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. 2018 Apr 17;9:1514. doi: 10.1038/s41467-018-03803-x

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© The Author(s) 2018

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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Fig. 6 — GOT2 expression in B-cells is up-regulated by NF-κB/STAT3 activation or MYC. a GOT2 mRNA expression in 24h-stimulated P493-6 MYC^low and unstimulated P493-6 MYC^high cells after inhibition of NF-κB signalling by ACHP or JAK/STAT signalling by Ruxolitinib. b Representative immunoblot of STAT3 and p65 protein levels 24 h after STAT3 (STAT3si) or RELA siRNA (RELAsi) transfection of P493-6 cells. Knockdown efficiencies (protein/GAPDH) relative to scrb control are presented under the images. c GOT2 mRNA expression in 24h-stimulated P493-6 MYC^low cells after siRNA transfection shown in b. d Chromatin immunoprecipitation of STAT3 and p65 1 h after stimulation of P493-6 MYC^low cells. Displayed are average qPCR results and technical errors (SD) of the GOT2 promoter (– 20 bp) from a representative stimulation out of three. Enrichment was calculated relative to an inactive control region (PRAME). e Full tyrosine and serine phosphorylation of STAT3 is only achieved after IL10 + CpG costimulation as revealed by immunoblot analysis. Cells were stimulated with IL10, CpG or both for 30 min. f GOT2 mRNA expression of TMD-8 and OCI-Ly3 cells in comparison with BJAB and CA-46 cells 24 h after ACHP or rRuxolitinib treatment. For additional details about the used cell lines also refer to Supplementary Fig. 7a. With the exception of d, all values are given as mean ± SD of three independent replicates. Results from Bonferroni post hoc test on a two-way ANOVA are presented (***p < 0.001, **p < 0.01)