Abstract
A conditional mutant of Epstein-Barr virus nuclear antigen 2 (EBNA2) regulated by estrogen was employed to study the effect of EBNA2 on the cellular phenotype. Activation of EBNA2 in lymphoblastoid cell lines (LCLs) and in B cell lymphoma lines resulted in down-regulation of cell surface IgM and Ig-mu steady-state RNA expression. In LCLs, activation of EBNA2 is required for maintaining proliferation, whereas in Burkitt's lymphoma (BL) cell lines with t(8;14) translocations, activation of EBNA2 induces growth arrest. In these cells, Northern and nuclear run-on analyses revealed rapid simultaneous repression of Ig-mu and c-myc transcription as early as 30 min after activation of EBNA2. Since c-myc expression is under the control of the Ig heavy chain locus in BL cell lines with a t(8;14) translocation, we propose that Ig-mu and c-myc are down-regulated by EBNA2 through a common mechanism.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Antigens, Viral / metabolism*
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Blotting, Northern
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Burkitt Lymphoma / genetics
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Cell Division
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Cell Nucleus / metabolism
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Chromosomes, Human, Pair 14
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Chromosomes, Human, Pair 8
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DNA-Binding Proteins / metabolism*
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Epstein-Barr Virus Nuclear Antigens
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Gene Expression Regulation, Neoplastic*
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Genes, myc*
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Humans
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Immunoglobulin M / biosynthesis
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Immunoglobulin mu-Chains / biosynthesis
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Kinetics
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Proto-Oncogene Proteins c-myc / biosynthesis
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Receptors, Antigen, B-Cell / biosynthesis
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Recombinant Fusion Proteins / metabolism
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Repressor Proteins / metabolism*
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Time Factors
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Transcription, Genetic
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Transfection
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Translocation, Genetic
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Tumor Cells, Cultured
Substances
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Antigens, Viral
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DNA-Binding Proteins
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Epstein-Barr Virus Nuclear Antigens
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Immunoglobulin M
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Immunoglobulin mu-Chains
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Proto-Oncogene Proteins c-myc
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Receptors, Antigen, B-Cell
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Recombinant Fusion Proteins
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Repressor Proteins