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Pim kinases are upregulated during Epstein-Barr virus infection and enhance EBNA2 activity.

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.
AuthorsEeva-Marja Rainio, Helena Ahlfors, Kara L Carter, Marja Ruuska, Sampsa Matikainen, Elliott Kieff, Päivi J Koskinen
JournalVirology (Virology) Vol. 333 Issue 2 Pg. 201-6 (Mar 15 2005) ISSN: 0042-6822 [Print] United States
PMID15721354 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)
Chemical References
  • EBNA-2 protein, Human herpesvirus 4
  • Epstein-Barr Virus Nuclear Antigens
  • Nuclear Proteins
  • PIM2 protein, human
  • Proto-Oncogene Proteins
  • Viral Proteins
  • DNA
  • PIM1 protein, human
  • Protein Serine-Threonine Kinases
  • Proto-Oncogene Proteins c-pim-1
  • Endonucleases
  • SND1 protein, human
Topics
  • B-Lymphocytes (enzymology, virology)
  • Base Sequence
  • Cell Line
  • DNA (genetics)
  • Endonucleases
  • Epstein-Barr Virus Infections (enzymology, etiology, genetics, virology)
  • Epstein-Barr Virus Nuclear Antigens (metabolism)
  • Herpesvirus 4, Human (genetics, metabolism, pathogenicity)
  • Humans
  • Nuclear Proteins (metabolism)
  • Phosphorylation
  • Protein Serine-Threonine Kinases (genetics)
  • Proto-Oncogene Proteins (genetics)
  • Proto-Oncogene Proteins c-pim-1
  • Transcriptional Activation
  • Up-Regulation
  • Viral Proteins

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