CCAAT/Enhancer Binding Proteins Are Not Required for HIV-1 Entry but Regulate Proviral Transcription by Recruiting Coactivators to the Long-Terminal Repeat in Monocytic Cells
| Autor: | Andrew J. Henderson, Deba Sarma, Huiyu Zhou, Eileen S. Lee |
|---|---|
| Jazyk: | angličtina |
| Předmět: |
Saccharomyces cerevisiae Proteins
Transcription Genetic Response element HIV Infections Transcription coregulator Biology Virus Replication Monocytes 03 medical and health sciences Proviruses Acetyltransferases Enhancer binding Virology Humans Enhancer 030304 developmental biology HIV Long Terminal Repeat Histone Acetyltransferases 0303 health sciences Ccaat-enhancer-binding proteins General transcription factor CCAAT-Enhancer-Binding Protein-beta 030302 biochemistry & molecular biology HIV Promoter U937 Cells Molecular biology 3. Good health TAF2 CCAAT-Enhancer-Binding Proteins HIV-1 chromatin transcription Protein Binding |
| Zdroj: | Virology. (1):20-31 |
| ISSN: | 0042-6822 |
| DOI: | 10.1006/viro.2002.1500 |
| Popis: | CCAAT/enhancer binding proteins (C/EBP) have been shown to be required for HIV-1 transcription and replication in macrophages. However, whether these transcription factors influence the ability of virus to establish infection by altering cytokine or receptor expression or primarily regulate HIV-1 transcription has not been determined. By inhibiting endogenous C/EBP activity with a dominant-negative protein, we demonstrate that functional C/EBPs are not required for HIV-1 infection and that these factors influence replication by a transcriptional mechanism. C/EBPβ recruits coactivators to the HIV-1 long-terminal repeat (LTR) and physically interacts with histone acetyltransferase (HAT) complexes, suggesting that C/EBPs participate in remodeling the chromatin organization of the HIV-1 provirus. Furthermore, overexpression of a C/EBP dominant-negative inhibits displacement of nucleosomes located at the HIV-1 transcriptional start site. These results provide insight into the general mechanisms by which C/EBPs regulate macrophage-restricted HIV-1 transcription. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|