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• W2151190049 endingPage "3552" @default.
• W2151190049 startingPage "3542" @default.
• W2151190049 abstract "The Epstein-Barr virus (EBV) nuclear antigen 2 (EBNA-2) is a key gene expressed in EBV type III latent infection that can transactivate numerous promoters, including those for all the other type III viral latency genes as well as cellular genes responsible for cell proliferation. EBNA-2 is essential for EBV-mediated immortalization of primary B lymphocytes. We now report that EBNA-2, a phosphoprotein, is hyperphosphorylated specifically in mitosis. Evidence that the cyclin-dependent kinase p34(cdc2) may be involved in this hyperphosphorylation includes (i) coimmunoprecipitation of EBNA-2 and p34(cdc2), suggesting physical association; (ii) temporal correlation between hyperphosphorylation of EBNA-2 and an increase in p34(cdc2) kinase activity; and (iii) ability of purified p34(cdc2)/cyclin B1 kinase to phosphorylate EBNA-2 in vitro. Hyperphosphorylation of EBNA-2 appears to suppress its ability to transactivate the latent membrane protein 1 (LMP-1) promoter by about 50%. The association between EBNA-2 and PU.1 is also decreased by about 50% in M-phase-arrested cells, as shown by coimmunoprecipitation from cell lysates, suggesting that hyperphosphorylation of EBNA-2 impairs its affinity for PU.1. Finally, endogenous LMP-1 mRNA levels in M phase are around 55% of those in asynchronously growing cells. These results suggest that regulation of gene expression during type III latency may be regulated in a cell-cycle-related manner." @default.
• W2151190049 created "2016-06-24" @default.
• W2151190049 creator A5014590662 @default.
• W2151190049 creator A5062701543 @default.
• W2151190049 creator A5075719027 @default.
• W2151190049 creator A5081306475 @default.
• W2151190049 date "2004-04-01" @default.
• W2151190049 modified "2023-09-26" @default.
• W2151190049 title "Mitosis-Specific Hyperphosphorylation of Epstein-Barr Virus Nuclear Antigen 2 Suppresses Its Function" @default.
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• W2151190049 doi "https://doi.org/10.1128/jvi.78.7.3542-3552.2004" @default.
• W2151190049 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/371044" @default.
• W2151190049 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15016877" @default.

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