scholarly journals Eradication of Latent Epstein‐Barr Virus by Hydroxyurea Alters the Growth‐Transformed Cell Phenotype

1998 ◽  
Vol 177 (5) ◽  
pp. 1194-1201 ◽  
Author(s):  
James Chodosh ◽  
Virgil P. Holder ◽  
Yan‐jun Gan ◽  
Asim Belgaumi ◽  
Jeffery Sample ◽  
...  
Keyword(s):  
Epstein Barr Virus ◽  
Cell Phenotype ◽  
Transformed Cell ◽  
Barr Virus ◽  
Epstein Barr

scholarly journals TRAF1 Is a Critical Regulator of JNK Signaling by the TRAF-Binding Domain of the Epstein-Barr Virus-Encoded Latent Infection Membrane Protein 1 but Not CD40

2003 ◽  
Vol 77 (2) ◽  
pp. 1316-1328 ◽  
Author(s):  
Aristides G. Eliopoulos ◽  
Elyse R. Waites ◽  
Sarah M. S. Blake ◽  
Clare Davies ◽  
Paul Murray ◽  
...  
Keyword(s):  
Membrane Protein ◽  
Epstein Barr Virus ◽  
Latent Infection ◽  
Binding Domain ◽  
Cell Phenotype ◽  
Tnf Receptor ◽  
Jnk Signaling ◽  
Barr Virus ◽  
Epstein Barr ◽  
Jnk Activation

ABSTRACT The oncogenic Epstein-Barr virus (EBV)-encoded latent infection membrane protein 1 (LMP1) mimics a constitutive active tumor necrosis factor (TNF) family receptor in its ability to recruit TNF receptor-associated factors (TRAFs) and TNF receptor-associated death domain protein (TRADD) in a ligand-independent manner. As a result, LMP1 constitutively engages signaling pathways, such as the JNK and p38 mitogen-activated protein kinases (MAPK), the transcription factor NF-κB, and the JAK/STAT cascade, and these activities may explain many of its pleiotropic effects on cell phenotype, growth, and transformation. In this study we demonstrate the ability of the TRAF-binding domain of LMP1 to signal on the JNK/AP-1 axis in a cell type- dependent manner that critically involves TRAF1 and TRAF2. Thus, expression of this LMP1 domain in TRAF1-positive lymphoma cells promotes significant JNK activation, which is blocked by dominant-negative TRAF2 but not TRAF5. However, TRAF1 is absent in many established epithelial cell lines and primary nasopharyngeal carcinoma (NPC) biopsy specimens. In these cells, JNK activation by the TRAF-binding domain of LMP1 depends on the reconstitution of TRAF1 expression. The critical role of TRAF1 in the regulation of TRAF2-dependent JNK signaling is particular to the TRAF-binding domain of LMP1, since a homologous region in the cytoplasmic tail of CD40 or the TRADD-interacting domain of LMP1 signal on the JNK axis independently of TRAF1 status. These data further dissect the signaling components used by LMP1 and identify a novel role for TRAF1 as a modulator of oncogenic signals.

Epstein-Barr virus status and tumour cell phenotype in sporadic Burkitt's lymphoma

1986 ◽  
Vol 37 (3) ◽  
pp. 367-373 ◽  
Author(s):  
M. Rowe ◽  
C. M. Rooney ◽  
C. F. Edwards ◽  
G. M. Lenoir ◽  
A. B. Rickinson
Keyword(s):  
Tumour Cell ◽  
Epstein Barr Virus ◽  
Burkitt’S Lymphoma ◽  
Burkitt's Lymphoma ◽  
Cell Phenotype ◽  
Barr Virus ◽  
Epstein Barr

scholarly journals Epstein-Barr Virus LMP2A Reduces Hyperactivation Induced by LMP1 to Restore Normal B Cell Phenotype in Transgenic Mice

2012 ◽  
Vol 8 (4) ◽  
pp. e1002662 ◽  
Author(s):  
Alexandra C. Vrazo ◽  
Maria Chauchard ◽  
Nancy Raab-Traub ◽  
Richard Longnecker
Keyword(s):  
Transgenic Mice ◽  
B Cell ◽  
Epstein Barr Virus ◽  
Cell Phenotype ◽  
Barr Virus ◽  
Epstein Barr
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