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. 2016 Jun 17;9:49. doi: 10.1186/s13045-016-0279-9

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© Song et al. 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 — Functions of wild-type MLL, LSD1 and onco-MLL fusion proteins. a MLL methylates H3K4 and initiates RNA polymerase II (Pol II) mediated gene transcription, while LSD1 removes the methyl group from H3K4me1 and 2 and keeps a balanced H3K4 methylation; b The onco-MLL protein complex involving AF4, AF9, AF10, or ENL can recruit DOT1L, which methylates H3K79 and causes overexpression of leukemia-relevant genes