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. 2021 Feb 17;11:3991. doi: 10.1038/s41598-021-83603-4

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© The Author(s) 2021

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Deficiency of p53 promotes increased HIF-1 signalling. (a,b,d–f) The indicated MYD88 constructs were introduced by retroviral infection to wild type and p53^−/−MEFs. Expressions of the indicated mRNAs were measured by qPCR. The y-axis values are relative fold change for gene transcripts normalised to β-actin. The data represent the mean ± s.d. (n = 3) using one-way ANOVA followed by Scheffe’s F test. *P < 0.05, **P < 0.01. The black asterisks show significance between WT and p53^−/−MEFs. The orange asterisks show significance between indicated cells and vector introduced WT MEFs. The blue asterisks show significance between indicated cells and vector introduced p53^−/−MEFs. (c) WT and p53^−/−MEFs from the same litter or same background were used for this experiment. Total cell lysates were analysed by immunoblotting.