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Expression of Gamma Interferon-Dependent Genes Is Blocked Independently by Virion Host Shutoff RNase and by U S 3 Protein Kinase
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| Zeitschriftentitel: | Journal of Virology |
|---|---|
| Personen und Körperschaften: | , |
| In: | Journal of Virology, 82, 2008, 10, S. 4688-4696 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
American Society for Microbiology
|
| Schlagwörter: |
| author_facet |
Liang, Li Roizman, Bernard Liang, Li Roizman, Bernard |
|---|---|
| author |
Liang, Li Roizman, Bernard |
| spellingShingle |
Liang, Li Roizman, Bernard Journal of Virology Expression of Gamma Interferon-Dependent Genes Is Blocked Independently by Virion Host Shutoff RNase and by U S 3 Protein Kinase Virology Insect Science Immunology Microbiology |
| author_sort |
liang, li |
| spelling |
Liang, Li Roizman, Bernard 0022-538X 1098-5514 American Society for Microbiology Virology Insect Science Immunology Microbiology http://dx.doi.org/10.1128/jvi.02763-07 <jats:title>ABSTRACT</jats:title> <jats:p> Gamma interferon receptor α (IFN-γRα) is stable but posttranslationally modified in herpes simplex virus 1(F) [HSV-1(F)]-infected cells. Studies with antibody directed to the phosphorylation site indicate that IFN-γRα is phosphorylated by the U <jats:sub>S</jats:sub> 3 kinase. The modification is abolished in cells infected with ΔU <jats:sub>S</jats:sub> 3, ΔU <jats:sub>L</jats:sub> 13, or Δ(U <jats:sub>S</jats:sub> 3/U <jats:sub>L</jats:sub> 13) mutant virus. Transcripts of the IFN-γ-dependent genes do not accumulate in cells transduced with the U <jats:sub>S</jats:sub> 3 protein kinase and treated with IFN-γ. In contrast, the accumulation of IFN-γ-dependent gene transcripts is suppressed in cells infected with the wild-type virus, in cells infected with the ΔU <jats:sub>S</jats:sub> 3 mutant virus, and to a lesser extent in the ΔU <jats:sub>L</jats:sub> 41 virus-infected cells. The accumulation of IFN-γ-dependent gene transcripts in ΔU <jats:sub>L</jats:sub> 41-infected cells could be due at least in part to a significant delay and reduction in the accumulation of the U <jats:sub>S</jats:sub> 3 protein. The results suggest that the expression of IFN-γ-dependent genes is blocked independently by the degradation of IFN-γ-dependent gene transcripts—a function of the virion host shutoff RNase—and by posttranslational modification of the IFN-γRα protein. </jats:p> Expression of Gamma Interferon-Dependent Genes Is Blocked Independently by Virion Host Shutoff RNase and by U <sub>S</sub> 3 Protein Kinase Journal of Virology |
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American Society for Microbiology, 2008 |
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American Society for Microbiology, 2008 |
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0022-538X 1098-5514 |
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49 |
| title |
Expression of Gamma Interferon-Dependent Genes Is Blocked Independently by Virion Host Shutoff RNase and by U S 3 Protein Kinase |
| title_unstemmed |
Expression of Gamma Interferon-Dependent Genes Is Blocked Independently by Virion Host Shutoff RNase and by U S 3 Protein Kinase |
| title_full |
Expression of Gamma Interferon-Dependent Genes Is Blocked Independently by Virion Host Shutoff RNase and by U S 3 Protein Kinase |
| title_fullStr |
Expression of Gamma Interferon-Dependent Genes Is Blocked Independently by Virion Host Shutoff RNase and by U S 3 Protein Kinase |
| title_full_unstemmed |
Expression of Gamma Interferon-Dependent Genes Is Blocked Independently by Virion Host Shutoff RNase and by U S 3 Protein Kinase |
| title_short |
Expression of Gamma Interferon-Dependent Genes Is Blocked Independently by Virion Host Shutoff RNase and by U S 3 Protein Kinase |
| title_sort |
expression of gamma interferon-dependent genes is blocked independently by virion host shutoff rnase and by u
<sub>s</sub>
3 protein kinase |
| topic |
Virology Insect Science Immunology Microbiology |
| url |
http://dx.doi.org/10.1128/jvi.02763-07 |
| publishDate |
2008 |
| physical |
4688-4696 |
| description |
<jats:title>ABSTRACT</jats:title>
<jats:p>
Gamma interferon receptor α (IFN-γRα) is stable but posttranslationally modified in herpes simplex virus 1(F) [HSV-1(F)]-infected cells. Studies with antibody directed to the phosphorylation site indicate that IFN-γRα is phosphorylated by the U
<jats:sub>S</jats:sub>
3 kinase. The modification is abolished in cells infected with ΔU
<jats:sub>S</jats:sub>
3, ΔU
<jats:sub>L</jats:sub>
13, or Δ(U
<jats:sub>S</jats:sub>
3/U
<jats:sub>L</jats:sub>
13) mutant virus. Transcripts of the IFN-γ-dependent genes do not accumulate in cells transduced with the U
<jats:sub>S</jats:sub>
3 protein kinase and treated with IFN-γ. In contrast, the accumulation of IFN-γ-dependent gene transcripts is suppressed in cells infected with the wild-type virus, in cells infected with the ΔU
<jats:sub>S</jats:sub>
3 mutant virus, and to a lesser extent in the ΔU
<jats:sub>L</jats:sub>
41 virus-infected cells. The accumulation of IFN-γ-dependent gene transcripts in ΔU
<jats:sub>L</jats:sub>
41-infected cells could be due at least in part to a significant delay and reduction in the accumulation of the U
<jats:sub>S</jats:sub>
3 protein. The results suggest that the expression of IFN-γ-dependent genes is blocked independently by the degradation of IFN-γ-dependent gene transcripts—a function of the virion host shutoff RNase—and by posttranslational modification of the IFN-γRα protein.
</jats:p> |
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| author | Liang, Li, Roizman, Bernard |
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| description | <jats:title>ABSTRACT</jats:title> <jats:p> Gamma interferon receptor α (IFN-γRα) is stable but posttranslationally modified in herpes simplex virus 1(F) [HSV-1(F)]-infected cells. Studies with antibody directed to the phosphorylation site indicate that IFN-γRα is phosphorylated by the U <jats:sub>S</jats:sub> 3 kinase. The modification is abolished in cells infected with ΔU <jats:sub>S</jats:sub> 3, ΔU <jats:sub>L</jats:sub> 13, or Δ(U <jats:sub>S</jats:sub> 3/U <jats:sub>L</jats:sub> 13) mutant virus. Transcripts of the IFN-γ-dependent genes do not accumulate in cells transduced with the U <jats:sub>S</jats:sub> 3 protein kinase and treated with IFN-γ. In contrast, the accumulation of IFN-γ-dependent gene transcripts is suppressed in cells infected with the wild-type virus, in cells infected with the ΔU <jats:sub>S</jats:sub> 3 mutant virus, and to a lesser extent in the ΔU <jats:sub>L</jats:sub> 41 virus-infected cells. The accumulation of IFN-γ-dependent gene transcripts in ΔU <jats:sub>L</jats:sub> 41-infected cells could be due at least in part to a significant delay and reduction in the accumulation of the U <jats:sub>S</jats:sub> 3 protein. The results suggest that the expression of IFN-γ-dependent genes is blocked independently by the degradation of IFN-γ-dependent gene transcripts—a function of the virion host shutoff RNase—and by posttranslational modification of the IFN-γRα protein. </jats:p> |
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| spelling | Liang, Li Roizman, Bernard 0022-538X 1098-5514 American Society for Microbiology Virology Insect Science Immunology Microbiology http://dx.doi.org/10.1128/jvi.02763-07 <jats:title>ABSTRACT</jats:title> <jats:p> Gamma interferon receptor α (IFN-γRα) is stable but posttranslationally modified in herpes simplex virus 1(F) [HSV-1(F)]-infected cells. Studies with antibody directed to the phosphorylation site indicate that IFN-γRα is phosphorylated by the U <jats:sub>S</jats:sub> 3 kinase. The modification is abolished in cells infected with ΔU <jats:sub>S</jats:sub> 3, ΔU <jats:sub>L</jats:sub> 13, or Δ(U <jats:sub>S</jats:sub> 3/U <jats:sub>L</jats:sub> 13) mutant virus. Transcripts of the IFN-γ-dependent genes do not accumulate in cells transduced with the U <jats:sub>S</jats:sub> 3 protein kinase and treated with IFN-γ. In contrast, the accumulation of IFN-γ-dependent gene transcripts is suppressed in cells infected with the wild-type virus, in cells infected with the ΔU <jats:sub>S</jats:sub> 3 mutant virus, and to a lesser extent in the ΔU <jats:sub>L</jats:sub> 41 virus-infected cells. The accumulation of IFN-γ-dependent gene transcripts in ΔU <jats:sub>L</jats:sub> 41-infected cells could be due at least in part to a significant delay and reduction in the accumulation of the U <jats:sub>S</jats:sub> 3 protein. The results suggest that the expression of IFN-γ-dependent genes is blocked independently by the degradation of IFN-γ-dependent gene transcripts—a function of the virion host shutoff RNase—and by posttranslational modification of the IFN-γRα protein. </jats:p> Expression of Gamma Interferon-Dependent Genes Is Blocked Independently by Virion Host Shutoff RNase and by U <sub>S</sub> 3 Protein Kinase Journal of Virology |
| spellingShingle | Liang, Li, Roizman, Bernard, Journal of Virology, Expression of Gamma Interferon-Dependent Genes Is Blocked Independently by Virion Host Shutoff RNase and by U S 3 Protein Kinase, Virology, Insect Science, Immunology, Microbiology |
| title | Expression of Gamma Interferon-Dependent Genes Is Blocked Independently by Virion Host Shutoff RNase and by U S 3 Protein Kinase |
| title_full | Expression of Gamma Interferon-Dependent Genes Is Blocked Independently by Virion Host Shutoff RNase and by U S 3 Protein Kinase |
| title_fullStr | Expression of Gamma Interferon-Dependent Genes Is Blocked Independently by Virion Host Shutoff RNase and by U S 3 Protein Kinase |
| title_full_unstemmed | Expression of Gamma Interferon-Dependent Genes Is Blocked Independently by Virion Host Shutoff RNase and by U S 3 Protein Kinase |
| title_short | Expression of Gamma Interferon-Dependent Genes Is Blocked Independently by Virion Host Shutoff RNase and by U S 3 Protein Kinase |
| title_sort | expression of gamma interferon-dependent genes is blocked independently by virion host shutoff rnase and by u <sub>s</sub> 3 protein kinase |
| title_unstemmed | Expression of Gamma Interferon-Dependent Genes Is Blocked Independently by Virion Host Shutoff RNase and by U S 3 Protein Kinase |
| topic | Virology, Insect Science, Immunology, Microbiology |
| url | http://dx.doi.org/10.1128/jvi.02763-07 |