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. 2021 Apr 15;147(7):2025–2033. doi: 10.1007/s00432-021-03626-2

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© The Author(s) 2021

Open AccessThis 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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Fig. 2 — Immunoblot analysis of intranuclear p53 protein level. a) U2OS and b) Hep3B cells were treated with DMSO, 0.1 µM Selinexor or 1.0 µM Selinexor under normoxia for 24 h and fractionated. Hep3B cells are deficient for the tumor suppressor protein p53 and were transiently transfected with a p53-pcDNA-plasmid. Relative protein levels of intranuclear p53 protein in % ± SD compared to DMSO control are shown. One-way ANOVA with Tukey posttest with *p < 0.05 and ***p < 0.001 (n = 3)