Abstract
Latent Epstein-Barr virus (EBV) infection is strongly associated with B-cell proliferative diseases such as Burkitt's lymphoma. Here we show that the oncogenic serine/threonine kinases Pim-1 and Pim-2 enhance the activity of the viral transcriptional activator EBNA2. During EBV infection of primary B-lymphocytes, the mRNA expression levels of pim genes, especially of pim-2, are upregulated and remain elevated in latently infected B-cell lines. Thus, EBV-induced upregulation of Pim kinases and Pim-stimulated EBNA2 transcriptional activity may contribute to the ability of EBV to immortalize B-cells and predispose them to malignant growth.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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B-Lymphocytes / enzymology
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B-Lymphocytes / virology
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Base Sequence
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Cell Line
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DNA / genetics
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Endonucleases
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Epstein-Barr Virus Infections / enzymology*
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Epstein-Barr Virus Infections / etiology
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Epstein-Barr Virus Infections / genetics*
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Epstein-Barr Virus Infections / virology
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Epstein-Barr Virus Nuclear Antigens / metabolism*
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Herpesvirus 4, Human / genetics
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Herpesvirus 4, Human / metabolism
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Herpesvirus 4, Human / pathogenicity
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Humans
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Nuclear Proteins / metabolism
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Phosphorylation
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Protein Serine-Threonine Kinases / genetics*
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Proto-Oncogene Proteins / genetics*
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Proto-Oncogene Proteins c-pim-1
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Transcriptional Activation
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Up-Regulation
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Viral Proteins
Substances
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EBNA-2 protein, Human herpesvirus 4
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Epstein-Barr Virus Nuclear Antigens
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Nuclear Proteins
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PIM2 protein, human
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Proto-Oncogene Proteins
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Viral Proteins
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DNA
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PIM1 protein, human
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Protein Serine-Threonine Kinases
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Proto-Oncogene Proteins c-pim-1
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Endonucleases
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SND1 protein, human