{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T16:48:23Z","timestamp":1790873303013,"version":"4.1.0"},"reference-count":48,"publisher":"American Society for Microbiology","issue":"23","license":[{"start":{"date-parts":[[2010,12,1]],"date-time":"2010-12-01T00:00:00Z","timestamp":1291161600000},"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":[[2010,12]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            The Epstein-Barr virus (EBV) lytic activator genes\n            <jats:italic>bzlf1<\/jats:italic>\n            and\n            <jats:italic>brlf1<\/jats:italic>\n            are conventionally referred to as immediate-early (IE) genes. However, previous studies showed that the earliest expression of these genes was blocked by cycloheximide when the EBV lytic cycle was induced by histone deacetylase (HDAC) inhibitors and protein kinase C agonists. Anti-IgG activates a complex signal transduction pathway that leads to EBV lytic activation in the Akata cell line. Here we demonstrate that in Akata cells, where lytic cycle activation occurs very rapidly after anti-IgG treatment,\n            <jats:italic>de novo<\/jats:italic>\n            protein synthesis is also required for induction of\n            <jats:italic>bzlf1<\/jats:italic>\n            and\n            <jats:italic>brlf1<\/jats:italic>\n            expression. New protein synthesis is required up to 1.25 h after application of anti-IgG;\n            <jats:italic>bzlf1<\/jats:italic>\n            and\n            <jats:italic>brlf1<\/jats:italic>\n            mRNAs can be detected 1.5 h after anti-IgG. Five cellular IE genes were shown to be expressed by 1 h after addition of anti-IgG, and their expression preceded that of\n            <jats:italic>bzlf1<\/jats:italic>\n            and\n            <jats:italic>brlf1<\/jats:italic>\n            . These include early growth response genes (\n            <jats:italic>egr1<\/jats:italic>\n            ,\n            <jats:italic>egr2<\/jats:italic>\n            , and\n            <jats:italic>egr3<\/jats:italic>\n            ) and nuclear orphan receptors (\n            <jats:italic>nr4a1<\/jats:italic>\n            and\n            <jats:italic>nr4a3<\/jats:italic>\n            ). These genes were activated by anti-IgG treatment of Akata cells with and without the EBV genome; therefore, their expression was not dependent on expression of any EBV gene product. EGR1, EGR2, and EGR3 proteins were kinetically upstream of ZEBRA and Rta proteins. Expression of EGR1, ZEBRA, and Rta proteins were inhibited by bisindolylmaleimide X, a selective inhibitor of PKC. The findings suggest a revised model in which the signal transduction cascade activated by cross-linking of the B cell receptor induces expression of cellular IE genes, such as early growth response and nuclear orphan receptor genes, whose products, in turn, regulate\n            <jats:italic>bzlf1<\/jats:italic>\n            and\n            <jats:italic>brlf1<\/jats:italic>\n            expression.\n          <\/jats:p>","DOI":"10.1128\/jvi.01415-10","type":"journal-article","created":{"date-parts":[[2010,9,23]],"date-time":"2010-09-23T04:30:04Z","timestamp":1285216204000},"page":"12405-12418","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":24,"title":["Cellular Immediate-Early Gene Expression Occurs Kinetically Upstream of Epstein-Barr Virus\n            <i>bzlf1<\/i>\n            and\n            <i>brlf1<\/i>\n            following Cross-Linking of the B Cell Antigen Receptor in the Akata Burkitt Lymphoma Cell Line"],"prefix":"10.1128","volume":"84","author":[{"given":"Jianjiang","family":"Ye","sequence":"first","affiliation":[{"name":"Departments of Molecular Biophysics and Biochemistry"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lyndle","family":"Gradoville","sequence":"additional","affiliation":[{"name":"Pediatrics"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"George","family":"Miller","sequence":"additional","affiliation":[{"name":"Departments of Molecular Biophysics and Biochemistry"},{"name":"Pediatrics"},{"name":"Epidemiology and Public Health, Yale University School of Medicine, New Haven, Connecticut 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