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. 2018 Nov 12;7(11):84. doi: 10.1038/s41389-018-0095-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. 5 — Indicated cell lines and primary cells were treated with 10 μM CX-4945 or with DMSO control and evaluated by qChIP for Ikaros binding (a, b) and the H3K4me3 histone mark (c, d) at the ARID5B promoter in the indicated cells. ***p < 0.001 compared to WT-anti-Ikaros control. Graphed data in a–d are the mean+/– SD of triplicates representative of one of 3 independent experiments or 3 patient samples