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dc.contributor.authorSairenji, Takeshi
dc.contributor.authorSpiro, Robert Christopher
dc.contributor.authorHumphreys, Robert E.
dc.date2022-08-11T08:08:47.000
dc.date.accessioned2022-08-23T16:08:39Z
dc.date.available2022-08-23T16:08:39Z
dc.date.issued1984-10-01
dc.date.submitted2008-12-09
dc.identifier.citation<p>Hematol Oncol. 1984 Oct-Dec;2(4):381-9.</p>
dc.identifier.issn0278-0232 (Print)
dc.identifier.doi10.1002/hon.2900020408
dc.identifier.pmid6098544
dc.identifier.urihttp://hdl.handle.net/20.500.14038/32499
dc.description.abstractThe aim of this study was to test whether EBV induction by TPA or n-butyrate was related directly to hyperexpression of Ii, an electrophoretically invariant, 35 000 dalton, HLA-DR antigen-associated glycoprotein which is abundantly detected in EBV freshly transformed cells and is enhanced by EBV superinfection of lymphoblastoid cell lines. P3HR-1 lymphoblasts were treated with n-butyrate or TPA in variable doses and durations. The augmented expression of Ii, EBV antigens (EA and VCA), DNA synthesis, and cell growth and viability were monitored. n-Butyrate induced hyperexpression of Ii at 2 days with a maximal effective dose of 4 mM, induced EBV antigens (EA and VCA) in 36 per cent of the cells at 2 days, inhibited DNA synthesis and cell growth, and was not cytolytic at 48 h when Ii induction was maximal. TPA did not induce hyperexpression of Ii, induced EBV antigens (EA) in 30 per cent of the cells at 4 days, did not inhibit DNA synthesis and cell growth, and was not cytolytic in the time course and doses studied. Ii expression, therefore, did not appear to be an obligatory consequence of EBV antigen induction. Ii induction might be related to an effect of EBV inducers on cellular DNA synthesis, or on control of the cell cycle, or directly upon Ii gene regulation.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=6098544&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://doi.org/10.1002/hon.2900020408
dc.subjectAntigens, Neoplasm; Antigens, Viral; Burkitt Lymphoma; Butyrates; Butyric Acid; Butyric Acids; *Capsid Proteins; Cell Line; Electrophoresis, Polyacrylamide Gel; HLA-DR Antigens; Herpesvirus 4, Human; Histocompatibility Antigens Class II; Humans; Leukemia, Hairy Cell; Lymphocytes; Phorbols; Tetradecanoylphorbol Acetate
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleDifferential effect of TPA and n-butyrate on induction of Ii and EBV antigens in the P3HR-1 lymphoblastoid cell line
dc.typeJournal Article
dc.source.journaltitleHematological oncology
dc.source.volume2
dc.source.issue4
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/1067
dc.identifier.contextkey678834
html.description.abstract<p>The aim of this study was to test whether EBV induction by TPA or n-butyrate was related directly to hyperexpression of Ii, an electrophoretically invariant, 35 000 dalton, HLA-DR antigen-associated glycoprotein which is abundantly detected in EBV freshly transformed cells and is enhanced by EBV superinfection of lymphoblastoid cell lines. P3HR-1 lymphoblasts were treated with n-butyrate or TPA in variable doses and durations. The augmented expression of Ii, EBV antigens (EA and VCA), DNA synthesis, and cell growth and viability were monitored. n-Butyrate induced hyperexpression of Ii at 2 days with a maximal effective dose of 4 mM, induced EBV antigens (EA and VCA) in 36 per cent of the cells at 2 days, inhibited DNA synthesis and cell growth, and was not cytolytic at 48 h when Ii induction was maximal. TPA did not induce hyperexpression of Ii, induced EBV antigens (EA) in 30 per cent of the cells at 4 days, did not inhibit DNA synthesis and cell growth, and was not cytolytic in the time course and doses studied. Ii expression, therefore, did not appear to be an obligatory consequence of EBV antigen induction. Ii induction might be related to an effect of EBV inducers on cellular DNA synthesis, or on control of the cell cycle, or directly upon Ii gene regulation.</p>
dc.identifier.submissionpathgsbs_sp/1067
dc.source.pages381-9


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