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. 2018 Jun;28(6):846–858. doi: 10.1101/gr.227280.117

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© 2018 Fukuda et al.; 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://genome.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 7. — Possible mechanism of MORC2A- and RESF1-mediated provirus silencing. MORC2A interacts with histone H3 tail through its CW domain and functions as transcriptional repressor when it colocalizes with H3K9me3. MORC2A-mediated silencing activity is ATPase activity dependent. RESF1 regulates SETDB1-mediated silencing by stabilizing SETDB1 enrichment on the target provirus loci.