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EBNA1 and Epstein-Barr Virus Associated Tumours by Lori Frappier

By Lori Frappier

This SpringerBrief is entire account of the services and results of the Epstein-Barr virus (EBV) EBNA1 protein that relate to EBV-associated cancers and facts for EBNA1 contributions to those cancers. EBNA1 used to be the 1st EBV protein detected and the main serious for EBV latent an infection. EBNA1 fulfills a number of services at EBV genomes that have been defined in lots of (sometimes complicated) stories over the past 28 years. whereas those have been at the start considered the one roles of EBNA1, many studies in recent times have proven that EBNA1 additionally at once impacts mobile approaches in ways in which will be anticipated to give a contribution to oncogenesis. even though, the measure to which EBNA1 promotes phone survival and oncogenesis in a variety of varieties of human tumours isn't totally transparent and a question of discussion. This e-book bargains a present synopsis of EBNA1 features in EBV latency, together with services in DNA replication, mitotic segregation and transcription. Mechanisms of those EBNA1 capabilities can also be mentioned in addition to implications for tumourigenesis. moreover, the mobile results of EBNA1 can be reviewed, together with how EBNA1 manipulates particular mobile proteins and relationships to EBV-associated lymphomas and carcinomas.

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Additional resources for EBNA1 and Epstein-Barr Virus Associated Tumours

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B. (1992). 7Å of the bovine papillomavirus-1 E2 DNA-binding protein bound to its DNA target. Nature, 359, 505–512. , Camiolo, S. , & Yates, J. L. (1993). Constitutive binding of EBNA1 protein to the Epstein-Barr virus replication origin, oriP, with distortion of DNA structure during latent infection. EMBO Journal, 12, 4933–4944. Jones, C. , Hayward, S. , & Rawlins, D. R. (1989). Interaction of the lymphocyte-derived Epstein-Barr virus nuclear antigen EBNA-1 with its DNA-binding sites. Journal of Virology, 63, 101–110.

2012a). Consistent with these p53 effects, the presence of EBNA1 in all of these cell lines resulted in decreased apoptosis after DNA damage, although this may not be entirely due to the lowered p53 levels. As discussed below, EBNA1 also induces the loss of PML nuclear bodies which are important for apoptosis, in part because they facilitate the activation of p53 through acetylation. Therefore, EBNA1 likely inhibits p53 function in multiple ways (at least in epithelial cells) thereby promoting cell survival.

In addition, PML nuclear bodies are part of the innate immune response and act to suppress productive infections of several viruses through inhibition of viral gene expression and replication (Everett and Chelbi-Alix 2007; Geoffroy and Chelbi-Alix 2011; Reichelt et al. 2011). PML proteins, which are comprised of six nuclear isoforms, interact with each other to form the structural basis of the PML nuclear body with which many additional proteins then interact. To counteract the inhibition of viral infection by PML nuclear bodies, many viruses encode proteins that disrupt them, either by inducing the degradation of the PML proteins or by interfering with the interactions of PML proteins to form the bodies (Everett 2001).

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