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. 2016 Nov 11;9:52. doi: 10.1186/s13072-016-0103-3

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© The Author(s) 2016

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 4 — Effect of KMT2A/MLL1 or Msk1 knockdown on H3K4me3, H3K9acS10ph and H3K27me3 distribution across HoxA4 and HoxA5. a Effect of KMT2A/MLL1 or Msk1 knockdown on H3K4me3, H3K9acS10ph and H3K27me3 levels at HoxA4 (upper panels) and HoxA5 (lower panels). Histograms present the modification abundance at these sites as a bound/unbound ratio, where 1.0 indicates there is no enrichment (n = 1 or 2, T test, *p < 0.05; **p < 0.01). b Proposed model of how the KMT2A/MLL1 and Msk1 interaction within the KMT2A/MLL1 complex facilitates H3K4 methylation at transcription start sites (TSSs). Msk1-catalysed H3S10 phosphorylation directly enhances KMT2A/MLL1-catalysed H3K4 methylation and, potentially, improves access of the complex to condensed chromatin by reversing chromatin compaction