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. 2018 Sep 20;8:14141. doi: 10.1038/s41598-018-32381-7

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Delocalization of HP1β and H3K9me3 from the decondensed transgene array bound by the HP1-binding-deficient mutant of p150. Cells were transfected with plasmids encoding EYFP-LacR fusion proteins as shown in (a) followed by ChIP assay using antibodies specific for HP1β or H3K9me3 (b). The fold enrichment was determined by normalizing the immunoprecipitation percentage of transgene sequences (CMVm promoter), defined as the ratio of immunoprecipitated DNA to input DNA, against that of the active ß-actin promoter region. Means and ranges from two independent experiments are shown.