LMP1 Regulation of ATM
in Epstein-Barr Virus Infected B Cells
Rico Wassather
Winona State University
Shannon C. Kenney, M.D.
Stacy R. Hagemeier, Ph.D.
McArdle Laboratory for Cancer Research
School of Medicine and Public Health
University of Wisconsin-Madison
Abstract
Epstein-Barr virus (EBV) is a human herpes virus associated with several B-cell and epithelial cell
cancers including Burkitt’s lymphoma and nasopharyngeal carcinoma (NPC). The EBV encoded
latent membrane protein 1 (LMP1) has been shown to be one of the major oncogenic factors, and
also down regulates the cellular protein kinase ataxia telangiectasia mutated (ATM). ATM is
activated in response to DNA damage and plays a key role in EBV lytic reactivation. In this study
we generated a lentivirus expressing LMP1 and green fluorescent protein (GFP) under the control
of a B-cell promoter to further examine the role of LMP1 and ATM during EBV infection. The
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lentivirus was used to infect the EBV B cell lines Mutu1 and Sal1. Neither LMP1 or GFP were
detected in either EBV infected cell line suggesting the lentivirus was either packaged inefficiently
or there is a problem with the construct. Additionally, we have not seen a significant decrease in
ATM expression when LMP1 is overexpressed in these cell lines, suggesting the effect of LMP1
on ATM expression may be cell type dependent.