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. 2019 Jan 18;9:208. doi: 10.1038/s41598-018-36312-4

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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LMP1 CTAR1 and CTAR2 contributed to LMP1-mediated increase in sumo levels via the activation of NF-κB. (a,b) 293 cells were transfected with 1 μg of a LMP1-expression plasmid, select LMP1 mutant-expression plasmid, or a pcDNA3 control plasmid. (a) RNA was harvested and cDNA was prepared. Real-time PCR was performed to quantitate relative sumo-1 and sumo-2/3 levels (relative to gapdh), The fold change in sumo-1 and sumo-2/3 levels (compared to control-expressing cells) was determined. Results are shown as the mean ± the standard deviation for samples performed in triplicate and independent experiments performed in triplicate. (b) Slot blots were performed to detect SUMO-1 and SUMO-2/3 levels. Actin was used as a loading control. Representative blots for experiments performed in triplicate are shown. (c,d) EBV-transformed LCLs were treated with Bay 11–7082 (1 μM), LY294002 (5 μM), or DMSO (the vehicle control; Control) for 24 hours. (c) RNA was harvested and cDNA was prepared. Real-time PCR was performed to quantitate relative sumo-1, and sumo-2/3 expression (relative to gapdh), and the fold change in sumo-1 and sumo-2/3 levels (relative to control-treated cells) was determined. Results are shown as the mean ± the standard deviation for samples performed in triplicate and independent experiments performed in triplicate. (d) Slot immunoblots and Western blots analyses were performed to detect SUMO-1 and SUMO-2/3 levels. GAPDH was used as a loading control. Representative blots for experiments performed in triplicate are shown. (e) cDNA generated from RNA harvested from BL41 EBV-negative, BL41 EBV WT, and BL41 EBV mut (P3HR1) cells that were treated with DMSO (the vehicle control; control) or Bay 11–7085 (1 μM) for 24 hours. Real-time PCR was performed was performed to quantitate relative sumo-1, and sumo-2/3 levels (relative to gapdh). The fold change in sumo-1 and sumo-2/3 levels (relative to control-treated BL41 EBV WT cells) was determined. Results are shown as the mean ± the standard deviation for samples performed in triplicate and independent experiments performed in triplicate.