The Epstein-Barr Virus Determined Nuclear Antigens EBNA-3A, -3B, and -3C Repress EBNA-2-Mediated Transactivation of the Viral Terminal Protein 1 Gene Promoter
| Autor: | Michel Perricaudet, A Le Roux, B Kerdiles, Dermot Walls, Jean-François Dedieu |
|---|---|
| Rok vydání: | 1994 |
| Předmět: |
Chloramphenicol O-Acetyltransferase
Herpesvirus 4 Human viruses Biology Transfection Virus Cell Line Chloramphenicol acetyltransferase Transactivation immune system diseases Transcription (biology) hemic and lymphatic diseases Virology Humans Promoter Regions Genetic Antigens Viral Gene Regulation of gene expression virus diseases Promoter Molecular biology Recombinant Proteins DNA-Binding Proteins Repressor Proteins Epstein-Barr Virus Nuclear Antigens Trans-Activators Plasmids |
| Zdroj: | Virology. 205:596-602 |
| ISSN: | 0042-6822 |
| DOI: | 10.1006/viro.1994.1687 |
| Popis: | The Epstein-Barr virus (EBV) nuclear antigen 2 (EBNA-2) has been shown to transactivate both cellular and viral gene promoters including the promoter for the viral terminal protein 1 gene (TP-1). We investigated whether three other EBV nuclear antigens EBNA-3A, -3B, and -3C (which themselves share a degree of primary sequence homology) could also play a role in TP-1 gene regulation. The TP-1 promoter sequence was linked to the chloramphenicol acetyltransferase (CAT) gene and used in cotransfection experiments in an EBV negative cell line with various combinations of vectors expressing individual EBNA-3s. In the absence of other EBV proteins, the EBNA-3s did not stimulate TP-1 promoter activity. In the presence of EBNA-2, the EBNA-3s were shown to be capable of reducing the level of TP-1 promoter-driven CAT activity. The EBNA-3s had no effect on a panel of heterologous promoters, indicating that EBNA-2 and/or transcription elements specific to the TP-1 promoter are essential for the observed activity of the EBNA-3s. The functional antagonism between the EBNA-2 and EBNA-3 proteins may be important in the overall viral strategy. |
| Databáze: | OpenAIRE |
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