scholarly journals 5-Azacytidine up regulates the expression of Epstein-Barr virus nuclear antigen 2 (EBNA-2) through EBNA-6 and latent membrane protein in the Burkitt's lymphoma line rael.

1989 ◽  
Vol 63 (7) ◽  
pp. 3135-3141 ◽  
Author(s):  
M G Masucci ◽  
B Contreras-Salazar ◽  
E Ragnar ◽  
K Falk ◽  
J Minarovits ◽  
...  
Keyword(s):  
Membrane Protein ◽  
Epstein Barr Virus ◽  
Burkitt’S Lymphoma ◽  
Latent Membrane Protein ◽  
Burkitt's Lymphoma ◽  
Nuclear Antigen ◽  
Barr Virus ◽  
Lymphoma Line ◽  
Epstein Barr

scholarly journals Epstein-Barr virus in Burkitt’s lymphoma: A role for latent membrane protein 2A

Cell Cycle ◽  
2010 ◽  
Vol 9 (5) ◽  
pp. 901-908 ◽  
Author(s):  
Kathryn T. Bieging ◽  
Michelle Swanson-Mungerson ◽  
Alexandra C. Amick ◽  
Richard Longnecker
Keyword(s):  
Membrane Protein ◽  
Epstein Barr Virus ◽  
Burkitt’S Lymphoma ◽  
Latent Membrane Protein ◽  
Burkitt's Lymphoma ◽  
Latent Membrane Protein 2A ◽  
Barr Virus ◽  
Epstein Barr

scholarly journals Silencing of latent membrane protein 2B reduces susceptibility to activation of lytic Epstein–Barr virus in Burkitt's lymphoma Akata cells

2007 ◽  
Vol 88 (5) ◽  
pp. 1454-1459 ◽  
Author(s):  
Markus P. Rechsteiner ◽  
Christoph Berger ◽  
Matthias Weber ◽  
Jürg A. Sigrist ◽  
David Nadal ◽  
...  
Keyword(s):  
Membrane Protein ◽  
Epstein Barr Virus ◽  
Cell Receptor ◽  
Burkitt’S Lymphoma ◽  
Latent Membrane Protein ◽  
Lytic Replication ◽  
Burkitt's Lymphoma ◽  
Cross Linking ◽  
Barr Virus ◽  
Epstein Barr

Epstein–Barr virus (EBV) latent membrane protein 2A (LMP2A) blocks B-cell receptor (BCR) signalling after BCR cross-linking to inhibit activation of lytic EBV, and ectopically expressed LMP2B negatively regulates LMP2A. Here, it is demonstrated that silencing of LMP2B in EBV-harbouring Burkitt's lymphoma Akata cells results in reduced expression of EBV immediate-early lytic BZLF1 gene mRNA and late lytic gp350/220 protein upon BCR cross-linking. Similarly, reduction of lytic EBV activation was observed in Akata cells overexpressing LMP2A. In contrast, silencing of LMP2A expression resulted in higher lytic EBV mRNA and protein expression in BCR cross-linked Akata cells. These observations indicate a role for LMP2B distinct from that of LMP2A in regulation of lytic EBV activation in the host cell and support the hypothesis that LMP2B exhibits a negative-regulatory effect on the ability of LMP2A to maintain EBV latency by preventing the switch to lytic replication.

Subcellular localization of the latent membrane protein LMP-1 in Epstein-Barr virus infected cells by immunogold EM

1994 ◽  
Vol 52 ◽  
pp. 248-249
Author(s):  
D. N. Misra ◽  
R. M. Agostini ◽  
E. J. Yunis
Keyword(s):  
Membrane Protein ◽  
Subcellular Localization ◽  
Cell Lines ◽  
Epstein Barr Virus ◽  
Hodgkin’S Disease ◽  
Burkitt’S Lymphoma ◽  
Latent Membrane Protein ◽  
Barr Virus ◽  
Infected Cells ◽  
Epstein Barr

Epstein-Barr virus (EBV) infection, prevalent in all human populations, is clinically silent in general, but causes infectious mononucleosis in some adolescents and B-lymphocyte proliferative disorders (LPDs) in immunocompromised individuals (e.g. AIDS infected; allograft recipients). EBV is also etiologically associated with African Burkitt’s lymphoma, nasopharyngeal carcinoma, and Hodgkin’s disease. The virus infects B lymphocytes and transforms them into lymphoblastoid cells which proliferate indefinitely in culture. The latently infected cells express an array of EBV gene products including 6 nuclear antigens (EBNAs), terminal proteins LMP-2A and LMP-2B, latent membrane protein LMP-1, and untranslated RNAs EBER 1 and EBER 2. These components are being extensively studied since they are involved in latency or proliferative transformation; LMP-1 has also shown oncogenic properties. In this work, we have used immunogold electron microscopy for precise subcellular localization of LMP-1 in EBV infected cell lines.Two human cell lines, P3HR-1 (Burkitt’s lymphoma) and CCL-113 (Hodgkin’s disease), obtained from ATCC, were grown in RPMI 1640 containing 20% fetal calf serum, 100 U/ml penicillin and 100 μg/ml streptomycin.

Expression of the Epstein-Barr Virus (EBV) latent membrane protein is tightly regulated, independently of EB nuclear antigen 2 and of EBV integration or copy number

1993 ◽  
Vol 27 (1) ◽  
pp. 55-69 ◽  
Author(s):  
Martine Cordier-Bussat ◽  
Alain Calender ◽  
Michéle Vuillaume ◽  
Georg W. Bornkamm ◽  
Gilbert M. Lenoir
Keyword(s):  
Membrane Protein ◽  
Copy Number ◽  
Epstein Barr Virus ◽  
Latent Membrane Protein ◽  
Nuclear Antigen ◽  
Barr Virus ◽  
Epstein Barr

scholarly journals Expression of bcl-2 in Burkitt's lymphoma cell lines: induction by latent Epstein-Barr virus genes

Blood ◽  
1992 ◽  
Vol 80 (2) ◽  
pp. 459-469 ◽  
Author(s):  
J Finke ◽  
R Fritzen ◽  
P Ternes ◽  
P Trivedi ◽  
KJ Bross ◽  
...  
Keyword(s):  
Cell Lines ◽  
Epstein Barr Virus ◽  
Burkitt’S Lymphoma ◽  
Burkitt's Lymphoma ◽  
Nuclear Antigen ◽  
Full Spectrum ◽  
Group Iii ◽  
Barr Virus ◽  
Group I ◽  
Epstein Barr

The bcl-2 oncogene blocks programmed cell death (apoptosis). Epstein- Barr virus (EBV) can immortalize B lymphocytes into continuously growing lymphoblastoid cell lines (LCL) by the coordinate expression of at least 9 latent genes (EBV nuclear antigen [EBNA] 1–6, latent membrane protein [LMP], and terminal proteins [TP] 1 and 2). We analyzed transcription and expression of bcl-2 and latent EBV genes in Burkitt's lymphoma (BL) cell lines with a germinal center phenotype (group I) as well as activated BL cell lines (group III) and LCLs. We found high expression of bcl-2 as well as the full spectrum of latent EBV genes in LCLs and activated group III BL cell lines. Group I BL cells expressed little or no bcl-2, EBNA-2, and LMP. Superinfection with nondefective EBV or an EBNA-2-defective virus as well as transfection with EBNA-2- or LMP-carrying vectors into the EBV-negative cell lines RAMOS, DG75, U698, or BJAB induced upregulation of bcl-2 expression. The strongest effect on bcl-2 was obtained by transfection with LMP, or infection with the nondefective virus. No change of bcl-2 expression was observed with EBNA-1. Our data indicate that the immortalization capacity of EBV and the growth advantage of EBV- positive compared with EBV-negative BL cells in vitro may predominantly be mediated via induction of bcl-2 and the main effectors are EBNA-2 and LMP.

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