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. 2019 Oct 1;33(19-20):1428–1440. doi: 10.1101/gad.328773.119

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© 2019 Lee 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://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 7. — A scheme showing a model by which EZH2 automethylation enhances the conversion of H3K27me2 to H3K27me3. (Left) In WT cells, PRC2 automethylates K510 and K514 of EZH2 which subsequently displaces the unstructured autoinhibitory loop and promotes PRC2 accessibility to nucleosomes. (Right) When EZH2 automethylation sites (EZH2-K510 and EZH2-K514) are mutated to alanine, automethylation fails and the loop may occlude the active site more frequently. This outcome significantly impairs the rate limiting step of PRC2 catalysis: conversion of H3K27me2 to H3K27me3.