Pim kinases are upregulated during Epstein-Barr virus infection and enhance EBNA2 activity
- Turku Centre for Biotechnology, University of Turku/Abo Akademi University, Tykistoekatu 6B, 20520 Turku (Finland)
- Department of Medicine and Microbiology, Harvard Medical School, Boston, MA 02115 (United States)
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.
- OSTI ID:
- 20637213
- Journal Information:
- Virology, Vol. 333, Issue 2; Other Information: DOI: 10.1016/j.virol.2005.01.001; PII: S0042-6822(05)00006-1; Copyright (c) 2005 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0042-6822
- Country of Publication:
- United States
- Language:
- English
Similar Records
KSHV encoded LANA upregulates Pim-1 and is a substrate for its kinase activity
Interleukin-21 regulates expression of key Epstein-Barr virus oncoproteins, EBNA2 and LMP1, in infected human B cells
Interaction of Epstein-Barr virus (EBV) with human B-lymphocytes
Journal Article
·
Thu Jul 20 00:00:00 EDT 2006
· Virology
·
OSTI ID:20637213
+3 more
Interleukin-21 regulates expression of key Epstein-Barr virus oncoproteins, EBNA2 and LMP1, in infected human B cells
Journal Article
·
Fri Apr 25 00:00:00 EDT 2008
· Virology
·
OSTI ID:20637213
Interaction of Epstein-Barr virus (EBV) with human B-lymphocytes
Journal Article
·
Fri May 21 00:00:00 EDT 2010
· Biochemical and Biophysical Research Communications
·
OSTI ID:20637213