Functional interplay of Epstein-Barr virus oncoproteins in a mouse model of B cell
Epstein-Barr virus (EBV) is a B cell transforming virus that causes B cell malignancies under conditions of immune suppression. EBV orchestrates B cell transformation through its latent membrane proteins (LMPs) and Epstein-Barr nuclear antigens (EBNAs). We here identify secondary mutations in mouse...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Sommermann, Thomas - 1982- [verfasserIn] Yasuda, Tomoharu [verfasserIn] Ronen, Jonathan [verfasserIn] Wirtz, Tristan [verfasserIn] Weber, Timm [verfasserIn] Sack, Ulrike [verfasserIn] Caeser, Rebecca [verfasserIn] Zhang, Jingwei [verfasserIn] Li, Xun [verfasserIn] Chu, Van Trung [verfasserIn] Jauch, Anna [verfasserIn] Unger, Kristian [verfasserIn] Hodson, Daniel J. [verfasserIn] Akalin, Altuna [verfasserIn] Rajewsky, Klaus [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
June 10, 2020 |
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| Schlagwörter: |
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| Anmerkung: |
Gesehen am 09.09.2020 |
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| Umfang: |
12 |
| Übergeordnetes Werk: |
Enthalten in: Proceedings of the National Academy of Sciences of the United States of America - National Academy of Sciences (Washington, DC), Washington, DC : National Acad. of Sciences, 1915, 117(2020), 25, Seite 14421-14432 |
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| Übergeordnetes Werk: |
volume:117 ; year:2020 ; number:25 ; pages:14421-14432 ; extent:12 |
| Links: |
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| DOI / URN: |
10.1073/pnas.1921139117 |
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| Katalog-ID: |
172919933X |
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| 100 | 1 | |a Sommermann, Thomas |d 1982- |e verfasserin |0 (DE-588)1023312697 |0 (DE-627)718353781 |0 (DE-576)366626019 |4 aut | |
| 245 | 1 | 0 | |a Functional interplay of Epstein-Barr virus oncoproteins in a mouse model of B cell |c Thomas Sommermann, Tomoharu Yasuda, Jonathan Ronen, Tristan Wirtz, Timm Weber, Ulrike Sack, Rebecca Caeser, Jingwei Zhang, Xun Li, Van Trung Chu, Anna Jauch, Kristian Unger, Daniel J. Hodson, Altuna Akalin, and Klaus Rajewsky |
| 264 | 1 | |c June 10, 2020 | |
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| 500 | |a Gesehen am 09.09.2020 | ||
| 520 | |a Epstein-Barr virus (EBV) is a B cell transforming virus that causes B cell malignancies under conditions of immune suppression. EBV orchestrates B cell transformation through its latent membrane proteins (LMPs) and Epstein-Barr nuclear antigens (EBNAs). We here identify secondary mutations in mouse B cell lymphomas induced by LMP1, to predict and identify key functions of other EBV genes during transformation. We find aberrant activation of early B cell factor 1 (EBF1) to promote transformation of LMP1-expressing B cells by inhibiting their differentiation to plasma cells. EBV EBNA3A phenocopies EBF1 activities in LMP1-expressing B cells, promoting transformation while inhibiting differentiation. In cells expressing LMP1 together with LMP2A, EBNA3A only promotes lymphomagenesis when the EBNA2 target Myc is also overexpressed. Collectively, our data support a model where proproliferative activities of LMP1, LMP2A, and EBNA2 in combination with EBNA3A-mediated inhibition of terminal plasma cell differentiation critically control EBV-mediated B cell lymphomagenesis. | ||
| 650 | 4 | |a B cell lymphomagenesis | |
| 650 | 4 | |a c-rel | |
| 650 | 4 | |a ebna | |
| 650 | 4 | |a ebv | |
| 650 | 4 | |a Epstein-Barr virus | |
| 650 | 4 | |a expression | |
| 650 | 4 | |a genome-wide | |
| 650 | 4 | |a in-vivo | |
| 650 | 4 | |a lmp1 | |
| 650 | 4 | |a lymphoma | |
| 650 | 4 | |a lymphoproliferative disorders | |
| 650 | 4 | |a nf-kappa-b | |
| 650 | 4 | |a nuclear antigen-1 | |
| 650 | 4 | |a plasma cell differentiation | |
| 650 | 4 | |a tumor-suppressor | |
| 700 | 1 | |a Yasuda, Tomoharu |e verfasserin |4 aut | |
| 700 | 1 | |a Ronen, Jonathan |e verfasserin |4 aut | |
| 700 | 1 | |a Wirtz, Tristan |e verfasserin |4 aut | |
| 700 | 1 | |a Weber, Timm |e verfasserin |4 aut | |
| 700 | 1 | |a Sack, Ulrike |e verfasserin |4 aut | |
| 700 | 1 | |a Caeser, Rebecca |e verfasserin |4 aut | |
| 700 | 1 | |a Zhang, Jingwei |e verfasserin |4 aut | |
| 700 | 1 | |a Li, Xun |e verfasserin |4 aut | |
| 700 | 1 | |a Chu, Van Trung |e verfasserin |4 aut | |
| 700 | 1 | |a Jauch, Anna |e verfasserin |0 (DE-588)1025525140 |0 (DE-627)722525362 |0 (DE-576)168357496 |4 aut | |
| 700 | 1 | |a Unger, Kristian |e verfasserin |4 aut | |
| 700 | 1 | |a Hodson, Daniel J. |e verfasserin |4 aut | |
| 700 | 1 | |a Akalin, Altuna |e verfasserin |4 aut | |
| 700 | 1 | |a Rajewsky, Klaus |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |a National Academy of Sciences (Washington, DC) |t Proceedings of the National Academy of Sciences of the United States of America |d Washington, DC : National Acad. of Sciences, 1915 |g 117(2020), 25, Seite 14421-14432 |h Online-Ressource |w (DE-627)254235379 |w (DE-600)1461794-8 |w (DE-576)073260509 |x 1091-6490 |7 nnns |
| 773 | 1 | 8 | |g volume:117 |g year:2020 |g number:25 |g pages:14421-14432 |g extent:12 |
| 856 | 4 | 0 | |u https://doi.org/10.1073/pnas.1921139117 |x Verlag |x Resolving-System |z lizenzpflichtig |3 Volltext |
| 912 | |a GBV_USEFLAG_U | ||
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| 912 | |a ISIL_DE-16-250 | ||
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| 912 | |a GBV_ILN_90 | ||
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| 912 | |a GBV_ILN_110 | ||
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| 912 | |a GBV_ILN_151 | ||
| 912 | |a GBV_ILN_161 | ||
| 912 | |a GBV_ILN_168 | ||
| 912 | |a GBV_ILN_170 | ||
| 912 | |a GBV_ILN_171 | ||
| 912 | |a GBV_ILN_211 | ||
| 912 | |a GBV_ILN_213 | ||
| 912 | |a GBV_ILN_230 | ||
| 912 | |a GBV_ILN_252 | ||
| 912 | |a GBV_ILN_285 | ||
| 912 | |a GBV_ILN_293 | ||
| 912 | |a GBV_ILN_370 | ||
| 912 | |a GBV_ILN_374 | ||
| 912 | |a GBV_ILN_381 | ||
| 912 | |a GBV_ILN_602 | ||
| 912 | |a GBV_ILN_702 | ||
| 912 | |a GBV_ILN_2001 | ||
| 912 | |a GBV_ILN_2003 | ||
| 912 | |a GBV_ILN_2005 | ||
| 912 | |a GBV_ILN_2006 | ||
| 912 | |a GBV_ILN_2009 | ||
| 912 | |a GBV_ILN_2010 | ||
| 912 | |a GBV_ILN_2011 | ||
| 912 | |a GBV_ILN_2014 | ||
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| 912 | |a GBV_ILN_2018 | ||
| 912 | |a GBV_ILN_2020 | ||
| 912 | |a GBV_ILN_2021 | ||
| 912 | |a GBV_ILN_2026 | ||
| 912 | |a GBV_ILN_2027 | ||
| 912 | |a GBV_ILN_2044 | ||
| 912 | |a GBV_ILN_2050 | ||
| 912 | |a GBV_ILN_2057 | ||
| 912 | |a GBV_ILN_2061 | ||
| 912 | |a GBV_ILN_2088 | ||
| 912 | |a GBV_ILN_2107 | ||
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| 912 | |a GBV_ILN_2190 | ||
| 912 | |a GBV_ILN_2360 | ||
| 912 | |a GBV_ILN_2943 | ||
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| 912 | |a GBV_ILN_2949 | ||
| 912 | |a GBV_ILN_2951 | ||
| 912 | |a GBV_ILN_4012 | ||
| 912 | |a GBV_ILN_4035 | ||
| 912 | |a GBV_ILN_4037 | ||
| 912 | |a GBV_ILN_4046 | ||
| 912 | |a GBV_ILN_4112 | ||
| 912 | |a GBV_ILN_4125 | ||
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| 912 | |a GBV_ILN_4242 | ||
| 912 | |a GBV_ILN_4249 | ||
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| 912 | |a GBV_ILN_4335 | ||
| 912 | |a GBV_ILN_4338 | ||
| 912 | |a GBV_ILN_4346 | ||
| 912 | |a GBV_ILN_4367 | ||
| 912 | |a GBV_ILN_4393 | ||
| 912 | |a GBV_ILN_4700 | ||
| 951 | |a AR | ||
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June 10, 2020 |
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2020 |
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10.1073/pnas.1921139117 doi (DE-627)172919933X (DE-599)KXP172919933X (OCoLC)1341359175 DE-627 ger DE-627 rda eng Sommermann, Thomas 1982- verfasserin (DE-588)1023312697 (DE-627)718353781 (DE-576)366626019 aut Functional interplay of Epstein-Barr virus oncoproteins in a mouse model of B cell Thomas Sommermann, Tomoharu Yasuda, Jonathan Ronen, Tristan Wirtz, Timm Weber, Ulrike Sack, Rebecca Caeser, Jingwei Zhang, Xun Li, Van Trung Chu, Anna Jauch, Kristian Unger, Daniel J. Hodson, Altuna Akalin, and Klaus Rajewsky June 10, 2020 12 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 09.09.2020 Epstein-Barr virus (EBV) is a B cell transforming virus that causes B cell malignancies under conditions of immune suppression. EBV orchestrates B cell transformation through its latent membrane proteins (LMPs) and Epstein-Barr nuclear antigens (EBNAs). We here identify secondary mutations in mouse B cell lymphomas induced by LMP1, to predict and identify key functions of other EBV genes during transformation. We find aberrant activation of early B cell factor 1 (EBF1) to promote transformation of LMP1-expressing B cells by inhibiting their differentiation to plasma cells. EBV EBNA3A phenocopies EBF1 activities in LMP1-expressing B cells, promoting transformation while inhibiting differentiation. In cells expressing LMP1 together with LMP2A, EBNA3A only promotes lymphomagenesis when the EBNA2 target Myc is also overexpressed. Collectively, our data support a model where proproliferative activities of LMP1, LMP2A, and EBNA2 in combination with EBNA3A-mediated inhibition of terminal plasma cell differentiation critically control EBV-mediated B cell lymphomagenesis. B cell lymphomagenesis c-rel ebna ebv Epstein-Barr virus expression genome-wide in-vivo lmp1 lymphoma lymphoproliferative disorders nf-kappa-b nuclear antigen-1 plasma cell differentiation tumor-suppressor Yasuda, Tomoharu verfasserin aut Ronen, Jonathan verfasserin aut Wirtz, Tristan verfasserin aut Weber, Timm verfasserin aut Sack, Ulrike verfasserin aut Caeser, Rebecca verfasserin aut Zhang, Jingwei verfasserin aut Li, Xun verfasserin aut Chu, Van Trung verfasserin aut Jauch, Anna verfasserin (DE-588)1025525140 (DE-627)722525362 (DE-576)168357496 aut Unger, Kristian verfasserin aut Hodson, Daniel J. verfasserin aut Akalin, Altuna verfasserin aut Rajewsky, Klaus verfasserin aut Enthalten in National Academy of Sciences (Washington, DC) Proceedings of the National Academy of Sciences of the United States of America Washington, DC : National Acad. of Sciences, 1915 117(2020), 25, Seite 14421-14432 Online-Ressource (DE-627)254235379 (DE-600)1461794-8 (DE-576)073260509 1091-6490 nnns volume:117 year:2020 number:25 pages:14421-14432 extent:12 https://doi.org/10.1073/pnas.1921139117 Verlag Resolving-System lizenzpflichtig Volltext GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_211 GBV_ILN_213 GBV_ILN_230 GBV_ILN_252 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_381 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2026 GBV_ILN_2027 GBV_ILN_2044 GBV_ILN_2050 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2088 GBV_ILN_2107 GBV_ILN_2110 GBV_ILN_2190 GBV_ILN_2360 GBV_ILN_2943 GBV_ILN_2946 GBV_ILN_2949 GBV_ILN_2951 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4346 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 117 2020 25 14421-14432 12 2013 01 DE-16-250 3748099940 00 --%%-- --%%-- --%%-- --%%-- l01 09-09-20 2013 01 DE-16-250 00 s hd2020 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_15 2013 01 DE-16-250 03 s s_12 2013 01 DE-16-250 04 p (DE-627)1440454388 Jauch, Anna 2013 01 DE-16-250 04 k (DE-627)1416741429 Institut für Humangenetik 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_11 |
| spelling |
10.1073/pnas.1921139117 doi (DE-627)172919933X (DE-599)KXP172919933X (OCoLC)1341359175 DE-627 ger DE-627 rda eng Sommermann, Thomas 1982- verfasserin (DE-588)1023312697 (DE-627)718353781 (DE-576)366626019 aut Functional interplay of Epstein-Barr virus oncoproteins in a mouse model of B cell Thomas Sommermann, Tomoharu Yasuda, Jonathan Ronen, Tristan Wirtz, Timm Weber, Ulrike Sack, Rebecca Caeser, Jingwei Zhang, Xun Li, Van Trung Chu, Anna Jauch, Kristian Unger, Daniel J. Hodson, Altuna Akalin, and Klaus Rajewsky June 10, 2020 12 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 09.09.2020 Epstein-Barr virus (EBV) is a B cell transforming virus that causes B cell malignancies under conditions of immune suppression. EBV orchestrates B cell transformation through its latent membrane proteins (LMPs) and Epstein-Barr nuclear antigens (EBNAs). We here identify secondary mutations in mouse B cell lymphomas induced by LMP1, to predict and identify key functions of other EBV genes during transformation. We find aberrant activation of early B cell factor 1 (EBF1) to promote transformation of LMP1-expressing B cells by inhibiting their differentiation to plasma cells. EBV EBNA3A phenocopies EBF1 activities in LMP1-expressing B cells, promoting transformation while inhibiting differentiation. In cells expressing LMP1 together with LMP2A, EBNA3A only promotes lymphomagenesis when the EBNA2 target Myc is also overexpressed. Collectively, our data support a model where proproliferative activities of LMP1, LMP2A, and EBNA2 in combination with EBNA3A-mediated inhibition of terminal plasma cell differentiation critically control EBV-mediated B cell lymphomagenesis. B cell lymphomagenesis c-rel ebna ebv Epstein-Barr virus expression genome-wide in-vivo lmp1 lymphoma lymphoproliferative disorders nf-kappa-b nuclear antigen-1 plasma cell differentiation tumor-suppressor Yasuda, Tomoharu verfasserin aut Ronen, Jonathan verfasserin aut Wirtz, Tristan verfasserin aut Weber, Timm verfasserin aut Sack, Ulrike verfasserin aut Caeser, Rebecca verfasserin aut Zhang, Jingwei verfasserin aut Li, Xun verfasserin aut Chu, Van Trung verfasserin aut Jauch, Anna verfasserin (DE-588)1025525140 (DE-627)722525362 (DE-576)168357496 aut Unger, Kristian verfasserin aut Hodson, Daniel J. verfasserin aut Akalin, Altuna verfasserin aut Rajewsky, Klaus verfasserin aut Enthalten in National Academy of Sciences (Washington, DC) Proceedings of the National Academy of Sciences of the United States of America Washington, DC : National Acad. of Sciences, 1915 117(2020), 25, Seite 14421-14432 Online-Ressource (DE-627)254235379 (DE-600)1461794-8 (DE-576)073260509 1091-6490 nnns volume:117 year:2020 number:25 pages:14421-14432 extent:12 https://doi.org/10.1073/pnas.1921139117 Verlag Resolving-System lizenzpflichtig Volltext GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_211 GBV_ILN_213 GBV_ILN_230 GBV_ILN_252 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_381 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2026 GBV_ILN_2027 GBV_ILN_2044 GBV_ILN_2050 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2088 GBV_ILN_2107 GBV_ILN_2110 GBV_ILN_2190 GBV_ILN_2360 GBV_ILN_2943 GBV_ILN_2946 GBV_ILN_2949 GBV_ILN_2951 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4346 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 117 2020 25 14421-14432 12 2013 01 DE-16-250 3748099940 00 --%%-- --%%-- --%%-- --%%-- l01 09-09-20 2013 01 DE-16-250 00 s hd2020 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_15 2013 01 DE-16-250 03 s s_12 2013 01 DE-16-250 04 p (DE-627)1440454388 Jauch, Anna 2013 01 DE-16-250 04 k (DE-627)1416741429 Institut für Humangenetik 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_11 |
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10.1073/pnas.1921139117 doi (DE-627)172919933X (DE-599)KXP172919933X (OCoLC)1341359175 DE-627 ger DE-627 rda eng Sommermann, Thomas 1982- verfasserin (DE-588)1023312697 (DE-627)718353781 (DE-576)366626019 aut Functional interplay of Epstein-Barr virus oncoproteins in a mouse model of B cell Thomas Sommermann, Tomoharu Yasuda, Jonathan Ronen, Tristan Wirtz, Timm Weber, Ulrike Sack, Rebecca Caeser, Jingwei Zhang, Xun Li, Van Trung Chu, Anna Jauch, Kristian Unger, Daniel J. Hodson, Altuna Akalin, and Klaus Rajewsky June 10, 2020 12 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 09.09.2020 Epstein-Barr virus (EBV) is a B cell transforming virus that causes B cell malignancies under conditions of immune suppression. EBV orchestrates B cell transformation through its latent membrane proteins (LMPs) and Epstein-Barr nuclear antigens (EBNAs). We here identify secondary mutations in mouse B cell lymphomas induced by LMP1, to predict and identify key functions of other EBV genes during transformation. We find aberrant activation of early B cell factor 1 (EBF1) to promote transformation of LMP1-expressing B cells by inhibiting their differentiation to plasma cells. EBV EBNA3A phenocopies EBF1 activities in LMP1-expressing B cells, promoting transformation while inhibiting differentiation. In cells expressing LMP1 together with LMP2A, EBNA3A only promotes lymphomagenesis when the EBNA2 target Myc is also overexpressed. Collectively, our data support a model where proproliferative activities of LMP1, LMP2A, and EBNA2 in combination with EBNA3A-mediated inhibition of terminal plasma cell differentiation critically control EBV-mediated B cell lymphomagenesis. B cell lymphomagenesis c-rel ebna ebv Epstein-Barr virus expression genome-wide in-vivo lmp1 lymphoma lymphoproliferative disorders nf-kappa-b nuclear antigen-1 plasma cell differentiation tumor-suppressor Yasuda, Tomoharu verfasserin aut Ronen, Jonathan verfasserin aut Wirtz, Tristan verfasserin aut Weber, Timm verfasserin aut Sack, Ulrike verfasserin aut Caeser, Rebecca verfasserin aut Zhang, Jingwei verfasserin aut Li, Xun verfasserin aut Chu, Van Trung verfasserin aut Jauch, Anna verfasserin (DE-588)1025525140 (DE-627)722525362 (DE-576)168357496 aut Unger, Kristian verfasserin aut Hodson, Daniel J. verfasserin aut Akalin, Altuna verfasserin aut Rajewsky, Klaus verfasserin aut Enthalten in National Academy of Sciences (Washington, DC) Proceedings of the National Academy of Sciences of the United States of America Washington, DC : National Acad. of Sciences, 1915 117(2020), 25, Seite 14421-14432 Online-Ressource (DE-627)254235379 (DE-600)1461794-8 (DE-576)073260509 1091-6490 nnns volume:117 year:2020 number:25 pages:14421-14432 extent:12 https://doi.org/10.1073/pnas.1921139117 Verlag Resolving-System lizenzpflichtig Volltext GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_211 GBV_ILN_213 GBV_ILN_230 GBV_ILN_252 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_381 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2026 GBV_ILN_2027 GBV_ILN_2044 GBV_ILN_2050 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2088 GBV_ILN_2107 GBV_ILN_2110 GBV_ILN_2190 GBV_ILN_2360 GBV_ILN_2943 GBV_ILN_2946 GBV_ILN_2949 GBV_ILN_2951 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4346 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 117 2020 25 14421-14432 12 2013 01 DE-16-250 3748099940 00 --%%-- --%%-- --%%-- --%%-- l01 09-09-20 2013 01 DE-16-250 00 s hd2020 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_15 2013 01 DE-16-250 03 s s_12 2013 01 DE-16-250 04 p (DE-627)1440454388 Jauch, Anna 2013 01 DE-16-250 04 k (DE-627)1416741429 Institut für Humangenetik 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_11 |
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10.1073/pnas.1921139117 doi (DE-627)172919933X (DE-599)KXP172919933X (OCoLC)1341359175 DE-627 ger DE-627 rda eng Sommermann, Thomas 1982- verfasserin (DE-588)1023312697 (DE-627)718353781 (DE-576)366626019 aut Functional interplay of Epstein-Barr virus oncoproteins in a mouse model of B cell Thomas Sommermann, Tomoharu Yasuda, Jonathan Ronen, Tristan Wirtz, Timm Weber, Ulrike Sack, Rebecca Caeser, Jingwei Zhang, Xun Li, Van Trung Chu, Anna Jauch, Kristian Unger, Daniel J. Hodson, Altuna Akalin, and Klaus Rajewsky June 10, 2020 12 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 09.09.2020 Epstein-Barr virus (EBV) is a B cell transforming virus that causes B cell malignancies under conditions of immune suppression. EBV orchestrates B cell transformation through its latent membrane proteins (LMPs) and Epstein-Barr nuclear antigens (EBNAs). We here identify secondary mutations in mouse B cell lymphomas induced by LMP1, to predict and identify key functions of other EBV genes during transformation. We find aberrant activation of early B cell factor 1 (EBF1) to promote transformation of LMP1-expressing B cells by inhibiting their differentiation to plasma cells. EBV EBNA3A phenocopies EBF1 activities in LMP1-expressing B cells, promoting transformation while inhibiting differentiation. In cells expressing LMP1 together with LMP2A, EBNA3A only promotes lymphomagenesis when the EBNA2 target Myc is also overexpressed. Collectively, our data support a model where proproliferative activities of LMP1, LMP2A, and EBNA2 in combination with EBNA3A-mediated inhibition of terminal plasma cell differentiation critically control EBV-mediated B cell lymphomagenesis. B cell lymphomagenesis c-rel ebna ebv Epstein-Barr virus expression genome-wide in-vivo lmp1 lymphoma lymphoproliferative disorders nf-kappa-b nuclear antigen-1 plasma cell differentiation tumor-suppressor Yasuda, Tomoharu verfasserin aut Ronen, Jonathan verfasserin aut Wirtz, Tristan verfasserin aut Weber, Timm verfasserin aut Sack, Ulrike verfasserin aut Caeser, Rebecca verfasserin aut Zhang, Jingwei verfasserin aut Li, Xun verfasserin aut Chu, Van Trung verfasserin aut Jauch, Anna verfasserin (DE-588)1025525140 (DE-627)722525362 (DE-576)168357496 aut Unger, Kristian verfasserin aut Hodson, Daniel J. verfasserin aut Akalin, Altuna verfasserin aut Rajewsky, Klaus verfasserin aut Enthalten in National Academy of Sciences (Washington, DC) Proceedings of the National Academy of Sciences of the United States of America Washington, DC : National Acad. of Sciences, 1915 117(2020), 25, Seite 14421-14432 Online-Ressource (DE-627)254235379 (DE-600)1461794-8 (DE-576)073260509 1091-6490 nnns volume:117 year:2020 number:25 pages:14421-14432 extent:12 https://doi.org/10.1073/pnas.1921139117 Verlag Resolving-System lizenzpflichtig Volltext GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_211 GBV_ILN_213 GBV_ILN_230 GBV_ILN_252 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_381 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2026 GBV_ILN_2027 GBV_ILN_2044 GBV_ILN_2050 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2088 GBV_ILN_2107 GBV_ILN_2110 GBV_ILN_2190 GBV_ILN_2360 GBV_ILN_2943 GBV_ILN_2946 GBV_ILN_2949 GBV_ILN_2951 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4346 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 117 2020 25 14421-14432 12 2013 01 DE-16-250 3748099940 00 --%%-- --%%-- --%%-- --%%-- l01 09-09-20 2013 01 DE-16-250 00 s hd2020 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_15 2013 01 DE-16-250 03 s s_12 2013 01 DE-16-250 04 p (DE-627)1440454388 Jauch, Anna 2013 01 DE-16-250 04 k (DE-627)1416741429 Institut für Humangenetik 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_11 |
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10.1073/pnas.1921139117 doi (DE-627)172919933X (DE-599)KXP172919933X (OCoLC)1341359175 DE-627 ger DE-627 rda eng Sommermann, Thomas 1982- verfasserin (DE-588)1023312697 (DE-627)718353781 (DE-576)366626019 aut Functional interplay of Epstein-Barr virus oncoproteins in a mouse model of B cell Thomas Sommermann, Tomoharu Yasuda, Jonathan Ronen, Tristan Wirtz, Timm Weber, Ulrike Sack, Rebecca Caeser, Jingwei Zhang, Xun Li, Van Trung Chu, Anna Jauch, Kristian Unger, Daniel J. Hodson, Altuna Akalin, and Klaus Rajewsky June 10, 2020 12 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Gesehen am 09.09.2020 Epstein-Barr virus (EBV) is a B cell transforming virus that causes B cell malignancies under conditions of immune suppression. EBV orchestrates B cell transformation through its latent membrane proteins (LMPs) and Epstein-Barr nuclear antigens (EBNAs). We here identify secondary mutations in mouse B cell lymphomas induced by LMP1, to predict and identify key functions of other EBV genes during transformation. We find aberrant activation of early B cell factor 1 (EBF1) to promote transformation of LMP1-expressing B cells by inhibiting their differentiation to plasma cells. EBV EBNA3A phenocopies EBF1 activities in LMP1-expressing B cells, promoting transformation while inhibiting differentiation. In cells expressing LMP1 together with LMP2A, EBNA3A only promotes lymphomagenesis when the EBNA2 target Myc is also overexpressed. Collectively, our data support a model where proproliferative activities of LMP1, LMP2A, and EBNA2 in combination with EBNA3A-mediated inhibition of terminal plasma cell differentiation critically control EBV-mediated B cell lymphomagenesis. B cell lymphomagenesis c-rel ebna ebv Epstein-Barr virus expression genome-wide in-vivo lmp1 lymphoma lymphoproliferative disorders nf-kappa-b nuclear antigen-1 plasma cell differentiation tumor-suppressor Yasuda, Tomoharu verfasserin aut Ronen, Jonathan verfasserin aut Wirtz, Tristan verfasserin aut Weber, Timm verfasserin aut Sack, Ulrike verfasserin aut Caeser, Rebecca verfasserin aut Zhang, Jingwei verfasserin aut Li, Xun verfasserin aut Chu, Van Trung verfasserin aut Jauch, Anna verfasserin (DE-588)1025525140 (DE-627)722525362 (DE-576)168357496 aut Unger, Kristian verfasserin aut Hodson, Daniel J. verfasserin aut Akalin, Altuna verfasserin aut Rajewsky, Klaus verfasserin aut Enthalten in National Academy of Sciences (Washington, DC) Proceedings of the National Academy of Sciences of the United States of America Washington, DC : National Acad. of Sciences, 1915 117(2020), 25, Seite 14421-14432 Online-Ressource (DE-627)254235379 (DE-600)1461794-8 (DE-576)073260509 1091-6490 nnns volume:117 year:2020 number:25 pages:14421-14432 extent:12 https://doi.org/10.1073/pnas.1921139117 Verlag Resolving-System lizenzpflichtig Volltext GBV_USEFLAG_U GBV_ILN_2013 ISIL_DE-16-250 SYSFLAG_1 GBV_KXP GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_211 GBV_ILN_213 GBV_ILN_230 GBV_ILN_252 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_374 GBV_ILN_381 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 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_2026 GBV_ILN_2027 GBV_ILN_2044 GBV_ILN_2050 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2088 GBV_ILN_2107 GBV_ILN_2110 GBV_ILN_2190 GBV_ILN_2360 GBV_ILN_2943 GBV_ILN_2946 GBV_ILN_2949 GBV_ILN_2951 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4346 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 117 2020 25 14421-14432 12 2013 01 DE-16-250 3748099940 00 --%%-- --%%-- --%%-- --%%-- l01 09-09-20 2013 01 DE-16-250 00 s hd2020 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_15 2013 01 DE-16-250 03 s s_12 2013 01 DE-16-250 04 p (DE-627)1440454388 Jauch, Anna 2013 01 DE-16-250 04 k (DE-627)1416741429 Institut für Humangenetik 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_11 |
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Hodson, Altuna Akalin, and Klaus Rajewsky</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">June 10, 2020</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">12</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">Gesehen am 09.09.2020</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Epstein-Barr virus (EBV) is a B cell transforming virus that causes B cell malignancies under conditions of immune suppression. 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Sommermann, Thomas 1982- misc B cell lymphomagenesis misc c-rel misc ebna misc ebv misc Epstein-Barr virus misc expression misc genome-wide misc in-vivo misc lmp1 misc lymphoma misc lymphoproliferative disorders misc nf-kappa-b misc nuclear antigen-1 misc plasma cell differentiation misc tumor-suppressor 2013 hd2020 2013 wissenschaftlicher Artikel (Zeitschrift) 2013 per_15 2013 s_12 2013 Jauch, Anna 2013 Institut für Humangenetik 2013 Verfasser 2013 pos_11 Functional interplay of Epstein-Barr virus oncoproteins in a mouse model of B cell |
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2013 01 DE-16-250 00 s hd2020 2013 01 DE-16-250 01 s (DE-627)1410508463 wissenschaftlicher Artikel (Zeitschrift) 2013 01 DE-16-250 02 s per_15 2013 01 DE-16-250 03 s s_12 2013 01 DE-16-250 04 p (DE-627)1440454388 Jauch, Anna 2013 01 DE-16-250 04 k (DE-627)1416741429 Institut für Humangenetik 2013 01 DE-16-250 04 s (DE-627)1410501914 Verfasser 2013 01 DE-16-250 04 s pos_11 Functional interplay of Epstein-Barr virus oncoproteins in a mouse model of B cell Thomas Sommermann, Tomoharu Yasuda, Jonathan Ronen, Tristan Wirtz, Timm Weber, Ulrike Sack, Rebecca Caeser, Jingwei Zhang, Xun Li, Van Trung Chu, Anna Jauch, Kristian Unger, Daniel J. Hodson, Altuna Akalin, and Klaus Rajewsky B cell lymphomagenesis c-rel ebna ebv Epstein-Barr virus expression genome-wide in-vivo lmp1 lymphoma lymphoproliferative disorders nf-kappa-b nuclear antigen-1 plasma cell differentiation tumor-suppressor |
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Functional interplay of Epstein-Barr virus oncoproteins in a mouse model of B cell Thomas Sommermann, Tomoharu Yasuda, Jonathan Ronen, Tristan Wirtz, Timm Weber, Ulrike Sack, Rebecca Caeser, Jingwei Zhang, Xun Li, Van Trung Chu, Anna Jauch, Kristian Unger, Daniel J. Hodson, Altuna Akalin, and Klaus Rajewsky |
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Sommermann, Thomas Yasuda, Tomoharu Ronen, Jonathan Wirtz, Tristan Weber, Timm Sack, Ulrike Caeser, Rebecca Zhang, Jingwei Li, Xun Chu, Van Trung Jauch, Anna Unger, Kristian Hodson, Daniel J. Akalin, Altuna Rajewsky, Klaus |
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functional interplay of epstein-barr virus oncoproteins in a mouse model of b cell |
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Functional interplay of Epstein-Barr virus oncoproteins in a mouse model of B cell |
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Epstein-Barr virus (EBV) is a B cell transforming virus that causes B cell malignancies under conditions of immune suppression. EBV orchestrates B cell transformation through its latent membrane proteins (LMPs) and Epstein-Barr nuclear antigens (EBNAs). We here identify secondary mutations in mouse B cell lymphomas induced by LMP1, to predict and identify key functions of other EBV genes during transformation. We find aberrant activation of early B cell factor 1 (EBF1) to promote transformation of LMP1-expressing B cells by inhibiting their differentiation to plasma cells. EBV EBNA3A phenocopies EBF1 activities in LMP1-expressing B cells, promoting transformation while inhibiting differentiation. In cells expressing LMP1 together with LMP2A, EBNA3A only promotes lymphomagenesis when the EBNA2 target Myc is also overexpressed. Collectively, our data support a model where proproliferative activities of LMP1, LMP2A, and EBNA2 in combination with EBNA3A-mediated inhibition of terminal plasma cell differentiation critically control EBV-mediated B cell lymphomagenesis. Gesehen am 09.09.2020 |
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Epstein-Barr virus (EBV) is a B cell transforming virus that causes B cell malignancies under conditions of immune suppression. EBV orchestrates B cell transformation through its latent membrane proteins (LMPs) and Epstein-Barr nuclear antigens (EBNAs). We here identify secondary mutations in mouse B cell lymphomas induced by LMP1, to predict and identify key functions of other EBV genes during transformation. We find aberrant activation of early B cell factor 1 (EBF1) to promote transformation of LMP1-expressing B cells by inhibiting their differentiation to plasma cells. EBV EBNA3A phenocopies EBF1 activities in LMP1-expressing B cells, promoting transformation while inhibiting differentiation. In cells expressing LMP1 together with LMP2A, EBNA3A only promotes lymphomagenesis when the EBNA2 target Myc is also overexpressed. Collectively, our data support a model where proproliferative activities of LMP1, LMP2A, and EBNA2 in combination with EBNA3A-mediated inhibition of terminal plasma cell differentiation critically control EBV-mediated B cell lymphomagenesis. Gesehen am 09.09.2020 |
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Epstein-Barr virus (EBV) is a B cell transforming virus that causes B cell malignancies under conditions of immune suppression. EBV orchestrates B cell transformation through its latent membrane proteins (LMPs) and Epstein-Barr nuclear antigens (EBNAs). We here identify secondary mutations in mouse B cell lymphomas induced by LMP1, to predict and identify key functions of other EBV genes during transformation. We find aberrant activation of early B cell factor 1 (EBF1) to promote transformation of LMP1-expressing B cells by inhibiting their differentiation to plasma cells. EBV EBNA3A phenocopies EBF1 activities in LMP1-expressing B cells, promoting transformation while inhibiting differentiation. In cells expressing LMP1 together with LMP2A, EBNA3A only promotes lymphomagenesis when the EBNA2 target Myc is also overexpressed. Collectively, our data support a model where proproliferative activities of LMP1, LMP2A, and EBNA2 in combination with EBNA3A-mediated inhibition of terminal plasma cell differentiation critically control EBV-mediated B cell lymphomagenesis. Gesehen am 09.09.2020 |
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