Artículos de revistas
Activation of the lytic program of the Epstein–Barr virus in Burkitt's lymphoma cells leads to a two steps downregulation of expression of the proapoptotic protein BimEL, one of which is EBV-late-gene expression dependent
Fecha
2009-02-28Registro en:
0042-6822
10.1016/j.virol.2009.02.009
Autor
Oussaief, Lassad
Hippocrate, Aurélie
Clybouw, Cyril
Rampanou, Aurore
Ramírez Mayorga, Vanessa
Claude, Desgranges
Vasquez, Aime
Khelifa, Ridha
Joab, Irène
Institución
Resumen
The Epstein–Barr virus (EBV) generally latently infects its target cells with expression of genes conferring resistance to apoptosis. However, the modulation of apoptotic signals during lytic cycle remains poorly understood. We show here that resulting from viral reactivation in the EBV-positive Mutu-I and Akata Burkitt's lymphoma cell lines, a two steps proteasome-dependent downregulation of expression of the proapoptotic protein BimEL occurs. The first drop might be EBV-independent, is ERK 1/2 dependent, and BimEL is phosphorylated on Ser69. A second dramatic drop of the BimEL level observed during the lytic cycle is dependent of EBV-late-gene expression, ERK 1/2 independent, and no further phosphorylation of BimEL on Ser69 occurred. These results demonstrate for the first time, that the lytic cycle contributes to downregulation of BimEL and then could add to protection against apoptosis.