The Epstein-Barr Virus Nuclear Antigen 2 (EBNA2), a Protein Required for B Lymphocyte Immortalization, Induces the Synthesis of Type I Interferon in Burkitts Lymphoma Cell Lines
Epstein-Barr virus nuclear antigen 2 (EBNA2), a protein involved in cell transformation, interferes with the cellular response to type I interferons (IFN-α/β). We investigated the function of conditionally expressed EBNA2 in the context of the IFN response in Burkitt's lymphoma cell lines. Expr...
Ausführliche Beschreibung
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Walter de Gruyter ; 2005 |
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Copyright © 1999 by Walter de Gruyter GmbH & Co. KG |
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9 |
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Walter de Gruyter Online Zeitschriften |
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Übergeordnetes Werk: |
In: 380(2005), 2 vom: 01. Juni, Seite 213-221 volume:380 ; year:2005 ; number:2 ; day:01 ; month:06 ; pages:213-221 ; extent:9 |
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10.1515/BC.1999.029 |
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10.1515/BC.1999.029 doi artikel_Grundlieferung.pp (DE-627)NLEJ246507977 DE-627 ger DE-627 rakwb The Epstein-Barr Virus Nuclear Antigen 2 (EBNA2), a Protein Required for B Lymphocyte Immortalization, Induces the Synthesis of Type I Interferon in Burkitts Lymphoma Cell Lines Walter de Gruyter 2005 9 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Copyright © 1999 by Walter de Gruyter GmbH & Co. KG Epstein-Barr virus nuclear antigen 2 (EBNA2), a protein involved in cell transformation, interferes with the cellular response to type I interferons (IFN-α/β). We investigated the function of conditionally expressed EBNA2 in the context of the IFN response in Burkitt's lymphoma cell lines. Expression of EBNA2 led to the transcriptional activation of both endogenous or transfected IFN-stimulated genes (ISGs), genes which contain within their promoters either the interferon-stimulated response element (ISRE) or the gamma interferon activation site (GAS). In search of a molecular mechanism for the transcriptional induction of ISGs, we observed an EBNA2-dependent synthesis of IFN-β mRNA at low levels and the secretion of low amounts of IFN. A transfected IFN-β promoter responded to EBNA2 activation, and a sequence closely resembling a RBP-Jκ binding site was pinpointed as a potential target of EBNA2 activity. EBNA2-dependent transcriptional induction of the IFN-β promoter occurred in EBV-negative Burkitt's lymphoma cells, indicating that other EBV genes were not required for the induction of IFN-β synthesis. Walter de Gruyter Online Zeitschriften Kanda, K. oth Kempkes, B. oth Bornkamm, G.W. oth Gabain, A. von oth Decker, T. oth In 380(2005), 2 vom: 01. Juni, Seite 213-221 volume:380 year:2005 number:2 day:01 month:06 pages:213-221 extent:9 https://doi.org/10.1515/BC.1999.029 Deutschlandweit zugänglich GBV_USEFLAG_U ZDB-1-DGR GBV_NL_ARTICLE AR 380 2005 2 01 06 213-221 9 |
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10.1515/BC.1999.029 doi artikel_Grundlieferung.pp (DE-627)NLEJ246507977 DE-627 ger DE-627 rakwb The Epstein-Barr Virus Nuclear Antigen 2 (EBNA2), a Protein Required for B Lymphocyte Immortalization, Induces the Synthesis of Type I Interferon in Burkitts Lymphoma Cell Lines Walter de Gruyter 2005 9 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Copyright © 1999 by Walter de Gruyter GmbH & Co. KG Epstein-Barr virus nuclear antigen 2 (EBNA2), a protein involved in cell transformation, interferes with the cellular response to type I interferons (IFN-α/β). We investigated the function of conditionally expressed EBNA2 in the context of the IFN response in Burkitt's lymphoma cell lines. Expression of EBNA2 led to the transcriptional activation of both endogenous or transfected IFN-stimulated genes (ISGs), genes which contain within their promoters either the interferon-stimulated response element (ISRE) or the gamma interferon activation site (GAS). In search of a molecular mechanism for the transcriptional induction of ISGs, we observed an EBNA2-dependent synthesis of IFN-β mRNA at low levels and the secretion of low amounts of IFN. A transfected IFN-β promoter responded to EBNA2 activation, and a sequence closely resembling a RBP-Jκ binding site was pinpointed as a potential target of EBNA2 activity. EBNA2-dependent transcriptional induction of the IFN-β promoter occurred in EBV-negative Burkitt's lymphoma cells, indicating that other EBV genes were not required for the induction of IFN-β synthesis. Walter de Gruyter Online Zeitschriften Kanda, K. oth Kempkes, B. oth Bornkamm, G.W. oth Gabain, A. von oth Decker, T. oth In 380(2005), 2 vom: 01. Juni, Seite 213-221 volume:380 year:2005 number:2 day:01 month:06 pages:213-221 extent:9 https://doi.org/10.1515/BC.1999.029 Deutschlandweit zugänglich GBV_USEFLAG_U ZDB-1-DGR GBV_NL_ARTICLE AR 380 2005 2 01 06 213-221 9 |
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10.1515/BC.1999.029 doi artikel_Grundlieferung.pp (DE-627)NLEJ246507977 DE-627 ger DE-627 rakwb The Epstein-Barr Virus Nuclear Antigen 2 (EBNA2), a Protein Required for B Lymphocyte Immortalization, Induces the Synthesis of Type I Interferon in Burkitts Lymphoma Cell Lines Walter de Gruyter 2005 9 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Copyright © 1999 by Walter de Gruyter GmbH & Co. KG Epstein-Barr virus nuclear antigen 2 (EBNA2), a protein involved in cell transformation, interferes with the cellular response to type I interferons (IFN-α/β). We investigated the function of conditionally expressed EBNA2 in the context of the IFN response in Burkitt's lymphoma cell lines. Expression of EBNA2 led to the transcriptional activation of both endogenous or transfected IFN-stimulated genes (ISGs), genes which contain within their promoters either the interferon-stimulated response element (ISRE) or the gamma interferon activation site (GAS). In search of a molecular mechanism for the transcriptional induction of ISGs, we observed an EBNA2-dependent synthesis of IFN-β mRNA at low levels and the secretion of low amounts of IFN. A transfected IFN-β promoter responded to EBNA2 activation, and a sequence closely resembling a RBP-Jκ binding site was pinpointed as a potential target of EBNA2 activity. EBNA2-dependent transcriptional induction of the IFN-β promoter occurred in EBV-negative Burkitt's lymphoma cells, indicating that other EBV genes were not required for the induction of IFN-β synthesis. Walter de Gruyter Online Zeitschriften Kanda, K. oth Kempkes, B. oth Bornkamm, G.W. oth Gabain, A. von oth Decker, T. oth In 380(2005), 2 vom: 01. Juni, Seite 213-221 volume:380 year:2005 number:2 day:01 month:06 pages:213-221 extent:9 https://doi.org/10.1515/BC.1999.029 Deutschlandweit zugänglich GBV_USEFLAG_U ZDB-1-DGR GBV_NL_ARTICLE AR 380 2005 2 01 06 213-221 9 |
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10.1515/BC.1999.029 doi artikel_Grundlieferung.pp (DE-627)NLEJ246507977 DE-627 ger DE-627 rakwb The Epstein-Barr Virus Nuclear Antigen 2 (EBNA2), a Protein Required for B Lymphocyte Immortalization, Induces the Synthesis of Type I Interferon in Burkitts Lymphoma Cell Lines Walter de Gruyter 2005 9 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Copyright © 1999 by Walter de Gruyter GmbH & Co. KG Epstein-Barr virus nuclear antigen 2 (EBNA2), a protein involved in cell transformation, interferes with the cellular response to type I interferons (IFN-α/β). We investigated the function of conditionally expressed EBNA2 in the context of the IFN response in Burkitt's lymphoma cell lines. Expression of EBNA2 led to the transcriptional activation of both endogenous or transfected IFN-stimulated genes (ISGs), genes which contain within their promoters either the interferon-stimulated response element (ISRE) or the gamma interferon activation site (GAS). In search of a molecular mechanism for the transcriptional induction of ISGs, we observed an EBNA2-dependent synthesis of IFN-β mRNA at low levels and the secretion of low amounts of IFN. A transfected IFN-β promoter responded to EBNA2 activation, and a sequence closely resembling a RBP-Jκ binding site was pinpointed as a potential target of EBNA2 activity. EBNA2-dependent transcriptional induction of the IFN-β promoter occurred in EBV-negative Burkitt's lymphoma cells, indicating that other EBV genes were not required for the induction of IFN-β synthesis. Walter de Gruyter Online Zeitschriften Kanda, K. oth Kempkes, B. oth Bornkamm, G.W. oth Gabain, A. von oth Decker, T. oth In 380(2005), 2 vom: 01. Juni, Seite 213-221 volume:380 year:2005 number:2 day:01 month:06 pages:213-221 extent:9 https://doi.org/10.1515/BC.1999.029 Deutschlandweit zugänglich GBV_USEFLAG_U ZDB-1-DGR GBV_NL_ARTICLE AR 380 2005 2 01 06 213-221 9 |
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10.1515/BC.1999.029 doi artikel_Grundlieferung.pp (DE-627)NLEJ246507977 DE-627 ger DE-627 rakwb The Epstein-Barr Virus Nuclear Antigen 2 (EBNA2), a Protein Required for B Lymphocyte Immortalization, Induces the Synthesis of Type I Interferon in Burkitts Lymphoma Cell Lines Walter de Gruyter 2005 9 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Copyright © 1999 by Walter de Gruyter GmbH & Co. KG Epstein-Barr virus nuclear antigen 2 (EBNA2), a protein involved in cell transformation, interferes with the cellular response to type I interferons (IFN-α/β). We investigated the function of conditionally expressed EBNA2 in the context of the IFN response in Burkitt's lymphoma cell lines. Expression of EBNA2 led to the transcriptional activation of both endogenous or transfected IFN-stimulated genes (ISGs), genes which contain within their promoters either the interferon-stimulated response element (ISRE) or the gamma interferon activation site (GAS). In search of a molecular mechanism for the transcriptional induction of ISGs, we observed an EBNA2-dependent synthesis of IFN-β mRNA at low levels and the secretion of low amounts of IFN. A transfected IFN-β promoter responded to EBNA2 activation, and a sequence closely resembling a RBP-Jκ binding site was pinpointed as a potential target of EBNA2 activity. EBNA2-dependent transcriptional induction of the IFN-β promoter occurred in EBV-negative Burkitt's lymphoma cells, indicating that other EBV genes were not required for the induction of IFN-β synthesis. Walter de Gruyter Online Zeitschriften Kanda, K. oth Kempkes, B. oth Bornkamm, G.W. oth Gabain, A. von oth Decker, T. oth In 380(2005), 2 vom: 01. Juni, Seite 213-221 volume:380 year:2005 number:2 day:01 month:06 pages:213-221 extent:9 https://doi.org/10.1515/BC.1999.029 Deutschlandweit zugänglich GBV_USEFLAG_U ZDB-1-DGR GBV_NL_ARTICLE AR 380 2005 2 01 06 213-221 9 |
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the epstein-barr virus nuclear antigen 2 (ebna2), a protein required for b lymphocyte immortalization, induces the synthesis of type i interferon in burkitts lymphoma cell lines |
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The Epstein-Barr Virus Nuclear Antigen 2 (EBNA2), a Protein Required for B Lymphocyte Immortalization, Induces the Synthesis of Type I Interferon in Burkitts Lymphoma Cell Lines |
abstract |
Epstein-Barr virus nuclear antigen 2 (EBNA2), a protein involved in cell transformation, interferes with the cellular response to type I interferons (IFN-α/β). We investigated the function of conditionally expressed EBNA2 in the context of the IFN response in Burkitt's lymphoma cell lines. Expression of EBNA2 led to the transcriptional activation of both endogenous or transfected IFN-stimulated genes (ISGs), genes which contain within their promoters either the interferon-stimulated response element (ISRE) or the gamma interferon activation site (GAS). In search of a molecular mechanism for the transcriptional induction of ISGs, we observed an EBNA2-dependent synthesis of IFN-β mRNA at low levels and the secretion of low amounts of IFN. A transfected IFN-β promoter responded to EBNA2 activation, and a sequence closely resembling a RBP-Jκ binding site was pinpointed as a potential target of EBNA2 activity. EBNA2-dependent transcriptional induction of the IFN-β promoter occurred in EBV-negative Burkitt's lymphoma cells, indicating that other EBV genes were not required for the induction of IFN-β synthesis. Copyright © 1999 by Walter de Gruyter GmbH & Co. KG |
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Epstein-Barr virus nuclear antigen 2 (EBNA2), a protein involved in cell transformation, interferes with the cellular response to type I interferons (IFN-α/β). We investigated the function of conditionally expressed EBNA2 in the context of the IFN response in Burkitt's lymphoma cell lines. Expression of EBNA2 led to the transcriptional activation of both endogenous or transfected IFN-stimulated genes (ISGs), genes which contain within their promoters either the interferon-stimulated response element (ISRE) or the gamma interferon activation site (GAS). In search of a molecular mechanism for the transcriptional induction of ISGs, we observed an EBNA2-dependent synthesis of IFN-β mRNA at low levels and the secretion of low amounts of IFN. A transfected IFN-β promoter responded to EBNA2 activation, and a sequence closely resembling a RBP-Jκ binding site was pinpointed as a potential target of EBNA2 activity. EBNA2-dependent transcriptional induction of the IFN-β promoter occurred in EBV-negative Burkitt's lymphoma cells, indicating that other EBV genes were not required for the induction of IFN-β synthesis. Copyright © 1999 by Walter de Gruyter GmbH & Co. KG |
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Epstein-Barr virus nuclear antigen 2 (EBNA2), a protein involved in cell transformation, interferes with the cellular response to type I interferons (IFN-α/β). We investigated the function of conditionally expressed EBNA2 in the context of the IFN response in Burkitt's lymphoma cell lines. Expression of EBNA2 led to the transcriptional activation of both endogenous or transfected IFN-stimulated genes (ISGs), genes which contain within their promoters either the interferon-stimulated response element (ISRE) or the gamma interferon activation site (GAS). In search of a molecular mechanism for the transcriptional induction of ISGs, we observed an EBNA2-dependent synthesis of IFN-β mRNA at low levels and the secretion of low amounts of IFN. A transfected IFN-β promoter responded to EBNA2 activation, and a sequence closely resembling a RBP-Jκ binding site was pinpointed as a potential target of EBNA2 activity. EBNA2-dependent transcriptional induction of the IFN-β promoter occurred in EBV-negative Burkitt's lymphoma cells, indicating that other EBV genes were not required for the induction of IFN-β synthesis. Copyright © 1999 by Walter de Gruyter GmbH & Co. KG |
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The Epstein-Barr Virus Nuclear Antigen 2 (EBNA2), a Protein Required for B Lymphocyte Immortalization, Induces the Synthesis of Type I Interferon in Burkitts Lymphoma Cell Lines |
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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">NLEJ246507977</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20220814134748.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">220814s2005 xx |||||o 00| ||und c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1515/BC.1999.029</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">artikel_Grundlieferung.pp</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ246507977</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="245" ind1="1" ind2="0"><subfield code="a">The Epstein-Barr Virus Nuclear Antigen 2 (EBNA2), a Protein Required for B Lymphocyte Immortalization, Induces the Synthesis of Type I Interferon in Burkitts Lymphoma Cell Lines</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="b">Walter de Gruyter</subfield><subfield code="c">2005</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">9</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">Copyright © 1999 by Walter de Gruyter GmbH & Co. KG</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Epstein-Barr virus nuclear antigen 2 (EBNA2), a protein involved in cell transformation, interferes with the cellular response to type I interferons (IFN-α/β). We investigated the function of conditionally expressed EBNA2 in the context of the IFN response in Burkitt's lymphoma cell lines. Expression of EBNA2 led to the transcriptional activation of both endogenous or transfected IFN-stimulated genes (ISGs), genes which contain within their promoters either the interferon-stimulated response element (ISRE) or the gamma interferon activation site (GAS). In search of a molecular mechanism for the transcriptional induction of ISGs, we observed an EBNA2-dependent synthesis of IFN-β mRNA at low levels and the secretion of low amounts of IFN. A transfected IFN-β promoter responded to EBNA2 activation, and a sequence closely resembling a RBP-Jκ binding site was pinpointed as a potential target of EBNA2 activity. EBNA2-dependent transcriptional induction of the IFN-β promoter occurred in EBV-negative Burkitt's lymphoma cells, indicating that other EBV genes were not required for the induction of IFN-β synthesis.</subfield></datafield><datafield tag="533" ind1=" " ind2=" "><subfield code="f">Walter de Gruyter Online Zeitschriften</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kanda, K.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kempkes, B.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Bornkamm, G.W.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Gabain, A. von</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Decker, T.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">In</subfield><subfield code="g">380(2005), 2 vom: 01. Juni, Seite 213-221</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:380</subfield><subfield code="g">year:2005</subfield><subfield code="g">number:2</subfield><subfield code="g">day:01</subfield><subfield code="g">month:06</subfield><subfield code="g">pages:213-221</subfield><subfield code="g">extent:9</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1515/BC.1999.029</subfield><subfield code="z">Deutschlandweit zugänglich</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">ZDB-1-DGR</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_NL_ARTICLE</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">380</subfield><subfield code="j">2005</subfield><subfield code="e">2</subfield><subfield code="b">01</subfield><subfield code="c">06</subfield><subfield code="h">213-221</subfield><subfield code="g">9</subfield></datafield></record></collection>
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