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. 2019 Sep 6;9:12827. doi: 10.1038/s41598-019-49289-5

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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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Phlda3 inhibition potentiated cytokine-induced activation of the NFκB pathway independently of AKT. MIN6 cells transfected with either control siRNA (si-C) or siRNA against Phlda3 (si-Ph3) were cultured in the absence (white bars) or presence (grey and black bars) of cytokines (15min-24h). Changes in the mRNA levels of iNos, Il1β and Ikbα (a–c). Changes in the phosphorylation of NFκB subunit p65 on serine 536 (d). Changes in phospho- and total AKT protein levels (e,f). n = 3–6 experiments. *p < 0.05, **p < 0.01, ***p < 0.001 vs untreated. ^#p < 0.05, ^##p < 0.01, ^###p < 0.001 vs control siRNA.