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Pim kinases are upregulated during Epstein-Barr virus infection and enhance EBNA2 activity
Tekijät: Rainio EM, Ahlfors H, Carter KL, Ruuska M, Matikainen S, Kieff E, Koskinen PJ
Kustantaja: ACADEMIC PRESS INC ELSEVIER SCIENCE
Julkaisuvuosi: 2005
Journal: Virology
Tietokannassa oleva lehden nimi: VIROLOGY
Lehden akronyymi: VIROLOGY
Vuosikerta: 333
Numero: 2
Aloitussivu: 201
Lopetussivu: 206
Sivujen määrä: 6
ISSN: 0042-6822
DOI: https://doi.org/10.1016/j.virol.2005.01.001
Tiivistelmä
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 pint 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. (C) 2005 Elsevier Inc. All rights reserved.
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 pint 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. (C) 2005 Elsevier Inc. All rights reserved.
Ladattava julkaisu This is an electronic reprint of the original article. |  |
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