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Role of Acetylases and Deacetylase Inhibitors in IRF‐1‐Mediated HIV‐1 Long Terminal Repeat Transcription
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| Zeitschriftentitel: | Annals of the New York Academy of Sciences |
|---|---|
| Personen und Körperschaften: | , , , |
| In: | Annals of the New York Academy of Sciences, 1030, 2004, 1, S. 636-643 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Wiley
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| Schlagwörter: |
| author_facet |
MARSILI, GIULIA REMOLI, ANNA LISA SGARBANTI, MARCO BATTISTINI, ANGELA MARSILI, GIULIA REMOLI, ANNA LISA SGARBANTI, MARCO BATTISTINI, ANGELA |
|---|---|
| author |
MARSILI, GIULIA REMOLI, ANNA LISA SGARBANTI, MARCO BATTISTINI, ANGELA |
| spellingShingle |
MARSILI, GIULIA REMOLI, ANNA LISA SGARBANTI, MARCO BATTISTINI, ANGELA Annals of the New York Academy of Sciences Role of Acetylases and Deacetylase Inhibitors in IRF‐1‐Mediated HIV‐1 Long Terminal Repeat Transcription History and Philosophy of Science General Biochemistry, Genetics and Molecular Biology General Neuroscience |
| author_sort |
marsili, giulia |
| spelling |
MARSILI, GIULIA REMOLI, ANNA LISA SGARBANTI, MARCO BATTISTINI, ANGELA 0077-8923 1749-6632 Wiley History and Philosophy of Science General Biochemistry, Genetics and Molecular Biology General Neuroscience http://dx.doi.org/10.1196/annals.1329.074 <jats:p><jats:bold>A<jats:sc>bstract</jats:sc>: </jats:bold> There is strong evidence that both transcriptional activation and silencing are mediated through the recruitment of enzymes that control reversible protein acetylation: histone acetylase (HAT) and histone deacetylase proteins. Acetylation is also a critical post‐translational modification of general and tissue‐specific transcription factors. In HIV‐1‐infected cells, the long terminal repeat (LTR) promoter, once organized into chromatin, is transcriptionally inactive in the absence of stimulation. LTR transcription is regulated by protein acetylation, since treatment with deacetylase inhibitors markedly induces transcriptional activity of the LTR. Besides cellular transcription factors involved in LTR activation, early in infection, and during reactivation from latency, we have previously shown that proteins of the IRF family play an important role. In particular, IRF‐1 is able <jats:italic>per se</jats:italic> to stimulate HIV‐1 LTR transcription even in the absence of Tat. IRF‐1 is also acetylated and associates with HATs such as p300/CBP and PCAF to form a multiprotein complex that assembles on the promoter of target genes. Here we show that CBP can be recruited by IRF‐1 to the HIV‐1 LTR promoter even in the absence of Tat and that treatment with deacetylase inhibitors, such as trichostatin A (TSA), increases LTR transactivation in response to both IRF‐1 and Tat. These results help to define the architecture of interactions between transcription factors binding HIV‐1 LTR and confirm the possibility that deacetylase inhibitors, such as TSA, combined with antiviral therapy may represent a valuable approach to control HIV‐1 infection.</jats:p> Role of Acetylases and Deacetylase Inhibitors in IRF‐1‐Mediated HIV‐1 Long Terminal Repeat Transcription Annals of the New York Academy of Sciences |
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| title |
Role of Acetylases and Deacetylase Inhibitors in IRF‐1‐Mediated HIV‐1 Long Terminal Repeat Transcription |
| title_unstemmed |
Role of Acetylases and Deacetylase Inhibitors in IRF‐1‐Mediated HIV‐1 Long Terminal Repeat Transcription |
| title_full |
Role of Acetylases and Deacetylase Inhibitors in IRF‐1‐Mediated HIV‐1 Long Terminal Repeat Transcription |
| title_fullStr |
Role of Acetylases and Deacetylase Inhibitors in IRF‐1‐Mediated HIV‐1 Long Terminal Repeat Transcription |
| title_full_unstemmed |
Role of Acetylases and Deacetylase Inhibitors in IRF‐1‐Mediated HIV‐1 Long Terminal Repeat Transcription |
| title_short |
Role of Acetylases and Deacetylase Inhibitors in IRF‐1‐Mediated HIV‐1 Long Terminal Repeat Transcription |
| title_sort |
role of acetylases and deacetylase inhibitors in irf‐1‐mediated hiv‐1 long terminal repeat transcription |
| topic |
History and Philosophy of Science General Biochemistry, Genetics and Molecular Biology General Neuroscience |
| url |
http://dx.doi.org/10.1196/annals.1329.074 |
| publishDate |
2004 |
| physical |
636-643 |
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<jats:p><jats:bold>A<jats:sc>bstract</jats:sc>: </jats:bold> There is strong evidence that both transcriptional activation and silencing are mediated through the recruitment of enzymes that control reversible protein acetylation: histone acetylase (HAT) and histone deacetylase proteins. Acetylation is also a critical post‐translational modification of general and tissue‐specific transcription factors. In HIV‐1‐infected cells, the long terminal repeat (LTR) promoter, once organized into chromatin, is transcriptionally inactive in the absence of stimulation. LTR transcription is regulated by protein acetylation, since treatment with deacetylase inhibitors markedly induces transcriptional activity of the LTR. Besides cellular transcription factors involved in LTR activation, early in infection, and during reactivation from latency, we have previously shown that proteins of the IRF family play an important role. In particular, IRF‐1 is able <jats:italic>per se</jats:italic> to stimulate HIV‐1 LTR transcription even in the absence of Tat. IRF‐1 is also acetylated and associates with HATs such as p300/CBP and PCAF to form a multiprotein complex that assembles on the promoter of target genes. Here we show that CBP can be recruited by IRF‐1 to the HIV‐1 LTR promoter even in the absence of Tat and that treatment with deacetylase inhibitors, such as trichostatin A (TSA), increases LTR transactivation in response to both IRF‐1 and Tat. These results help to define the architecture of interactions between transcription factors binding HIV‐1 LTR and confirm the possibility that deacetylase inhibitors, such as TSA, combined with antiviral therapy may represent a valuable approach to control HIV‐1 infection.</jats:p> |
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| description | <jats:p><jats:bold>A<jats:sc>bstract</jats:sc>: </jats:bold> There is strong evidence that both transcriptional activation and silencing are mediated through the recruitment of enzymes that control reversible protein acetylation: histone acetylase (HAT) and histone deacetylase proteins. Acetylation is also a critical post‐translational modification of general and tissue‐specific transcription factors. In HIV‐1‐infected cells, the long terminal repeat (LTR) promoter, once organized into chromatin, is transcriptionally inactive in the absence of stimulation. LTR transcription is regulated by protein acetylation, since treatment with deacetylase inhibitors markedly induces transcriptional activity of the LTR. Besides cellular transcription factors involved in LTR activation, early in infection, and during reactivation from latency, we have previously shown that proteins of the IRF family play an important role. In particular, IRF‐1 is able <jats:italic>per se</jats:italic> to stimulate HIV‐1 LTR transcription even in the absence of Tat. IRF‐1 is also acetylated and associates with HATs such as p300/CBP and PCAF to form a multiprotein complex that assembles on the promoter of target genes. Here we show that CBP can be recruited by IRF‐1 to the HIV‐1 LTR promoter even in the absence of Tat and that treatment with deacetylase inhibitors, such as trichostatin A (TSA), increases LTR transactivation in response to both IRF‐1 and Tat. These results help to define the architecture of interactions between transcription factors binding HIV‐1 LTR and confirm the possibility that deacetylase inhibitors, such as TSA, combined with antiviral therapy may represent a valuable approach to control HIV‐1 infection.</jats:p> |
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| imprint_str_mv | Wiley, 2004 |
| institution | DE-Ch1, DE-L229, DE-D275, DE-Bn3, DE-Brt1, DE-D161, DE-Gla1, DE-Zi4, DE-15, DE-Pl11, DE-Rs1, DE-105, DE-14 |
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| spelling | MARSILI, GIULIA REMOLI, ANNA LISA SGARBANTI, MARCO BATTISTINI, ANGELA 0077-8923 1749-6632 Wiley History and Philosophy of Science General Biochemistry, Genetics and Molecular Biology General Neuroscience http://dx.doi.org/10.1196/annals.1329.074 <jats:p><jats:bold>A<jats:sc>bstract</jats:sc>: </jats:bold> There is strong evidence that both transcriptional activation and silencing are mediated through the recruitment of enzymes that control reversible protein acetylation: histone acetylase (HAT) and histone deacetylase proteins. Acetylation is also a critical post‐translational modification of general and tissue‐specific transcription factors. In HIV‐1‐infected cells, the long terminal repeat (LTR) promoter, once organized into chromatin, is transcriptionally inactive in the absence of stimulation. LTR transcription is regulated by protein acetylation, since treatment with deacetylase inhibitors markedly induces transcriptional activity of the LTR. Besides cellular transcription factors involved in LTR activation, early in infection, and during reactivation from latency, we have previously shown that proteins of the IRF family play an important role. In particular, IRF‐1 is able <jats:italic>per se</jats:italic> to stimulate HIV‐1 LTR transcription even in the absence of Tat. IRF‐1 is also acetylated and associates with HATs such as p300/CBP and PCAF to form a multiprotein complex that assembles on the promoter of target genes. Here we show that CBP can be recruited by IRF‐1 to the HIV‐1 LTR promoter even in the absence of Tat and that treatment with deacetylase inhibitors, such as trichostatin A (TSA), increases LTR transactivation in response to both IRF‐1 and Tat. These results help to define the architecture of interactions between transcription factors binding HIV‐1 LTR and confirm the possibility that deacetylase inhibitors, such as TSA, combined with antiviral therapy may represent a valuable approach to control HIV‐1 infection.</jats:p> Role of Acetylases and Deacetylase Inhibitors in IRF‐1‐Mediated HIV‐1 Long Terminal Repeat Transcription Annals of the New York Academy of Sciences |
| spellingShingle | MARSILI, GIULIA, REMOLI, ANNA LISA, SGARBANTI, MARCO, BATTISTINI, ANGELA, Annals of the New York Academy of Sciences, Role of Acetylases and Deacetylase Inhibitors in IRF‐1‐Mediated HIV‐1 Long Terminal Repeat Transcription, History and Philosophy of Science, General Biochemistry, Genetics and Molecular Biology, General Neuroscience |
| title | Role of Acetylases and Deacetylase Inhibitors in IRF‐1‐Mediated HIV‐1 Long Terminal Repeat Transcription |
| title_full | Role of Acetylases and Deacetylase Inhibitors in IRF‐1‐Mediated HIV‐1 Long Terminal Repeat Transcription |
| title_fullStr | Role of Acetylases and Deacetylase Inhibitors in IRF‐1‐Mediated HIV‐1 Long Terminal Repeat Transcription |
| title_full_unstemmed | Role of Acetylases and Deacetylase Inhibitors in IRF‐1‐Mediated HIV‐1 Long Terminal Repeat Transcription |
| title_short | Role of Acetylases and Deacetylase Inhibitors in IRF‐1‐Mediated HIV‐1 Long Terminal Repeat Transcription |
| title_sort | role of acetylases and deacetylase inhibitors in irf‐1‐mediated hiv‐1 long terminal repeat transcription |
| title_unstemmed | Role of Acetylases and Deacetylase Inhibitors in IRF‐1‐Mediated HIV‐1 Long Terminal Repeat Transcription |
| topic | History and Philosophy of Science, General Biochemistry, Genetics and Molecular Biology, General Neuroscience |
| url | http://dx.doi.org/10.1196/annals.1329.074 |