{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T12:05:09Z","timestamp":1791115509304,"version":"4.1.0"},"reference-count":65,"publisher":"American Society for Microbiology","issue":"1","license":[{"start":{"date-parts":[[2002,1,1]],"date-time":"2002-01-01T00:00:00Z","timestamp":1009843200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[2002,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>The Epstein-Barr virus (EBV) nuclear antigen 3C (EBNA-3C) regulates virus and cell genes and is essential for EBV-mediated transformation of primary B lymphocytes. EBNA-3C associates with the cellular DNA sequence-specific transcription factors RBP-J\u03ba and PU.1 and coactivates the EBV LMP1 promoter with EBNA-2 in BL2 and Raji cells under conditions of restrictive growth. We now find that EBNA-3C is similar to EBNA-LP in coactivating the LMP1 promoter with EBNA-2 in non-EBV-infected Burkitt lymphoma cells under conditions of maximal cell growth, whereas the EBV Cp promoter is repressed under the same conditions. EBNA-3A and EBNA-3B coactivation are at most 40% that of EBNA-3C. The RBP-J\u03ba binding sites of EBNA-2 and the LMP1 promoter are not required for EBNA-3C coactivation, whereas the PU.1 site in the LMP1 promoter is required for EBNA-2-mediated activation and EBNA-3C coactivation. EBNA-3C amino acids (aa) 365 to 545, including most of the previously identified repression domain (M. Bain, R. J. Watson, P. J. Farrell, and M. J. Allday, J. Virol. 70:2481\u20132489, 1996), are necessary and sufficient for coactivation with wild-type EBNA-2. EBNA-3C can also coactivate with the EBNA-2 acidic activating domain; this activation does not require aa 343 to 545. These data indicate that there are at least two mechanisms by which EBNA-3C coactivates the LMP1 promoter with EBNA-2. Of the proteins that interact with EBNA-3C in a yeast two-hybrid screen, only the ubiquitin-like proteins SUMO-1 and SUMO-3\/hSMT3B map to aa 365 to 545, implicating these molecules in EBNA-3C coactivation. In addition, SUMO-1 associates at a high level with EBNA-3C in lymphoblasts. Promoter coactivation by EBNA-3C is likely to be important in ensuring adequate levels of LMP1, while inhibition of the EBNA-Cp promoter under the same conditions prevents uncontrolled up-regulation of EBNA expression from a positive-feedback loop.<\/jats:p>","DOI":"10.1128\/jvi.76.1.232-242.2002","type":"journal-article","created":{"date-parts":[[2002,7,27]],"date-time":"2002-07-27T09:55:53Z","timestamp":1027763753000},"page":"232-242","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":85,"title":["Epstein-Barr Virus Nuclear Antigen 3C Putative Repression Domain Mediates Coactivation of the LMP1 Promoter with EBNA-2"],"prefix":"10.1128","volume":"76","author":[{"given":"Jeffrey","family":"Lin","sequence":"first","affiliation":[{"name":"Virology Program and Departments of Medicine and Microbiology and Molecular Genetics, Channing Laboratory, Brigham and Women\u2019s Hospital and Harvard Medical School, Boston, Massachusetts 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eric","family":"Johannsen","sequence":"additional","affiliation":[{"name":"Virology Program and Departments of Medicine and Microbiology and Molecular Genetics, Channing Laboratory, Brigham and Women\u2019s Hospital and Harvard Medical School, Boston, Massachusetts 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Erle","family":"Robertson","sequence":"additional","affiliation":[{"name":"Virology Program and Departments of Medicine and Microbiology and Molecular Genetics, Channing Laboratory, Brigham and Women\u2019s Hospital and Harvard Medical School, Boston, Massachusetts 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elliott","family":"Kieff","sequence":"additional","affiliation":[{"name":"Virology Program and Departments of Medicine and Microbiology and Molecular Genetics, Channing Laboratory, Brigham and Women\u2019s Hospital and Harvard Medical School, Boston, Massachusetts 02115"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1099\/0022-1317-74-3-361"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1128\/jvi.68.6.3491-3498.1994"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1128\/jvi.70.4.2481-2489.1996"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1128\/jvi.65.11.5880-5885.1991"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.20.15.5722-5735.2000"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1101\/gad.10.15.1858"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1097-2765(00)80133-1"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1128\/mcb.14.5.3310-3319.1994"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1006\/viro.1993.1347"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1006\/abio.1993.1170"},{"key":"e_1_3_2_12_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.74.17.8166-8175.2000"},{"key":"e_1_3_2_13_2","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/18.22.6462"},{"key":"e_1_3_2_14_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.91.16.7568"},{"key":"e_1_3_2_15_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.27.19136"},{"key":"e_1_3_2_16_2","doi-asserted-by":"publisher","DOI":"10.1128\/jvi.63.6.2469-2475.1989"},{"key":"e_1_3_2_17_2","doi-asserted-by":"publisher","DOI":"10.1128\/jvi.71.9.6611-6618.1997"},{"key":"e_1_3_2_18_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.75.5.2482-2487.2001"},{"key":"e_1_3_2_19_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.8016657"},{"key":"e_1_3_2_20_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.7725102"},{"key":"e_1_3_2_21_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.1.23"},{"key":"e_1_3_2_22_2","doi-asserted-by":"publisher","DOI":"10.1128\/jvi.69.1.253-262.1995"},{"key":"e_1_3_2_23_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.73.5.4481-4484.1999"},{"key":"e_1_3_2_24_2","doi-asserted-by":"publisher","DOI":"10.1101\/gad.12.15.2269"},{"key":"e_1_3_2_25_2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1203365"},{"key":"e_1_3_2_26_2","first-page":"2511","year":"2001","unstructured":"Kieff, E., and A. 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