Abstract
The archetypical system for regulating heterologous gene expression in mammalian cells involves tetracycline-activated transactivators (rtTA). Binding of such transactivators to tet-operator-controlled promoters induces transcription. Immune responses directed against the transactivator proteins may limit the applicability of this system in immune-competent hosts. To circumvent such immune responses the immune evasion mechanism of the Epstein-Barr virus Nuclear-Antigen 1 was exploited. Our data show that fusion of the rtTA with the EBNA-1 derived Gly-Ala repeat yielded an efficient transactivator with no detectable activity in absence of inducer. Antigenic peptides of the fusion protein were not presented in MHC class I.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Antigen Presentation
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Cell Line
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Epstein-Barr Virus Nuclear Antigens / biosynthesis*
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Epstein-Barr Virus Nuclear Antigens / genetics*
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Epstein-Barr Virus Nuclear Antigens / immunology
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Gene Expression
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Herpesvirus 4, Human / genetics
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Histocompatibility Antigens Class I / immunology
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Humans
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Immune Evasion
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Recombinant Fusion Proteins / biosynthesis
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Recombinant Fusion Proteins / genetics
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Recombinant Fusion Proteins / immunology
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Tetracycline / metabolism*
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Trans-Activators / biosynthesis*
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Trans-Activators / genetics*
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Trans-Activators / immunology
Substances
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Epstein-Barr Virus Nuclear Antigens
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Histocompatibility Antigens Class I
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Recombinant Fusion Proteins
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Trans-Activators
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Tetracycline
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EBV-encoded nuclear antigen 1