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• W2017481656 startingPage "6608" @default.
• W2017481656 abstract "The Epstein–Barr virus (EBV)-encoded latent membrane protein-1 (LMP1), a functional homologue of the tumor necrosis factor receptor family, substantially contributes to EBV's oncogenic potential by activating nuclear factor-κB (NF-κB). miR-155 is an oncogenic miRNA critical for B-cell maturation and immunoglobulin production in response to antigen. We report that miR-155 expression is much higher in EBV-immortalized B cells than in EBV-negative B cells. LMP1, but not LMP2, up-regulated the expression of miR-155, when transfected in EBV-negative B cells. We analyzed two putative NF-κB binding sites in the miR-155 promoter; both sites recruited NF-κB complex, in nuclear extract from EBV-immortalized cells. The exogenous expression of LMP1, in EBV-negative background, is temporally correlated to induction of p65 with binding on both NF-κB sites and with miR-155 overexpression. The induction of p65 binding together with increased RNA polymerase II binding, confirms that LMP1-mediated activation of miR-155 occurs transcriptionally. In reporter assays, miR-155 promoter lacking NF-κB binding sites was no longer activated by LMP1 expression and an intact AP1 site is needed to attain maximum activation. Finally, we demonstrate that LMP1-mediated activation of miR-155 in an EBV-negative background correlates with reduction of protein PU.1, which is a possible miR target." @default.
• W2017481656 created "2016-06-24" @default.
• W2017481656 creator A5025632358 @default.
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• W2017481656 date "2008-10-21" @default.
• W2017481656 modified "2023-09-27" @default.
• W2017481656 title "Epstein–Barr virus latent membrane protein 1 trans-activates miR-155 transcription through the NF-κB pathway" @default.
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• W2017481656 doi "https://doi.org/10.1093/nar/gkn666" @default.
• W2017481656 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2582607" @default.
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