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. 2020 Feb 29;69(11):2016–2024. doi: 10.1136/gutjnl-2019-319637

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© Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.

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A model for DLEU2-PRC2/EZH2-HBx interaction. Left panel: PRC2-mediated epigenetic silencing of target genes; middle panel: DLEU2 recruitment displaces PRC2/EZH2 from close contact with target chromatin, resulting in a reduction of the methyl groups at lysine 27 of histone H3 (H3K27me3) repressive mark; right panel: in the presence of HBx (HBV-infected hepatocytes and HBV-related HCCs expressing HBx), the increase in DLEU2 levels and DLEU2 interaction with PRC2/EZH2 lead to a progressive increase of active chromatin marks associated with active transcription. HBx is part of the DLEU2-PRC2/EZH2 complex and recruited at the chromatin level together with transcription factors and co-activators to contribute to transcriptional activation (not shown in the cartoon). EZH2, enhancer of zeste homolog 2; PRC2, polycomb repressor complex 2.