and HPV typing. Clin Dermatol 1997; 15: 199–206
   Google Scholar
• Favre M, Ramoz N, Orth G. Human papillomaviruses: general features. Clin Dermatol 1997; 15: 181–98
   PubMedGoogle Scholar
• Jablonska S, Majewski S, Obalek S, Orth G. Cutaneous warts. Clin Dermatol 1997; 15: 309–19
   Google Scholar
• Orth G, Jablonska S. Papillomavirus: part one. Clin Dermatol 1997; 15: 179–80
   Google Scholar
• Wright T C, Sun X W. Anogenital papillomavirus infection and neoplasia in immunodeficient women. Obstet Gynecol Clin North Am 1996; 23: 861–93
   Google Scholar
• Pfister H, Fuchs P G. Anatomy, taxonomy and evolution of papillomaviruses. Intervirology 1994; 37: 143–9
   PubMed Web of Science ®Google Scholar
• Fuchs P G, Pfister H. Transcription of papillomavirus genomes. Intervirology 1994; 37: 159–67
   PubMed Web of Science ®Google Scholar
• Turek L P. The structure, function, and regulation of papillomaviral genes in infection and cervical cancer. Adv Virus Res 1994; 44: 305–56
   PubMed Web of Science ®Google Scholar
• Hoppe-Seyler F, Butz K. Cellular control of human papillomavirus oncogene transcription. Mol Carcinog 1994; 10: 134–41
   PubMed Web of Science ®Google Scholar
• Auborn K J, Wang H, Vaccariello M A, Taichman L B. Kinetics of HPV11 DNA replication after infection of keratinocytes with virions. Virus Res 1996; 43: 85–90
   Google Scholar
• Sherr C J. Mammalian Gl cyclins. Cell 1993; 73: 1059–65
   PubMed Web of Science ®Google Scholar
• O'Connor P M. Mammalian G1 and G2 phase checkpoints. Cancer Surv 1997; 29: 151–82
   PubMedGoogle Scholar
• Grana X, Reddy E P. Cell cycle control in mammalian cells: role of cyclins, cyclin dependent kinases (CDKs), growth suppressor genes and cyclin-dependent kinase inhibitors (CKIs). Oncogene 1995; 11: 211–9
   PubMed Web of Science ®Google Scholar
• Arellano M, Moreno S. Regulation of CDK/cyclin complexes during the cell cycle. Int J Biochem Cell Biol 1997; 29: 559–73
   PubMed Web of Science ®Google Scholar
• Desdouets C, Sobczak-Thepot J, Murphy M, Brechot C. Cyclin A: function and expression during cell proliferation. Prog Cell Cycle Res 1995; 1: 115–23
   PubMedGoogle Scholar
• Gao C Y, Zelenka P S. Cyclins, cyclin-dependent kinases and differentiation. Bioessays 1997; 19: 307–15
   PubMed Web of Science ®Google Scholar
• Pines J. The cell cycle kinases. Semin Cancer Biol 1994; 5: 305–13
   PubMed Web of Science ®Google Scholar
• Drexler H G. Review of alterations of the cyclin-dependent kinase inhibitor INK4 family genes p15, p16, p18 and p19 in human leukemia-lymphoma cells. Leukemia 1998; 12: 845–59
   PubMed Web of Science ®Google Scholar
• Livneh E, Fishman D D. Linking protein kinase C to cell-cycle control. Eur] Biochem 1997; 248: 1–9
   PubMedGoogle Scholar
• MacLachlan T K, Sang N, Giordano A. Cyclins, cyclin-dependent kinases and cdk inhibitors: implications in cell cycle control and cancer. Crit Rev Eukaryot Gene Expr 1995; 5: 127–56
   PubMed Web of Science ®Google Scholar
• Lawrence D A. Transforming growth factor-beta: a general review. Eur Cytokine Netw 1996; 7: 363–74
   PubMed Web of Science ®Google Scholar
• Mayol X, Grana X. pRB, p107 and p130 as transcriptional regulators: role in cell growth and differentiation. Prog Cell Cycle Res 1997; 3: 157–69
   PubMedGoogle Scholar
• Phelps W C, Bagchi S, Barnes J A. Analysis of trans activation by human papillomavirus type 16 E7 and adenovirus 12S E1A suggests a common mechanism. J Virol 1991; 65: 6922–30
   PubMedGoogle Scholar
• Morris J D, Crook T, Bandara L R, Davies R, Lathangue N B, Vousden K H. Human papillomavirus type 16 E7 regulates E2F and contributes to mitogenic signalling. Oncogene 1993; 8: 893–8
   PubMedGoogle Scholar
• Kubbutat M HG, Vousden K H. Role of E6 and E7 oncoproteins in HPV-induced anogenital malignancies. Semin Virol 1996; 7: 295–304
   Google Scholar
• Weintraub S J, Prater C A, Dean D C. Retinoblastoma protein switches the E2F site from positive to negative element. Nature 1992; 358: 259–61
   PubMed Web of Science ®Google Scholar
• Helin K, Wu C L, Fattaey A R, Lees J A, Dynlacht B D, Ngwu C, et al. Heterodimerization of the transcription factors E2F-1 and DP-1 leads to cooperative trans-activation. Genes Dev 1993; 7: 1850–61
   PubMed Web of Science ®Google Scholar
• Hickman E S, Bates S, Vousden K H. Perturbation of the p53 response by human papillomavirus type 16 E7. J Virol 1997; 71: 3710–8
   PubMedGoogle Scholar
• Donehower L A, Harvey M, Slagle B L, McArthur M J, Montgomery C A, Butel J S, et al. Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours. Nature 1992; 356: 215–21
   PubMed Web of Science ®Google Scholar
• El-Deiry W S, Tokino T, Velculescu V E, Levy D B, Parsons R, Trent J M, et al. WAF1, a potential mediator of p53 tumor suppression. Cell 1993; 75: 817–25
   PubMed Web of Science ®Google Scholar
• Kastan M B, Zhan Q, El Deiry W S, Fornace A J, Jr. A mammalian cell cycle checkpoint pathway utilizing p53 and GADD45 is defective in ataxia-telangiectasia. Cell 1992; 71: 587–97
   PubMed Web of Science ®Google Scholar
• Miyashita T, Reed J C. Tumor suppressor p53 is a direct transcriptional activator of the human bax gene. Cell 1995; 80: 293–9
   PubMed Web of Science ®Google Scholar
• Barak Y, Juven T, Haffner R, Oren M. mdm2 expression is induced by wild type p53 activity. EMBO J 1993; 12: 461–8
   PubMed Web of Science ®Google Scholar
• Okamoto K, Beach D. Cyclin G is a transcriptional target of the p53 tumor suppressor protein. EMBO J 1994; 13: 4816–22
   PubMed Web of Science ®Google Scholar
• Buckbinder L, Talbott R, Velasco-Miguel S, Takenaka I, Faha B, Seizinger B R, et al. Induction of the growth inhibitor IGF-binding protein 3 by p53. Nature 1995; 377: 646–9
   PubMed Web of Science ®Google Scholar
• Harper J W, Adami G R, Wei N, Keyomarsi K, Elledge S J. The p21 Cdk-interacting protein Cip1 is a potent inhibitor of G1 cyclin-dependent kinases. Cell 1993; 75: 805–16
   PubMed Web of Science ®Google Scholar
• Galloway D A, Demers G W, Foster S A, Halbert C L, Russell K. Cell cycle checkpoint control is bypassed by human papillomavirus oncogenes. Cold Spring Harb Symp Quant Biol 1994; 59: 297–306
   Google Scholar
• Jones D L, Munger K. Analysis of the p53-mediated G(1) growth arrest pathway in cells expressing the human papillomavirus type 16 E7 oncoprotein. J Virol 1997; 71: 2905–12
   PubMedGoogle Scholar
• Bernard H U. Controls in the papillomavirus life cycle. FEMS Microbiol Immunol 1990; 64: 201–6
   Google Scholar
• Ham J, Dostatni N, Gauthier J M, Yaniv M. The papillomavirus E2 protein: a factor with many talents. Trends Biochem Sci 1991; 16: 440–4
   Google Scholar
• McBride A A, Romanczuk H, Howley P M. The papillomavirus E2 regulatory proteins. J Biol Cbem 1991; 266: 18411–4
   Google Scholar
• Giri I, Yaniv M. Study of the E2 gene product of the cottontail rabbit papillomavirus reveals a common mechanism of transactivation among papillomaviruses. J Virol 1988; 62: 1573–81
   PubMedGoogle Scholar
• Barsoum J, Prakash S S, Han P, Androphy E J. Mechanism of action of the papillomavirus E2 repressor: repression in the absence of DNA binding. J Virol 1992; 66: 3941–5
   PubMedGoogle Scholar
• Desaintes C, Hallez S, Detremmerie O, Burny A. Wild-type p53 down-regulates transcription from oncogenic human papillomavirus promoters through the epithelial specific enhancer. Oncogene 1995; 10: 2155–61
   Google Scholar
• Drummond-Barbosa D A, Vaillancourt R R, Kazlauskas A, DiMaio D. Ligand-independent activation of the platelet-derived growth factor beta receptor: requirements for bovine papillomavirus E5-induced mitogenic signaling. Mol Cell Biol 1995; 15: 2570-–81
   PubMedGoogle Scholar
• Drummond-Barbosa D, DiMaio D. Virocrine transformation. Biochim Biophys Acta 1997; 1332: Ml–17
   Google Scholar
• Flores E R, Lambert P F. Evidence for a switch in the mode of human papillomavirus type 16 DNA replication during the viral life cycle. J Virol 1997; 71: 7167–79
   PubMed Web of Science ®Google Scholar
• Desaintes C, Demeret C, Goyat S, Yaniv M, Thierry F. Expression of the papillomavirus E2 protein in HeLa cells leads to apoptosis. EMBO J 1997; 16: 504–14
   PubMed Web of Science ®Google Scholar
• Bubb V, McCance D J, Schlegel R. DNA sequence of the HPV-16 E5 ORF and the structural conservation of its encoded protein. Virology 1988; 163: 243–6
   Google Scholar
• Halbert C L, Galloway D A. Identification of the E5 open reading frame of human papillomavirus type 16. J Virol 1988; 62: 1071–5
   Google Scholar
• Leptak C, Ramon Y, Kulke R, Horwitz B H, Riese D J, Dotto G P, et al. Tumorigenic transformation of murine keratino-cytes by the E5 genes of bovine papillomavirus type 1 and human papillomavirus type 16. J Virol 1991; 65: 7078–83
   PubMed Web of Science ®Google Scholar
• Leechanachai P, Banks L, Moreau F, Matlashewski G. The E5 gene from human papillomavirus type 16 is an oncogene which enhances growth factor-mediated signal transduction to the nucleus. Oncogene 1992; 7: 19–25
   PubMed Web of Science ®Google Scholar
• Pim D, Collins M, Banks L. Human papillomavirus type 16 E5 gene stimulates the transforming activity of the epidermal growth factor receptor. Oncogene 1992; 7: 27–32
   PubMed Web of Science ®Google Scholar
• Straight S W, Hinkle P M, Jewers R J, McCance D J. The E5 oncoprotein of human papillomavirus type 16 transforms fibroblasts and effects the downregulation of the epidermal growth factor receptor in keratinocytes. J Virol 1993; 67: 4521–32
   PubMed Web of Science ®Google Scholar
• Bouvard V, Matlashewski G, Gu Z M, Storey A, Banks L. The human papillomavirus type 16 E5 gene cooperates with the E7 gene to stimulate proliferation of primary cells and increases viral gene expression. Virology 1994; 203: 73–80
   PubMed Web of Science ®Google Scholar
• Hwang J Y, Lin B Y, Tang F M, Yu W CY. Tamoxifen stimulates human papillomavirus type-16 gene expression and cell proliferation in a cervical cancer cell line. Cancer Res 1992; 52: 6848–52
   Web of Science ®Google Scholar
• Straight S W, Herman B, McCance D J. The E5 oncoprotein of human papillomavirus type 16 inhibits the acidification of endosomes in human keratinocytes. J Virol 1995; 69: 3185–92
   PubMed Web of Science ®Google Scholar
• Crusius K, Auvinen E, Steuer B, Gaissert H, Alonso A. The human papillomavirus type 16 E5-protein modulates ligand-dependent activation of the EGF receptor family in the human epithelial cell line HaCaT. Exp Cell Res 1998; 241: 76–83
   PubMed Web of Science ®Google Scholar
• Conrad M, Goldstein D, Andresson T, Schlegel R. The e5 protein of HPV-6, but not HPV-16, associates efficiently with cellular growth factor receptors. Virology 1994; 200: 796–800
   PubMed Web of Science ®Google Scholar
• Kulke R, DiMaio D. Biological properties of the deer papillomavirus E5 gene in mouse C127 cells: growth transformation, induction of transformation. J Virol 1991; 4943–9
   Google Scholar
• Petti L, DiMaio D. Stable association between the bovine papillomavirus E5 transforming protein and activated platelet-derived growth factor receptor in transformed mouse cells. Proc Natl Acad Sci USA 1992; 89: 6736–40
   PubMedGoogle Scholar
• Meyer A N, Xu Y F, Webster M K, Smith A E, Donoghue D J. Cellular transformation by a transmembrane peptide: structural requirements for the bovine papillomavirus e5 oncoprotein. Proc Natl Acad Sci USA 1994; 91: 4634–8
   PubMedGoogle Scholar
• Nilson L A, Gottlieb R L, Polack G W, DiMaio D. Mutational analysis of the interaction between the bovine papillomavirus e5 transforming protein and the endogenous beta receptor for platelet-derived growth factor in mouse c127 cells. J Virol 1995; 69: 5869–74
   Google Scholar
• Sparkowski J, Anders J, Schlegel R. E5 oncoprotein retained in the endoplasmic reticulum/cis golgi still induces PDGF receptor autophosphorylation but does not transform cells. EMBO J 1995; 14: 3055–63
   PubMed Web of Science ®Google Scholar
• Petti L, DiMaio D. Specific interaction between the bovine papillomavirus e5 transforming protein and the beta receptor for platelet-derived growth factor in stably transformed and acutely transfected cells. J Virol 1994; 68: 3582–92
   PubMedGoogle Scholar
• Petti L M, Reddy V, Smith S O, DiMaio D. Identification of amino acids in the transmembrane and juxtamembrane domains of the platelet-derived growth factor receptor required for productive interaction with the bovine papillomavirus E5 protein. J Virol 1997; 71: 7318–27
   Google Scholar
• Goldstein D J, Andresson T, Sparkowski J J, Schlegel R. The BPV-1 e5-protein, the 16-kda membrane pore-forming protein and the PDGF receptor exist in a complex that is dependent on hydrophobic transmembrane interactions. EMBO J 1992; 11: 4851-–9
   PubMedGoogle Scholar
• Maher D W, Strawn L M, Donoghue D J. Alanine mutagenesis of conserved residues in the platelet-derived growth factor family - identification of residues necessary for dimerization and transformation. Oncogene 1993; 8: 533–41
   Google Scholar
• Cohen B D, Goldstein D J, Rutledge L, Vass W C, Lowy D R, Schlegel R, et al. Transformation-specific interaction of the bovine papillomavirus E5 oncoprotein with the platelet-derived growth factor receptor transmembrane domain and the epidermal growth factor receptor cytoplasmic domain. J Virol 1993; 67: 5303–11
   PubMedGoogle Scholar
• Gu Z, Matlashewski G. Effect of human papillomavirus type 16 oncogenes on MAP kinase activity. J Virol 1995; 69: 8051–6
   Google Scholar
• Crusius K, Auvinen E, Alonso A. Enhancement of EGF- and PMA-mediated MAP kinase activation in cells expressing the human papillomavirus type 16 E5 protein. Oncogene 1997; 15: 1437–44
   PubMed Web of Science ®Google Scholar
• Tsao Y P, Li L Y, Tsai T C, Chen S L. Human papillomavirus type 11 and 16 E5 represses p(21WafI/SdiI/CipI) gene expression in fibroblasts and keratinocytes. J Virol 1996; 70: 7535–9
   Google Scholar
• Chen J J, Reid C E, Band V, Androphy E J. Interaction of papillomavirus e6 oncoproteins with a putative calcium-binding protein. Science 1995; 269: 529–31
   PubMed Web of Science ®Google Scholar
• Chen S L, Tsai T C, Han C P, Tsao Y P. Mutational analysis of human papillomavirus type 11 E5a oncoprotein. J Virol 1996; 70: 3502–8
   Google Scholar
• Halbert C L, Demers G W, Galloway D A. The E7 gene of human papillomavirus type 16 is sufficient for immortalization of human epithelial cells. J Virol 1991; 65: 473–8
   PubMed Web of Science ®Google Scholar
• Sedman S A, Barbosa M S, Vass W C, Hubbert N L, Haas J A, Lowy D R, et al. The full-length E6 protein of human papillomavirus type 16 has transforming and trans-activating activities and cooperates with E7 to immortalize keratinocytes in culture. J Virol 1991; 65: 4860–6
   PubMedGoogle Scholar
• Band V, Zajchowski D, Kulesa V, Sager R. Human papilloma virus DNAs immortalize normal human mammary epithelial cells and reduce their growth factor requirements. Proc Natl Acad Sci USA 1990; 87: 463–7
   PubMed Web of Science ®Google Scholar
• Werness B A, Levine A J, Howley P M. Association of human papillomavirus type 16 and 18 E6 proteins with p53. Science 1990; 248: 76–9
   PubMed Web of Science ®Google Scholar
• Keen N, Elston R, Crawford L. Interaction of the e6 protein of human papillomavirus with cellular proteins. Oncogene 1994; 9: 1493–9
   Google Scholar
• Weis K, Griffiths G, Lamond A L. The endoplasmic reticulum calcium-binding protein of 55 kDa is a novel EF-hand protein retained in the endoplasmic reticulum by a carboxyl-terminal His-Asp-Glu-Leu motif. J Biol Chem 1994; 269: 19142–50
   PubMedGoogle Scholar
• Kim K H, Yoon D J, Moon Y A, Kim Y S. Expression and localization of human papillomavirus type 16 E6 and E7 open reading frame proteins in human epidermal keratino-cyte. Yonsei Med] 1994; 35: 1–9
   Google Scholar
• Etscheid B G, Foster S A, Galloway D A. The E6 protein of human papillomavirus type 16 functions as a transcriptional repressor in a mechanism independent of the tumor suppressor protein, p53. Virology 1994; 205: 583–5
   PubMed Web of Science ®Google Scholar
• Kiyono T, Hiraiwa A, Fujita M, Hayashi Y, Akiyama T, Ishibashi M. Binding of high-risk human papillomavirus E6 oncoproteins to the human homologue of the Drosophila discs large tumor suppressor protein. Proc Natl Acad Sci USA 1997; 94: 11612–6
   PubMed Web of Science ®Google Scholar
• Scheffner M, Huibregtse J M, Vierstra R D, Howley P M. The HPV-16 E6 and E6-AP complex functions as a ubiquitin-protein ligase in the ubiquitination of p53. Cell 1993; 75: 495–505
   PubMed Web of Science ®Google Scholar
• Marston N J, Crook T, Vousden K H. Interaction of p53 with MDM2 is independent of e6 and does not mediate wild type transformation suppressor function. Oncogene 1994; 9: 2707–16
   PubMedGoogle Scholar
• Mansur C P, Marcus B, Dalai S, Androphy E J. The domain of p53 required for binding HPV 16 E6 is separable from the degradation domain. Oncogene 1995; 10: 457–65
   PubMedGoogle Scholar
• Huibregtse J M, Scheffner M, Howley P M. A cellular protein mediates association of p53 with the E6 oncoprotein of human papillomavirus types 16 or 18. EMBO J 1991; 10: 4129–35
   PubMed Web of Science ®Google Scholar
• Scheffner M, Takahashi T, Huibregtse J M, Minna J D, Howley P M. Interaction of the human papillomavirus type 16 E6 oncoprotein with wild-type and mutant human p53 proteins. J Virol 1992; 66: 5100–5
   PubMed Web of Science ®Google Scholar
• Ciechanover A. The ubiquitin-mediated proteolytic pathway: mechanisms of action and cellular physiology. Biol Chem Hoppe Seyler 1994; 375: 565–81
   Google Scholar
• Hochstrasser M, Papa F R, Chen P, Swaminathan S, Johnson P, Stillman L, et al. The DOA pathway: studies on the functions and mechanisms of ubiquitin-dependent protein degradation in the yeast Saccharomyces cerevisiae. Cold Spring Harb Symp Quant Biol 1995; 60: 503–13
   PubMedGoogle Scholar
• Crook T, Tidy J A, Vousden K H. Degradation of p53 can be targeted by HPV E6 sequences distinct from those required for p53 binding and trans-activation. Cell 1991; 67: 547–56
   PubMed Web of Science ®Google Scholar
• Crook T, Vousden K H. Interaction of HPV E6 with p53 and associated proteins. Biochem Soc Trans 1994; 22: 52–5
   PubMed Web of Science ®Google Scholar
• Pim D, Storey A, Thomas M, Massimi P, Banks L. Mutational analysis of HPV-18 e6 identifies domains required for p53 degradation in vitro, abolition of p53 transactivation in vivo and immortalisation of primary BMK cells. Oncogene 1994; 9: 1869–76
   Google Scholar
• Dalai S, Gao Q S, Androphy E J, Band V. Mutational analysis of human papillomavirus type 16 E6 demonstrates that p53 degradation is necessary for immortalization of mammary epithelial cells. J Virol 1996; 70: 683–8
   Google Scholar
• Nuber U, Schwarz S E, Scheffner M. The ubiquitin-protein ligase E6-associated protein (E6-AP) serves as its own substrate. Eur J Biochem 1998; 254: 643–9
   PubMedGoogle Scholar
• Pim D, Massimi P, Banks L. Alternatively spliced HPV-18 E6* protein inhibits E6 mediated degradation of p53 and suppresses transformed cell growth. Oncogene 1997; 15: 257–64
   PubMed Web of Science ®Google Scholar
• Lepik D, Iives I, Kristjuhan A, Maimers T, Ustav M. p53 protein is a suppressor of papillomavirus DNA amplifi-cational replication. J Virol 1998; 72: 6822–31
   Google Scholar
• Lechner M S, Laimins L A. Inhibition of p53 DNA binding by human papillomavirus E6 proteins. J Virol 1994; 68: 4262–73
   PubMed Web of Science ®Google Scholar
• Kinoshita T, Shirasawa H, Shino Y, Moriya H, Desbarats L, Eilers M, et al. Transactivation of prothymosin alpha and c-myc promoters by human papillomavirus type 16 E6 protein. Virology 1997; 232: 53–61
   PubMedGoogle Scholar
• Gross-Mesilaty S, Reinstein E, Bercovich B, Tobias K E, Schwartz A L, Kahana C, et al. Basal and human papillomavirus E6 oncoprotein-induced degradation of Myc proteins by the ubiquitin pathway. Proc Natl Acad Sci USA 1998; 95: 8058–63
   PubMed Web of Science ®Google Scholar
• Dyson N, Howley P M, Munger K, Harlow E. The human papilloma virus-16 E7 oncoprotein is able to bind to the retinoblastoma gene product. Science 1989; 243: 934–7
   PubMed Web of Science ®Google Scholar
• Dyson N, Guida P, Munger K, Harlow E. Homologous sequences in adenovirus E1A and human papillomavirus E7 proteins mediate interaction with the same set of cellular proteins. J Virol 1992; 66: 6893–902
   PubMed Web of Science ®Google Scholar
• Firzlaff J M, Galloway D A, Eisenman R N, Luscher B. The E7 protein of human papillomavirus type 16 is phosphorylated by casein kinase II. New Biol 1989; 1: 44–53
   PubMedGoogle Scholar
• Vousden K. Interactions of human papillomavirus transforming proteins with the products of tumor suppressor genes. FASEB J 1993; 7: 872–9
   PubMed Web of Science ®Google Scholar
• Ciccolini F, Dipasquale G, Carlotti F, Crawford L, Tommasino M. Functional studies of E7 proteins from different HPV types. Oncogene 1994; 9: 2633–8
   PubMedGoogle Scholar
• Massimi P, Pim D, Storey A, Banks L. HPV-16 E7 and adenovirus Ela complex formation with TATA box binding protein is enhanced by casein kinase II phosphorylation. Oncogene 1996; 12: 2325–30
   PubMedGoogle Scholar
• Massimi P, Banks L. Repression of p53 transcriptional activity by the HPV E7 proteins. Virology 1997; 227: 255–9
   Google Scholar
• Huang P S, Patrick D R, Edwards G. Protein domains governing interactions between E2F, the retinoblastoma gene product, and human papillomavirus type 16 E7 protein. Mol Cell Biol 1993; 13: 953-–60
   PubMedGoogle Scholar
• Davies R, Hicks R, Crook T, Morris J, Vousden K. Human papillomavirus type 16 E7 associates with a histone HI kinase and with p107 through sequences necessary for transformation. J Virol 1993; 67: 2521–8
   PubMedGoogle Scholar
• Tommasino M, Adamczewski J P, Carlotti F, Barth C F, Manetti R, Contorni M, et al. HPV16 E7 protein associates with the protein kinase p33CDK2 and cyclin A. Oncogene 1993; 8: 195–202
   PubMed Web of Science ®Google Scholar
• McIntyre M C, Ruesch M N, Laimins L A. Human papillomavirus E7 oncoproteins bind a single form of cyclin E in a complex with cdk2 and p107. Virology 1996; 215: 73–82
   PubMedGoogle Scholar
• Zerfass K, Levy L M, Cremonesi C, Ciccolini F, Jansen-Durr P, Crawford L, et al. Cell cycle-dependent disruption of E2F-p107 complexes by human papillomavirus type 16 E7. J Gen Virol 1995; 76: 1815–20
   Google Scholar
• Antinore M J, Birrer M J, Patel D, Nader L, McCance D J. The human papillomavirus type 16 E7 gene product interacts with and trans-activates the API family of transcription factors. EMBO J 1996; 15: 1950–60
   PubMedGoogle Scholar
• Shan B, Farmer A A, Lee W H. The molecular basis of E2F-1/ DP-1-induced S-phase entry and apoptosis. Cell Growth Differ 1996; 7: 689–97
   PubMedGoogle Scholar
• Ruesch M N, Laimins L A. Initiation of DNA synthesis by human papillomavirus E7 oncoproteins is resistant to p21-mediated inhibition of cyclin E-cdk2 activity. J Virol 1997; 71: 5570–8
   PubMedGoogle Scholar
• Wang Y S, Okan I, Pokrovskaja K, Wiman K G. Abrogation of p53-induced Gl arrest by the HPV 16 E7 protein does not inhibit p53-induced apoptosis. Oncogene 1996; 12: 2731–5
   Google Scholar
• Rowan S, Ludwig R L, Haupt Y, Bates S, Lu X, Oren M, et al. Specific loss of apoptotic but not cell-cycle arrest function in a human tumor derived p53 mutant. EMBO J 1996; 15: 827–38
   PubMed Web of Science ®Google Scholar
• Xu C, Meikrantz W, Schlegel R, Sager R. The human papilloma virus 16E6 gene sensitizes human mammary epithelial cells to apoptosis induced by DNA damage. Proc Natl Acad Sci USA 1995; 92: 7829–33
   PubMedGoogle Scholar