Interactions Between Papillomavirus Proteins and Tumor Suppressor Gene Products

作者: Karen H. Vousden

DOI: 10.1016/S0065-230X(08)60833-7

关键词:

摘要: Publisher Summary Human papillomaviruses (HPVs) have provided unique insight into the mechanisms that regulate growth and oncogenic progression of human cells. The genital HPV types cause lesions are not strictly benign; malignant HPV-infected cells appears to give rise almost all cervical cancers. paradigm for tumor suppressor genes has now been joined by a growing number whose loss function contributes cancer development; subsequently, many these shown play role in preventing or delaying progress through cell cycle. Studies somatic mutation within loci frequently development sporadic Several cell-encoded proteins detected association with viral E6 E7, identification some as products revealed at least oncoprotein function. Viral oncoproteins identified enormous advances unraveling their mechanism action participated convergence different areas research. application understanding interactions between host directly treating such common disease may be fitting culmination studies.

参考文章(148)
A. Storey, D. Pim, A. Murray, K. Osborn, L. Banks, L. Crawford, Comparison of the in vitro transforming activities of human papillomavirus types. The EMBO Journal. ,vol. 7, pp. 1815- 1820 ,(1988) , 10.1002/J.1460-2075.1988.TB03013.X
N. B. Lathangue, L. R. Bandara, R. Davies, K. H. Vousden, T. Crook, J. D. H. Morris, Human papillomavirus type 16 E7 regulates E2F and contributes to mitogenic signalling Oncogene. ,vol. 8, pp. 893- 898 ,(1993)
P. Hawley-Nelson, K.H. Vousden, N.L. Hubbert, D.R. Lowy, J.T. Schiller, HPV16 E6 and E7 proteins cooperate to immortalize human foreskin keratinocytes. The EMBO Journal. ,vol. 8, pp. 3905- 3910 ,(1989) , 10.1002/J.1460-2075.1989.TB08570.X
J A DiPaolo, N C Popescu, C D Woodworth, J Doniger, V Notario, Induction of human cervical squamous cell carcinoma by sequential transfection with human papillomavirus 16 DNA and viral Harvey ras. Oncogene. ,vol. 4, pp. 395- 399 ,(1989)
Castellsagué X, Guerrero E, Aristizabal N, Bosch Fx, de Sanjosé S, Alonso de Ruiz P, Santamaria M, HPV types in women with normal cervical cytology. IARC scientific publications. pp. 75- 84 ,(1992)
Wrede D, Vousden Kh, Crook T, p53 point mutation in HPV negative human cervical carcinoma cell lines. Oncogene. ,vol. 6, pp. 873- ,(1991)
J-Y Kato, H Matsushime, SW Hiebert, ME Ewen, CJ Sherr, Direct binding of cyclin D to the retinoblastoma gene product (pRb) and pRb phosphorylation by the cyclin D-dependent kinase CDK4. Genes & Development. ,vol. 7, pp. 331- 342 ,(1993) , 10.1101/GAD.7.3.331
T Hunt, J P Adamczewski, F Carlotti, F Cavalieri, M Contorni, C F Barth, R Manetti, L Crawford, M Tommasino, HPV16 E7 protein associates with the protein kinase p33CDK2 and cyclin A. Oncogene. ,vol. 8, pp. 195- 202 ,(1993)
J.M. Huibregtse, M. Scheffner, P.M. Howley, A cellular protein mediates association of p53 with the E6 oncoprotein of human papillomavirus types 16 or 18. The EMBO Journal. ,vol. 10, pp. 4129- 4135 ,(1991) , 10.1002/J.1460-2075.1991.TB04990.X