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Human immunodeficiency virus type 1 Tat prevents dephosphorylation of Sp1 by TCF-4 in astrocytes
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| Zeitschriftentitel: | Journal of General Virology |
|---|---|
| Personen und Körperschaften: | , , , , , |
| In: | Journal of General Virology, 87, 2006, 6, S. 1613-1623 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Microbiology Society
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| Schlagwörter: |
| author_facet |
Rossi, Andrea Mukerjee, Ruma Ferrante, Pasquale Khalili, Kamel Amini, Shohreh Sawaya, Bassel E. Rossi, Andrea Mukerjee, Ruma Ferrante, Pasquale Khalili, Kamel Amini, Shohreh Sawaya, Bassel E. |
|---|---|
| author |
Rossi, Andrea Mukerjee, Ruma Ferrante, Pasquale Khalili, Kamel Amini, Shohreh Sawaya, Bassel E. |
| spellingShingle |
Rossi, Andrea Mukerjee, Ruma Ferrante, Pasquale Khalili, Kamel Amini, Shohreh Sawaya, Bassel E. Journal of General Virology Human immunodeficiency virus type 1 Tat prevents dephosphorylation of Sp1 by TCF-4 in astrocytes Virology |
| author_sort |
rossi, andrea |
| spelling |
Rossi, Andrea Mukerjee, Ruma Ferrante, Pasquale Khalili, Kamel Amini, Shohreh Sawaya, Bassel E. 0022-1317 1465-2099 Microbiology Society Virology http://dx.doi.org/10.1099/vir.0.81691-0 <jats:p>Previous examination of the effect of TCF-4 on transcription of the human immunodeficiency virus type 1 (HIV-1) promoter in human astrocytic cells found that TCF-4 affects the HIV-1 promoter through the GC-rich domain (nt −80 to nt −68). Here, the physical interaction and a functional consequence of TCF4–Sp1 contact were characterized. It was shown that expression of TCF-4 in U-87 MG (human astrocytic) cells decreased basal and Sp1-mediated transcription of the HIV-1 promoter. Results from a GST pull-down assay, as well as combined immunoprecipitation and Western blot analysis of protein extracts from U-87 MG cells, revealed an interaction of Sp1 with TCF-4. Using <jats:italic>in vitro</jats:italic> protein chromatography, the region of Sp1 that contacts TCF-4 was mapped to aa 266–350. It was also found that, in cell-free extracts, TCF-4 prevented dsDNA-dependent protein kinase (DNA-PK)-mediated Sp1 phosphorylation. Surprisingly, TCF-4 failed to decrease Sp1-mediated transcription of the HIV-1 long terminal repeat (LTR) and Sp1 phosphorylation in cells expressing HIV-1 Tat. Results from immunoprecipitation/Western blotting demonstrated that TCF-4 lost its ability to interact with Sp1, but not with Tat, in Tat-transfected cells. Taken together, these findings suggest that activity at the HIV-1 promoter is influenced by phosphorylation of Sp1, which is affected by Tat and DNA-PK. Interactions among TCF-4, Sp1 and/or Tat may determine the level of viral gene transcription in human astrocytic cells.</jats:p> Human immunodeficiency virus type 1 Tat prevents dephosphorylation of Sp1 by TCF-4 in astrocytes Journal of General Virology |
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Microbiology Society, 2006 |
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| title |
Human immunodeficiency virus type 1 Tat prevents dephosphorylation of Sp1 by TCF-4 in astrocytes |
| title_unstemmed |
Human immunodeficiency virus type 1 Tat prevents dephosphorylation of Sp1 by TCF-4 in astrocytes |
| title_full |
Human immunodeficiency virus type 1 Tat prevents dephosphorylation of Sp1 by TCF-4 in astrocytes |
| title_fullStr |
Human immunodeficiency virus type 1 Tat prevents dephosphorylation of Sp1 by TCF-4 in astrocytes |
| title_full_unstemmed |
Human immunodeficiency virus type 1 Tat prevents dephosphorylation of Sp1 by TCF-4 in astrocytes |
| title_short |
Human immunodeficiency virus type 1 Tat prevents dephosphorylation of Sp1 by TCF-4 in astrocytes |
| title_sort |
human immunodeficiency virus type 1 tat prevents dephosphorylation of sp1 by tcf-4 in astrocytes |
| topic |
Virology |
| url |
http://dx.doi.org/10.1099/vir.0.81691-0 |
| publishDate |
2006 |
| physical |
1613-1623 |
| description |
<jats:p>Previous examination of the effect of TCF-4 on transcription of the human immunodeficiency virus type 1 (HIV-1) promoter in human astrocytic cells found that TCF-4 affects the HIV-1 promoter through the GC-rich domain (nt −80 to nt −68). Here, the physical interaction and a functional consequence of TCF4–Sp1 contact were characterized. It was shown that expression of TCF-4 in U-87 MG (human astrocytic) cells decreased basal and Sp1-mediated transcription of the HIV-1 promoter. Results from a GST pull-down assay, as well as combined immunoprecipitation and Western blot analysis of protein extracts from U-87 MG cells, revealed an interaction of Sp1 with TCF-4. Using <jats:italic>in vitro</jats:italic> protein chromatography, the region of Sp1 that contacts TCF-4 was mapped to aa 266–350. It was also found that, in cell-free extracts, TCF-4 prevented dsDNA-dependent protein kinase (DNA-PK)-mediated Sp1 phosphorylation. Surprisingly, TCF-4 failed to decrease Sp1-mediated transcription of the HIV-1 long terminal repeat (LTR) and Sp1 phosphorylation in cells expressing HIV-1 Tat. Results from immunoprecipitation/Western blotting demonstrated that TCF-4 lost its ability to interact with Sp1, but not with Tat, in Tat-transfected cells. Taken together, these findings suggest that activity at the HIV-1 promoter is influenced by phosphorylation of Sp1, which is affected by Tat and DNA-PK. Interactions among TCF-4, Sp1 and/or Tat may determine the level of viral gene transcription in human astrocytic cells.</jats:p> |
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| author | Rossi, Andrea, Mukerjee, Ruma, Ferrante, Pasquale, Khalili, Kamel, Amini, Shohreh, Sawaya, Bassel E. |
| author_facet | Rossi, Andrea, Mukerjee, Ruma, Ferrante, Pasquale, Khalili, Kamel, Amini, Shohreh, Sawaya, Bassel E., Rossi, Andrea, Mukerjee, Ruma, Ferrante, Pasquale, Khalili, Kamel, Amini, Shohreh, Sawaya, Bassel E. |
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| description | <jats:p>Previous examination of the effect of TCF-4 on transcription of the human immunodeficiency virus type 1 (HIV-1) promoter in human astrocytic cells found that TCF-4 affects the HIV-1 promoter through the GC-rich domain (nt −80 to nt −68). Here, the physical interaction and a functional consequence of TCF4–Sp1 contact were characterized. It was shown that expression of TCF-4 in U-87 MG (human astrocytic) cells decreased basal and Sp1-mediated transcription of the HIV-1 promoter. Results from a GST pull-down assay, as well as combined immunoprecipitation and Western blot analysis of protein extracts from U-87 MG cells, revealed an interaction of Sp1 with TCF-4. Using <jats:italic>in vitro</jats:italic> protein chromatography, the region of Sp1 that contacts TCF-4 was mapped to aa 266–350. It was also found that, in cell-free extracts, TCF-4 prevented dsDNA-dependent protein kinase (DNA-PK)-mediated Sp1 phosphorylation. Surprisingly, TCF-4 failed to decrease Sp1-mediated transcription of the HIV-1 long terminal repeat (LTR) and Sp1 phosphorylation in cells expressing HIV-1 Tat. Results from immunoprecipitation/Western blotting demonstrated that TCF-4 lost its ability to interact with Sp1, but not with Tat, in Tat-transfected cells. Taken together, these findings suggest that activity at the HIV-1 promoter is influenced by phosphorylation of Sp1, which is affected by Tat and DNA-PK. Interactions among TCF-4, Sp1 and/or Tat may determine the level of viral gene transcription in human astrocytic cells.</jats:p> |
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| spelling | Rossi, Andrea Mukerjee, Ruma Ferrante, Pasquale Khalili, Kamel Amini, Shohreh Sawaya, Bassel E. 0022-1317 1465-2099 Microbiology Society Virology http://dx.doi.org/10.1099/vir.0.81691-0 <jats:p>Previous examination of the effect of TCF-4 on transcription of the human immunodeficiency virus type 1 (HIV-1) promoter in human astrocytic cells found that TCF-4 affects the HIV-1 promoter through the GC-rich domain (nt −80 to nt −68). Here, the physical interaction and a functional consequence of TCF4–Sp1 contact were characterized. It was shown that expression of TCF-4 in U-87 MG (human astrocytic) cells decreased basal and Sp1-mediated transcription of the HIV-1 promoter. Results from a GST pull-down assay, as well as combined immunoprecipitation and Western blot analysis of protein extracts from U-87 MG cells, revealed an interaction of Sp1 with TCF-4. Using <jats:italic>in vitro</jats:italic> protein chromatography, the region of Sp1 that contacts TCF-4 was mapped to aa 266–350. It was also found that, in cell-free extracts, TCF-4 prevented dsDNA-dependent protein kinase (DNA-PK)-mediated Sp1 phosphorylation. Surprisingly, TCF-4 failed to decrease Sp1-mediated transcription of the HIV-1 long terminal repeat (LTR) and Sp1 phosphorylation in cells expressing HIV-1 Tat. Results from immunoprecipitation/Western blotting demonstrated that TCF-4 lost its ability to interact with Sp1, but not with Tat, in Tat-transfected cells. Taken together, these findings suggest that activity at the HIV-1 promoter is influenced by phosphorylation of Sp1, which is affected by Tat and DNA-PK. Interactions among TCF-4, Sp1 and/or Tat may determine the level of viral gene transcription in human astrocytic cells.</jats:p> Human immunodeficiency virus type 1 Tat prevents dephosphorylation of Sp1 by TCF-4 in astrocytes Journal of General Virology |
| spellingShingle | Rossi, Andrea, Mukerjee, Ruma, Ferrante, Pasquale, Khalili, Kamel, Amini, Shohreh, Sawaya, Bassel E., Journal of General Virology, Human immunodeficiency virus type 1 Tat prevents dephosphorylation of Sp1 by TCF-4 in astrocytes, Virology |
| title | Human immunodeficiency virus type 1 Tat prevents dephosphorylation of Sp1 by TCF-4 in astrocytes |
| title_full | Human immunodeficiency virus type 1 Tat prevents dephosphorylation of Sp1 by TCF-4 in astrocytes |
| title_fullStr | Human immunodeficiency virus type 1 Tat prevents dephosphorylation of Sp1 by TCF-4 in astrocytes |
| title_full_unstemmed | Human immunodeficiency virus type 1 Tat prevents dephosphorylation of Sp1 by TCF-4 in astrocytes |
| title_short | Human immunodeficiency virus type 1 Tat prevents dephosphorylation of Sp1 by TCF-4 in astrocytes |
| title_sort | human immunodeficiency virus type 1 tat prevents dephosphorylation of sp1 by tcf-4 in astrocytes |
| title_unstemmed | Human immunodeficiency virus type 1 Tat prevents dephosphorylation of Sp1 by TCF-4 in astrocytes |
| topic | Virology |
| url | http://dx.doi.org/10.1099/vir.0.81691-0 |