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Viruses 2012, 4(9), 1537-1547; doi:10.3390/v4091537

Contributions of Epstein–Barr Nuclear Antigen 1 (EBNA1) to Cell Immortalization and Survival

Department of Molecular Genetics, University of Toronto, 1 Kings College Circle, Toronto, ON M5S 1A8, Canada
Received: 19 July 2012 / Revised: 14 August 2012 / Accepted: 27 August 2012 / Published: 13 September 2012
(This article belongs to the Special Issue Modulation of Apoptosis by Viral Infection)
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Abstract

Epstein–Barr virus (EBV) immortalizes host cells as part of its latent mode of infection. As a result of this ability to promote cell proliferation and survival, EBV infection contributes to the development of several kinds of B-cell lymphomas and epithelial tumours. The EBV Epstein–Barr nuclear antigen 1 (EBNA1) protein is the only EBV protein expressed in all EBV-associated tumours and plays multiple important roles in EBV latency. In addition to its well-studied roles in viral DNA replication, segregation and transcriptional activation, several studies have identified roles of EBNA1 in manipulating cellular processes that result in reduced apoptosis and increased cell survival. This review discusses these cellular effects of EBNA1 and mechanisms by which they occur.
Keywords: EBNA1; USP7; PML; p53; survivin; Nm23-H1; ROS; oxidative stress; NFκB; STAT1 EBNA1; USP7; PML; p53; survivin; Nm23-H1; ROS; oxidative stress; NFκB; STAT1
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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MDPI and ACS Style

Frappier, L. Contributions of Epstein–Barr Nuclear Antigen 1 (EBNA1) to Cell Immortalization and Survival. Viruses 2012, 4, 1537-1547.

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