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Impairment of Interferon-Induced IRF-7 Gene Expression due to Inhibition of ISGF3 Formation by Trichostatin A.
- Source :
-
Journal of Virology . Jun2003, Vol. 77 Issue 12, p7113. 7p. 7 Graphs. - Publication Year :
- 2003
-
Abstract
- Two members of the signal transducer and activator of transcription family, STAT1 and STAT2, form, together with interferon regulatory factor 9 (IRF-9), the ISGF3 complex that activates the expression of the interferon-stimulated genes (ISG). The ISGF3 complex also participates in the virus-induced alpha/beta interferon (IFN-α/β) gene amplification cascade by up-regulating IRF-7 gene expression. Here, we show that treatment of cells with trichostatin A (TSA), a deacetylase inhibitor, inhibits the virus-induced activation of IFN-α/β promoters and dramatically reduces the ability of different ISG promoters to respond to IFN stimulation. Impairment of IFN-α/β and ISG expression by TSA in infected cells is due to the blockage of interferon-stimulated ISGF3 complex formation, which leads to the abolition of IRF-7 gene expression. We also show that the TSA-dependent inhibition of ISGF3 is related to impaired nuclear accumulation of STAT2. Our data suggest that an acetylation/deacetylation mechanism participates in the regulation of cellular distribution and function of STAT2 in IFN-α/β signaling. [ABSTRACT FROM AUTHOR]
- Subjects :
- *GENE expression
*INTERFERONS
*GENE amplification
Subjects
Details
- Language :
- English
- ISSN :
- 0022538X
- Volume :
- 77
- Issue :
- 12
- Database :
- Academic Search Index
- Journal :
- Journal of Virology
- Publication Type :
- Academic Journal
- Accession number :
- 10345057
- Full Text :
- https://doi.org/10.1128/JVI.77.12.7113-7119.2003