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Semin Cancer Biol. 2003 Feb;13(1):59-67.

Human papillomavirus-induced carcinogenesis and the ubiquitin-proteasome system.

Author information

1
Institute of Biochemistry I, Faculty of Medicine, University of Cologne, Joseph-Stelzmann-Str 52, 50931 Köln, Germany. martin.scheffner@uni-koeln.de

Abstract

Certain types of human papillomaviruses have been etiologically associated with malignant lesions, most notably with cervical cancer. The major oncoproteins of these cancer-associated viruses are encoded by the viral E6 and E7 genes. Thorough characterization of these oncoproteins and their interaction with cellular proteins has shown that both E6 and E7 exploit the ubiquitin-proteasome system to degrade and, thus, to functionally inactivate negative cell-regulatory proteins including members of the p110(RB) family and p53. This act of piracy is assumed to contribute to both the efficient propagation of HPVs and HPV-induced carcinogenesis.

PMID:
12507557
DOI:
10.1016/s1044-579x(02)00100-1
[Indexed for MEDLINE]

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