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. 2017 Nov 15;31(22):2201–2203. doi: 10.1101/gad.310359.117

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© 2017 Sump and Brickner; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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Figure 1. — Model for Nup98 and Nup98-Nsd1 regulation of chromatin modification and gene expression. (A) In wild-type mouse HPCs, Nup98 facilitates the recruitment of the WSC complex to active promoters, which catalyzes H3K4 trimethylation, promoting RNA polymerase II-dependent transcription. (B) In cells expressing the Nup98-Nsd1 fusion protein, the WSC complex is recruited by Nup98-Nsd1 to ectopic sites, leading to inappropriate methylation of H3K4. This promotes inappropriate expression of genes such as HoxA9 and Meis1, leading to AML.