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EBV infection of human B lymphocytes leads to down-regulation of Bim expression: relationship to resistance to apoptosis.

Authors
  • Clybouw, Cyril1
  • McHichi, Bouchra
  • Mouhamad, Shahul
  • Auffredou, Marie Thérèse
  • Bourgeade, Marie Françoise
  • Sharma, Surendra
  • Leca, Gerald
  • Vazquez, Aimé
  • 1 Institut National de la Santé et de la Recherche Médicale, Unité 542, Université Paris-Sud, Hôpital Paul Brousse, Villejuif, France. , (France)
Type
Published Article
Journal
Journal of immunology (Baltimore, Md. : 1950)
Publication Date
Sep 01, 2005
Volume
175
Issue
5
Pages
2968–2973
Identifiers
PMID: 16116183
Source
Medline
License
Unknown

Abstract

EBV infects a large proportion of the human population worldwide and is one of the major viruses with human B lymphocyte tropism. It can immortalize human B lymphocytes and controls their resistance to apoptosis. EBV infection is associated with several lymphomas, including Burkitt's lymphoma. In this report we show that EBV infection leads to the post-transcriptional down-regulation of expression of the proapoptotic protein Bim. This process involves the phosphorylation of BimEL by the constitutive EBV-activated kinase ERK1/2, followed by its degradation through the proteasome pathway. We also show that ectopic expression of BimEL in EBV-positive Burkitt's lymphoma cells can enhance the sensitivity of these cells to serum deprivation-dependent apoptosis. Thus, EBV-mediated resistance to growth factor deprivation in human B lymphocytes is dependent on BimEL expression. Our data suggest that this regulatory pathway is an important contributor to the oncogenic potential of EBV.

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