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| SUPPRESSION OF CELLULAR PROLIFERATION BY THE PAPILLOMAVIRUS E2 PROTEIN |
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| Author(s): DOWHANICK JJ, MCBRIDE AA, HOWLEY PM |
| Source: JOURNAL OF VIROLOGY Volume: 69 Issue: 12 Pages: 7791-7799 Published: DEC 1995 |
| Times Cited: 117 References: 62 |
| Abstract: Carcinogenic progression of a human papillomavirus (HPV)-infected cell is often associated with integration of the viral genome in a manner which results in the loss of expression of the viral regulatory protein E2. One function of E2 is the regulation of expression of the viral oncogenes, E6 and E7. Introduction of the bovine papillomavirus type 1 (BPV-1) E2 transactivator (E2-TA) in HeLa cells, an HPV type 18 (HPV-IS)-positive cervical carcinoma cell line results in growth arrest. In this study, we have found that the HPV-16 and HPV-18 E2 proteins share with BPV-1 E2-TA the ability to suppress HeLa cell growth. This property was not observed for the BPV-1 E2 transcriptional repressor (E2-TR). Analysis of various mutant E2 proteins for growth suppression revealed a requirement for the intact transactivation and DNA binding domains. A HeLa cell line (HeLa-tsE2) which expressed a conditional mutant E2 protein that was functional only at the permissive temperature (32 degrees C) was established, permitting an analysis of the molecular and cellular consequences of E2 expression. Our data indicate that one mechanism by which E2 suppresses cellular growth is through repression of E6 and E7 expression, thereby enabling the cellular targets of E6 and E7 to resume regulation of the cell cycle. |
| Document Type: Article |
| Language: English |
Addresses:
1. HARVARD UNIV, SCH MED, DEPT PATHOL, BOSTON, MA 02115 USA
2. NIH, VIRAL DIS LAB, BETHESDA, MD 20892 USA |
| Publisher: AMER SOC MICROBIOLOGY, 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 |
| Subject Category: Virology |
| IDS Number: TE366 |
| ISSN: 0022-538X |
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