Cooperative interaction of Ets‐1 with USF‐1 required for HIV‐1 enhancer activity in T cells
Abstract The distal enhancer region of the human immunodeficiency virus 1 (HIV‐1) long terminal repeat (LTR) is known to be essential for HIV replication and to contain immediately adjacent E‐box and Ets binding sites. Based on a yeast one‐hybrid screen we have identified the E‐box binding protein U...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Sieweke, Michael H. [verfasserIn] Tekotte, Hildegard [verfasserIn] Jarosch, Ursula [verfasserIn] Graf, Thomas [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
1998 |
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| Schlagwörter: |
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| Anmerkung: |
© European Molecular Biology Organization 1998 |
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| Übergeordnetes Werk: |
Enthalten in: The EMBO Journal - Nature Publishing Group UK, 2023, 17(1998), 6 vom: 16. März, Seite 1728-1739 |
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| Übergeordnetes Werk: |
volume:17 ; year:1998 ; number:6 ; day:16 ; month:03 ; pages:1728-1739 |
| Links: |
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| DOI / URN: |
10.1093/emboj/17.6.1728 |
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| Katalog-ID: |
SPR058002235 |
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| 100 | 1 | |a Sieweke, Michael H. |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Cooperative interaction of Ets‐1 with USF‐1 required for HIV‐1 enhancer activity in T cells |
| 264 | 1 | |c 1998 | |
| 336 | |a Text |b txt |2 rdacontent | ||
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| 500 | |a © European Molecular Biology Organization 1998 | ||
| 520 | |a Abstract The distal enhancer region of the human immunodeficiency virus 1 (HIV‐1) long terminal repeat (LTR) is known to be essential for HIV replication and to contain immediately adjacent E‐box and Ets binding sites. Based on a yeast one‐hybrid screen we have identified the E‐box binding protein USF‐1 as a direct interaction partner of Ets‐1 and found that the complex acts on this enhancer element. The binding surfaces of USF‐1 and Ets‐1 map to their DNA‐binding domains and although these domains are highly conserved, the interaction is very selective within the respective protein family. USF‐1 and Ets‐1 synergize in specific DNA binding as well as in the transactivation of reporter constructs containing the enhancer element, and mutations of the individual binding sites dramatically reduce reporter activity in T cells. In addition, a dominant negative Ets‐1 mutant inhibits both USF‐1‐mediated transactivation and the activity of the HIV‐1 LTR in T cells. The inhibition is independent of Ets DNA‐binding sites but requires the Ets binding surface on USF‐1, highlighting the importance of the direct protein–protein interaction. Together these results indicate that the interaction between Ets‐1 and USF‐1 is required for full transcriptional activity of the HIV‐1 LTR in T cells. | ||
| 650 | 4 | |a Ets proteins |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a HIV‐1 |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a HLH proteins |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a protein–protein interaction |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a transcription factors |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Tekotte, Hildegard |e verfasserin |4 aut | |
| 700 | 1 | |a Jarosch, Ursula |e verfasserin |4 aut | |
| 700 | 1 | |a Graf, Thomas |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t The EMBO Journal |d Nature Publishing Group UK, 2023 |g 17(1998), 6 vom: 16. März, Seite 1728-1739 |w (DE-627)266022529 |w (DE-600)1467419-1 |x 1460-2075 |7 nnns |
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| 912 | |a GBV_ILN_2038 | ||
| 912 | |a GBV_ILN_2044 | ||
| 912 | |a GBV_ILN_2048 | ||
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| 912 | |a GBV_ILN_2061 | ||
| 912 | |a GBV_ILN_2064 | ||
| 912 | |a GBV_ILN_2068 | ||
| 912 | |a GBV_ILN_2088 | ||
| 912 | |a GBV_ILN_2093 | ||
| 912 | |a GBV_ILN_2106 | ||
| 912 | |a GBV_ILN_2108 | ||
| 912 | |a GBV_ILN_2110 | ||
| 912 | |a GBV_ILN_2111 | ||
| 912 | |a GBV_ILN_2113 | ||
| 912 | |a GBV_ILN_2118 | ||
| 912 | |a GBV_ILN_2119 | ||
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| 912 | |a GBV_ILN_2148 | ||
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| 912 | |a GBV_ILN_2153 | ||
| 912 | |a GBV_ILN_2188 | ||
| 912 | |a GBV_ILN_2190 | ||
| 912 | |a GBV_ILN_2232 | ||
| 912 | |a GBV_ILN_2336 | ||
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| 912 | |a GBV_ILN_4251 | ||
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| 912 | |a GBV_ILN_4307 | ||
| 912 | |a GBV_ILN_4311 | ||
| 912 | |a GBV_ILN_4313 | ||
| 912 | |a GBV_ILN_4314 | ||
| 912 | |a GBV_ILN_4318 | ||
| 912 | |a GBV_ILN_4322 | ||
| 912 | |a GBV_ILN_4323 | ||
| 912 | |a GBV_ILN_4324 | ||
| 912 | |a GBV_ILN_4325 | ||
| 912 | |a GBV_ILN_4326 | ||
| 912 | |a GBV_ILN_4328 | ||
| 912 | |a GBV_ILN_4333 | ||
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| 951 | |a AR | ||
| 952 | |d 17 |j 1998 |e 6 |b 16 |c 03 |h 1728-1739 | ||
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1998 |
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1998 |
| allfields |
10.1093/emboj/17.6.1728 doi (DE-627)SPR058002235 (SPR)17.6.1728-e DE-627 ger DE-627 rakwb eng Sieweke, Michael H. verfasserin aut Cooperative interaction of Ets‐1 with USF‐1 required for HIV‐1 enhancer activity in T cells 1998 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 1998 Abstract The distal enhancer region of the human immunodeficiency virus 1 (HIV‐1) long terminal repeat (LTR) is known to be essential for HIV replication and to contain immediately adjacent E‐box and Ets binding sites. Based on a yeast one‐hybrid screen we have identified the E‐box binding protein USF‐1 as a direct interaction partner of Ets‐1 and found that the complex acts on this enhancer element. The binding surfaces of USF‐1 and Ets‐1 map to their DNA‐binding domains and although these domains are highly conserved, the interaction is very selective within the respective protein family. USF‐1 and Ets‐1 synergize in specific DNA binding as well as in the transactivation of reporter constructs containing the enhancer element, and mutations of the individual binding sites dramatically reduce reporter activity in T cells. In addition, a dominant negative Ets‐1 mutant inhibits both USF‐1‐mediated transactivation and the activity of the HIV‐1 LTR in T cells. The inhibition is independent of Ets DNA‐binding sites but requires the Ets binding surface on USF‐1, highlighting the importance of the direct protein–protein interaction. Together these results indicate that the interaction between Ets‐1 and USF‐1 is required for full transcriptional activity of the HIV‐1 LTR in T cells. Ets proteins (dpeaa)DE-He213 HIV‐1 (dpeaa)DE-He213 HLH proteins (dpeaa)DE-He213 protein–protein interaction (dpeaa)DE-He213 transcription factors (dpeaa)DE-He213 Tekotte, Hildegard verfasserin aut Jarosch, Ursula verfasserin aut Graf, Thomas verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 17(1998), 6 vom: 16. März, Seite 1728-1739 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:17 year:1998 number:6 day:16 month:03 pages:1728-1739 https://dx.doi.org/10.1093/emboj/17.6.1728 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4116 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4311 GBV_ILN_4313 GBV_ILN_4314 GBV_ILN_4318 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4598 GBV_ILN_4700 AR 17 1998 6 16 03 1728-1739 |
| spelling |
10.1093/emboj/17.6.1728 doi (DE-627)SPR058002235 (SPR)17.6.1728-e DE-627 ger DE-627 rakwb eng Sieweke, Michael H. verfasserin aut Cooperative interaction of Ets‐1 with USF‐1 required for HIV‐1 enhancer activity in T cells 1998 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 1998 Abstract The distal enhancer region of the human immunodeficiency virus 1 (HIV‐1) long terminal repeat (LTR) is known to be essential for HIV replication and to contain immediately adjacent E‐box and Ets binding sites. Based on a yeast one‐hybrid screen we have identified the E‐box binding protein USF‐1 as a direct interaction partner of Ets‐1 and found that the complex acts on this enhancer element. The binding surfaces of USF‐1 and Ets‐1 map to their DNA‐binding domains and although these domains are highly conserved, the interaction is very selective within the respective protein family. USF‐1 and Ets‐1 synergize in specific DNA binding as well as in the transactivation of reporter constructs containing the enhancer element, and mutations of the individual binding sites dramatically reduce reporter activity in T cells. In addition, a dominant negative Ets‐1 mutant inhibits both USF‐1‐mediated transactivation and the activity of the HIV‐1 LTR in T cells. The inhibition is independent of Ets DNA‐binding sites but requires the Ets binding surface on USF‐1, highlighting the importance of the direct protein–protein interaction. Together these results indicate that the interaction between Ets‐1 and USF‐1 is required for full transcriptional activity of the HIV‐1 LTR in T cells. Ets proteins (dpeaa)DE-He213 HIV‐1 (dpeaa)DE-He213 HLH proteins (dpeaa)DE-He213 protein–protein interaction (dpeaa)DE-He213 transcription factors (dpeaa)DE-He213 Tekotte, Hildegard verfasserin aut Jarosch, Ursula verfasserin aut Graf, Thomas verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 17(1998), 6 vom: 16. März, Seite 1728-1739 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:17 year:1998 number:6 day:16 month:03 pages:1728-1739 https://dx.doi.org/10.1093/emboj/17.6.1728 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4116 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4311 GBV_ILN_4313 GBV_ILN_4314 GBV_ILN_4318 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4598 GBV_ILN_4700 AR 17 1998 6 16 03 1728-1739 |
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10.1093/emboj/17.6.1728 doi (DE-627)SPR058002235 (SPR)17.6.1728-e DE-627 ger DE-627 rakwb eng Sieweke, Michael H. verfasserin aut Cooperative interaction of Ets‐1 with USF‐1 required for HIV‐1 enhancer activity in T cells 1998 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 1998 Abstract The distal enhancer region of the human immunodeficiency virus 1 (HIV‐1) long terminal repeat (LTR) is known to be essential for HIV replication and to contain immediately adjacent E‐box and Ets binding sites. Based on a yeast one‐hybrid screen we have identified the E‐box binding protein USF‐1 as a direct interaction partner of Ets‐1 and found that the complex acts on this enhancer element. The binding surfaces of USF‐1 and Ets‐1 map to their DNA‐binding domains and although these domains are highly conserved, the interaction is very selective within the respective protein family. USF‐1 and Ets‐1 synergize in specific DNA binding as well as in the transactivation of reporter constructs containing the enhancer element, and mutations of the individual binding sites dramatically reduce reporter activity in T cells. In addition, a dominant negative Ets‐1 mutant inhibits both USF‐1‐mediated transactivation and the activity of the HIV‐1 LTR in T cells. The inhibition is independent of Ets DNA‐binding sites but requires the Ets binding surface on USF‐1, highlighting the importance of the direct protein–protein interaction. Together these results indicate that the interaction between Ets‐1 and USF‐1 is required for full transcriptional activity of the HIV‐1 LTR in T cells. Ets proteins (dpeaa)DE-He213 HIV‐1 (dpeaa)DE-He213 HLH proteins (dpeaa)DE-He213 protein–protein interaction (dpeaa)DE-He213 transcription factors (dpeaa)DE-He213 Tekotte, Hildegard verfasserin aut Jarosch, Ursula verfasserin aut Graf, Thomas verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 17(1998), 6 vom: 16. März, Seite 1728-1739 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:17 year:1998 number:6 day:16 month:03 pages:1728-1739 https://dx.doi.org/10.1093/emboj/17.6.1728 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4116 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4311 GBV_ILN_4313 GBV_ILN_4314 GBV_ILN_4318 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4598 GBV_ILN_4700 AR 17 1998 6 16 03 1728-1739 |
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10.1093/emboj/17.6.1728 doi (DE-627)SPR058002235 (SPR)17.6.1728-e DE-627 ger DE-627 rakwb eng Sieweke, Michael H. verfasserin aut Cooperative interaction of Ets‐1 with USF‐1 required for HIV‐1 enhancer activity in T cells 1998 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 1998 Abstract The distal enhancer region of the human immunodeficiency virus 1 (HIV‐1) long terminal repeat (LTR) is known to be essential for HIV replication and to contain immediately adjacent E‐box and Ets binding sites. Based on a yeast one‐hybrid screen we have identified the E‐box binding protein USF‐1 as a direct interaction partner of Ets‐1 and found that the complex acts on this enhancer element. The binding surfaces of USF‐1 and Ets‐1 map to their DNA‐binding domains and although these domains are highly conserved, the interaction is very selective within the respective protein family. USF‐1 and Ets‐1 synergize in specific DNA binding as well as in the transactivation of reporter constructs containing the enhancer element, and mutations of the individual binding sites dramatically reduce reporter activity in T cells. In addition, a dominant negative Ets‐1 mutant inhibits both USF‐1‐mediated transactivation and the activity of the HIV‐1 LTR in T cells. The inhibition is independent of Ets DNA‐binding sites but requires the Ets binding surface on USF‐1, highlighting the importance of the direct protein–protein interaction. Together these results indicate that the interaction between Ets‐1 and USF‐1 is required for full transcriptional activity of the HIV‐1 LTR in T cells. Ets proteins (dpeaa)DE-He213 HIV‐1 (dpeaa)DE-He213 HLH proteins (dpeaa)DE-He213 protein–protein interaction (dpeaa)DE-He213 transcription factors (dpeaa)DE-He213 Tekotte, Hildegard verfasserin aut Jarosch, Ursula verfasserin aut Graf, Thomas verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 17(1998), 6 vom: 16. März, Seite 1728-1739 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:17 year:1998 number:6 day:16 month:03 pages:1728-1739 https://dx.doi.org/10.1093/emboj/17.6.1728 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4116 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4311 GBV_ILN_4313 GBV_ILN_4314 GBV_ILN_4318 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4598 GBV_ILN_4700 AR 17 1998 6 16 03 1728-1739 |
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10.1093/emboj/17.6.1728 doi (DE-627)SPR058002235 (SPR)17.6.1728-e DE-627 ger DE-627 rakwb eng Sieweke, Michael H. verfasserin aut Cooperative interaction of Ets‐1 with USF‐1 required for HIV‐1 enhancer activity in T cells 1998 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 1998 Abstract The distal enhancer region of the human immunodeficiency virus 1 (HIV‐1) long terminal repeat (LTR) is known to be essential for HIV replication and to contain immediately adjacent E‐box and Ets binding sites. Based on a yeast one‐hybrid screen we have identified the E‐box binding protein USF‐1 as a direct interaction partner of Ets‐1 and found that the complex acts on this enhancer element. The binding surfaces of USF‐1 and Ets‐1 map to their DNA‐binding domains and although these domains are highly conserved, the interaction is very selective within the respective protein family. USF‐1 and Ets‐1 synergize in specific DNA binding as well as in the transactivation of reporter constructs containing the enhancer element, and mutations of the individual binding sites dramatically reduce reporter activity in T cells. In addition, a dominant negative Ets‐1 mutant inhibits both USF‐1‐mediated transactivation and the activity of the HIV‐1 LTR in T cells. The inhibition is independent of Ets DNA‐binding sites but requires the Ets binding surface on USF‐1, highlighting the importance of the direct protein–protein interaction. Together these results indicate that the interaction between Ets‐1 and USF‐1 is required for full transcriptional activity of the HIV‐1 LTR in T cells. Ets proteins (dpeaa)DE-He213 HIV‐1 (dpeaa)DE-He213 HLH proteins (dpeaa)DE-He213 protein–protein interaction (dpeaa)DE-He213 transcription factors (dpeaa)DE-He213 Tekotte, Hildegard verfasserin aut Jarosch, Ursula verfasserin aut Graf, Thomas verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 17(1998), 6 vom: 16. März, Seite 1728-1739 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:17 year:1998 number:6 day:16 month:03 pages:1728-1739 https://dx.doi.org/10.1093/emboj/17.6.1728 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4116 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4311 GBV_ILN_4313 GBV_ILN_4314 GBV_ILN_4318 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4598 GBV_ILN_4700 AR 17 1998 6 16 03 1728-1739 |
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Enthalten in The EMBO Journal 17(1998), 6 vom: 16. März, Seite 1728-1739 volume:17 year:1998 number:6 day:16 month:03 pages:1728-1739 |
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Enthalten in The EMBO Journal 17(1998), 6 vom: 16. März, Seite 1728-1739 volume:17 year:1998 number:6 day:16 month:03 pages:1728-1739 |
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Ets proteins HIV‐1 HLH proteins protein–protein interaction transcription factors |
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The EMBO Journal |
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Sieweke, Michael H. @@aut@@ Tekotte, Hildegard @@aut@@ Jarosch, Ursula @@aut@@ Graf, Thomas @@aut@@ |
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1998-03-16T00:00:00Z |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000naa a22002652 4500</leader><controlfield tag="001">SPR058002235</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20241024065047.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">241024s1998 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1093/emboj/17.6.1728</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR058002235</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)17.6.1728-e</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Sieweke, Michael H.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Cooperative interaction of Ets‐1 with USF‐1 required for HIV‐1 enhancer activity in T cells</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">1998</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="500" ind1=" " ind2=" "><subfield code="a">© European Molecular Biology Organization 1998</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract The distal enhancer region of the human immunodeficiency virus 1 (HIV‐1) long terminal repeat (LTR) is known to be essential for HIV replication and to contain immediately adjacent E‐box and Ets binding sites. Based on a yeast one‐hybrid screen we have identified the E‐box binding protein USF‐1 as a direct interaction partner of Ets‐1 and found that the complex acts on this enhancer element. The binding surfaces of USF‐1 and Ets‐1 map to their DNA‐binding domains and although these domains are highly conserved, the interaction is very selective within the respective protein family. USF‐1 and Ets‐1 synergize in specific DNA binding as well as in the transactivation of reporter constructs containing the enhancer element, and mutations of the individual binding sites dramatically reduce reporter activity in T cells. In addition, a dominant negative Ets‐1 mutant inhibits both USF‐1‐mediated transactivation and the activity of the HIV‐1 LTR in T cells. The inhibition is independent of Ets DNA‐binding sites but requires the Ets binding surface on USF‐1, highlighting the importance of the direct protein–protein interaction. 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Sieweke, Michael H. |
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Sieweke, Michael H. misc Ets proteins misc HIV‐1 misc HLH proteins misc protein–protein interaction misc transcription factors Cooperative interaction of Ets‐1 with USF‐1 required for HIV‐1 enhancer activity in T cells |
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Cooperative interaction of Ets‐1 with USF‐1 required for HIV‐1 enhancer activity in T cells Ets proteins (dpeaa)DE-He213 HIV‐1 (dpeaa)DE-He213 HLH proteins (dpeaa)DE-He213 protein–protein interaction (dpeaa)DE-He213 transcription factors (dpeaa)DE-He213 |
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misc Ets proteins misc HIV‐1 misc HLH proteins misc protein–protein interaction misc transcription factors |
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Cooperative interaction of Ets‐1 with USF‐1 required for HIV‐1 enhancer activity in T cells |
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Cooperative interaction of Ets‐1 with USF‐1 required for HIV‐1 enhancer activity in T cells |
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Sieweke, Michael H. |
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Sieweke, Michael H. Tekotte, Hildegard Jarosch, Ursula Graf, Thomas |
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cooperative interaction of ets‐1 with usf‐1 required for hiv‐1 enhancer activity in t cells |
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Cooperative interaction of Ets‐1 with USF‐1 required for HIV‐1 enhancer activity in T cells |
| abstract |
Abstract The distal enhancer region of the human immunodeficiency virus 1 (HIV‐1) long terminal repeat (LTR) is known to be essential for HIV replication and to contain immediately adjacent E‐box and Ets binding sites. Based on a yeast one‐hybrid screen we have identified the E‐box binding protein USF‐1 as a direct interaction partner of Ets‐1 and found that the complex acts on this enhancer element. The binding surfaces of USF‐1 and Ets‐1 map to their DNA‐binding domains and although these domains are highly conserved, the interaction is very selective within the respective protein family. USF‐1 and Ets‐1 synergize in specific DNA binding as well as in the transactivation of reporter constructs containing the enhancer element, and mutations of the individual binding sites dramatically reduce reporter activity in T cells. In addition, a dominant negative Ets‐1 mutant inhibits both USF‐1‐mediated transactivation and the activity of the HIV‐1 LTR in T cells. The inhibition is independent of Ets DNA‐binding sites but requires the Ets binding surface on USF‐1, highlighting the importance of the direct protein–protein interaction. Together these results indicate that the interaction between Ets‐1 and USF‐1 is required for full transcriptional activity of the HIV‐1 LTR in T cells. © European Molecular Biology Organization 1998 |
| abstractGer |
Abstract The distal enhancer region of the human immunodeficiency virus 1 (HIV‐1) long terminal repeat (LTR) is known to be essential for HIV replication and to contain immediately adjacent E‐box and Ets binding sites. Based on a yeast one‐hybrid screen we have identified the E‐box binding protein USF‐1 as a direct interaction partner of Ets‐1 and found that the complex acts on this enhancer element. The binding surfaces of USF‐1 and Ets‐1 map to their DNA‐binding domains and although these domains are highly conserved, the interaction is very selective within the respective protein family. USF‐1 and Ets‐1 synergize in specific DNA binding as well as in the transactivation of reporter constructs containing the enhancer element, and mutations of the individual binding sites dramatically reduce reporter activity in T cells. In addition, a dominant negative Ets‐1 mutant inhibits both USF‐1‐mediated transactivation and the activity of the HIV‐1 LTR in T cells. The inhibition is independent of Ets DNA‐binding sites but requires the Ets binding surface on USF‐1, highlighting the importance of the direct protein–protein interaction. Together these results indicate that the interaction between Ets‐1 and USF‐1 is required for full transcriptional activity of the HIV‐1 LTR in T cells. © European Molecular Biology Organization 1998 |
| abstract_unstemmed |
Abstract The distal enhancer region of the human immunodeficiency virus 1 (HIV‐1) long terminal repeat (LTR) is known to be essential for HIV replication and to contain immediately adjacent E‐box and Ets binding sites. Based on a yeast one‐hybrid screen we have identified the E‐box binding protein USF‐1 as a direct interaction partner of Ets‐1 and found that the complex acts on this enhancer element. The binding surfaces of USF‐1 and Ets‐1 map to their DNA‐binding domains and although these domains are highly conserved, the interaction is very selective within the respective protein family. USF‐1 and Ets‐1 synergize in specific DNA binding as well as in the transactivation of reporter constructs containing the enhancer element, and mutations of the individual binding sites dramatically reduce reporter activity in T cells. In addition, a dominant negative Ets‐1 mutant inhibits both USF‐1‐mediated transactivation and the activity of the HIV‐1 LTR in T cells. The inhibition is independent of Ets DNA‐binding sites but requires the Ets binding surface on USF‐1, highlighting the importance of the direct protein–protein interaction. Together these results indicate that the interaction between Ets‐1 and USF‐1 is required for full transcriptional activity of the HIV‐1 LTR in T cells. © European Molecular Biology Organization 1998 |
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Cooperative interaction of Ets‐1 with USF‐1 required for HIV‐1 enhancer activity in T cells |
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https://dx.doi.org/10.1093/emboj/17.6.1728 |
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Tekotte, Hildegard Jarosch, Ursula Graf, Thomas |
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| score |
7.4006395 |