Transcriptional Activation of Gammaherpesviral Oncogene Promoters by the Hepatitis B Viral X Protein (HBx)
| Autor: | Barnabe Dossou Assogba, Hyune Mo Rho, Nak Whan Paik |
|---|---|
| Rok vydání: | 2004 |
| Předmět: |
Transcriptional Activation
Oncogene Proteins viruses Biology medicine.disease_cause Jurkat cells Virus Jurkat Cells Gammaherpesvirinae Genetics medicine Humans Viral Regulatory and Accessory Proteins RNA Messenger Promoter Regions Genetic Molecular Biology Hepatitis B virus Mutation Oncogene NF-kappa B virus diseases Promoter Oncogene Proteins Viral Cell Biology General Medicine Virology Molecular biology HBx Trans-Activators |
| Zdroj: | DNA and Cell Biology. 23:141-148 |
| ISSN: | 1557-7430 1044-5498 |
| DOI: | 10.1089/104454904322964733 |
| Popis: | The latent membrane protein-1 (LMP1) of Epstein-Barr Virus (EBV), saimiri transformation protein (STP) of Herpesvirus saimiri (HVS), and K1 protein of Kaposi's sarcoma-associated herpesvirus (KSHV) are potent gammaherpesvirus oncogenes. To study the possible effects of double viral infection, we investigated the effects of oncogenic early proteins of DNA viruses E1A and E1B (adenovirus-5), E6 and E7 (human papillomavirus-16), HBx (hepatitis B virus), Tag (SV40), and gammaherpesviral oncogene during co-infection in human B-lymphoma (Ramos) and human T-cell leukemia (Jurkat) cell lines. HBx transactivated the promoters of LMP1, STP, and K1 the most, by about six-, three-, and twofold, respectively. Analyses of site-directed mutation and the heterologous promoter system showed that HBx activated the promoter activity of these genes via the NF-kappaB site. These results suggest that HBV (HBx) infection of cells previously infected by gammaherpesviruses transactivates their oncogenes, resulting in possible virus-related disease pathogenesis. |
| Databáze: | OpenAIRE |
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