scholarly journals The Zipper Region of Epstein-Barr Virus bZIP Transcription Factor Zta Is Necessary but Not Sufficient To Direct DNA Binding

2003 ◽  
Vol 77 (14) ◽  
pp. 8173-8177 ◽  
Author(s):  
Matthew R. Hicks ◽  
Salama S. Al-Mehairi ◽  
Alison J. Sinclair
Keyword(s):  
Transcription Factor ◽  
Dna Binding ◽  
Epstein Barr Virus ◽  
Bzip Transcription Factor ◽  
Barr Virus ◽  
Binding Function ◽  
Sequence Elements ◽  
Epstein Barr ◽  
Bzip Proteins

ABSTRACT The viral bZIP transcription factor Zta (BZLF1, EB1, ZEBRA) mediates the switch between the latent and lytic cycles of Epstein-Barr virus (EBV). In part, its activity requires the formation of homodimers and interaction with specific DNA sequence elements (ZREs). Zta has an atypical zipper motif that has a lower stability than do typical bZIP proteins. Here we show that a synthetic peptide directed against the zipper can disrupt the DNA-binding function of Zta. This highlights the relevance of this region for the function of Zta and demonstrates that the zipper region is a potential target for therapeutic agents. We also unmask the relevance of a region adjacent to the zipper (CT region), which is required to direct the interaction of Zta with DNA and to transactivate ZRE-dependent promoters in vivo.

scholarly journals Domains of the Epstein-Barr virus (EBV) transcription factor R required for dimerization, DNA binding and activation

1991 ◽  
Vol 19 (10) ◽  
pp. 2661-2667 ◽  
Author(s):  
E. Manet ◽  
A. Rigolet ◽  
H. Gruffat ◽  
J.-F. Giot ◽  
A. Sergeant
Keyword(s):  
Transcription Factor ◽  
Dna Binding ◽  
Epstein Barr Virus ◽  
Barr Virus ◽  
Epstein Barr

The role of DNA hypomethylation, histone acetylation and in vivo protein-DNA binding in Epstein–Barr virus-induced CD23 upregulation

2013 ◽  
Vol 435 (1) ◽  
pp. 8-15 ◽  
Author(s):  
Kalman Szenthe ◽  
Anita Koroknai ◽  
Ferenc Banati ◽  
Zoltan Bathori ◽  
Hans Helmut Niller ◽  
...  
Keyword(s):  
Dna Binding ◽  
Histone Acetylation ◽  
Epstein Barr Virus ◽  
Dna Hypomethylation ◽  
Barr Virus ◽  
Epstein Barr

Epstein-Barr virus nuclear antigen 2 induces FcRH5 expression through CBF1

Blood ◽  
2006 ◽  
Vol 107 (11) ◽  
pp. 4433-4439 ◽  
Author(s):  
Joanne Mohan ◽  
Jessica Dement-Brown ◽  
Sabine Maier ◽  
Tomoko Ise ◽  
Bettina Kempkes ◽  
...  
Keyword(s):  
Dna Binding ◽  
B Cell ◽  
Burkitt Lymphoma ◽  
Epstein Barr Virus ◽  
De Novo ◽  
Nuclear Antigen ◽  
Barr Virus ◽  
Epstein Barr ◽  
Chromosome 1Q21

AbstractFc-receptor homolog 5 (FcRH5) is a recently identified B-cell membrane protein of unknown function. In Burkitt lymphoma cell lines with chromosome 1q21 abnormalities, FcRH5 expression is deregulated, implicating FcRH5 in lymphomagenesis. Epstein-Barr virus infects and immortalizes B cells, and is implicated in the etiology of several tumors of B-cell origin. Overexpression of genes located on 1q21-25 has been proposed as a surrogate for Epstein-Barr virus in Burkitt lymphoma. We now report that Epstein-Barr virus nuclear antigen 2 (EBNA2) markedly induces the expression of the FcRH5 gene, encoded on chromosome 1q21. Induction occurred in the absence of other viral proteins and did not require de novo protein synthesis. EBNA2 lacks a DNA-binding domain and can target responsive genes through the host DNA binding protein CBF1. We show that induction of FcRH5 by EBNA2 is strictly CBF1 dependent, as it was abolished in CBF1-deficient cells. Accordingly, EBNA2 targeted CBF1 binding sites present in the FcRH5 promoter in vivo, as detected by chromatin immunoprecipitation. These results identify FcRH5 as a novel, direct target of EBNA2 that may contribute to the development of Epstein-Barr virus–associated tumors.

scholarly journals EBV-LMP1 promotes radioresistance by inducing protective autophagy through BNIP3 in nasopharyngeal carcinoma

2021 ◽  
Vol 12 (4) ◽  
Author(s):  
San Xu ◽  
Zhuan Zhou ◽  
Xingzhi Peng ◽  
Xuxiu Tao ◽  
Peijun Zhou ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Crucial Role ◽  
Epstein Barr Virus ◽  
Interacting Protein ◽  
Multiple Tumors ◽  
Barr Virus ◽  
Signaling Axis ◽  
Epstein Barr ◽  
Adenovirus E1b

AbstractStudies have indicated that dysfunction of autophagy is involved in the initiation and progression of multiple tumors and their chemoradiotherapy. Epstein–Barr virus (EBV) is a lymphotropic human gamma herpes virus that has been implicated in the pathogenesis of nasopharyngeal carcinoma (NPC). EBV encoded latent membrane protein1 (LMP1) exhibits the properties of a classical oncoprotein. In previous studies, we experimentally demonstrated that LMP1 could increase the radioresistance of NPC. However, how LMP1 contributes to the radioresistance in NPC is still not clear. In the present study, we found that LMP1 could enhance autophagy by upregulating the expression of BCL2/adenovirus E1B 19 kDa protein-interacting protein 3 (BNIP3). Knockdown of BNIP3 could increase the apoptosis and decrease the radioresistance mediated by protective autophagy in LMP1-positive NPC cells. The data showed that increased BNIP3 expression is mediated by LMP1 through the ERK/HIF1α signaling axis, and LMP1 promotes the binding of BNIP3 to Beclin1 and competitively reduces the binding of Bcl-2 to Beclin1, thus upregulating autophagy. Furthermore, knockdown of BNIP3 can reduce the radioresistance promoted by protective autophagy in vivo. These data clearly indicated that, through BNIP3, LMP1 induced autophagy, which has a crucial role in the protection of LMP1-positive NPC cells against irradiation. It provides a new basis and potential target for elucidating LMP1-mediated radioresistance.

scholarly journals Epstein-Barr virus, B cell lymphoproliferative disease, and SCID mice: Modeling T cell immunotherapy in vivo

2011 ◽  
Vol 83 (9) ◽  
pp. 1585-1596 ◽  
Author(s):  
I. Johannessen ◽  
L. Bieleski ◽  
G. Urquhart ◽  
S.L. Watson ◽  
P. Wingate ◽  
...  
Keyword(s):  
T Cell ◽  
B Cell ◽  
Epstein Barr Virus ◽  
Lymphoproliferative Disease ◽  
Scid Mice ◽  
Barr Virus ◽  
Cell Immunotherapy ◽  
Epstein Barr ◽  
T Cell Immunotherapy
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