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. 2019 Apr 26;10:1935. doi: 10.1038/s41467-019-09970-9

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© The Author(s) 2019

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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Fig. 9 — CSF-1R is abnormally expressed and recruited on chromatin in CMML monocytes. a Total proteins were extracted from isolated control or CMML monocytes and analyzed by immunoblotting with antibodies that recognize CSF-1R and actin. b CFMS expression was assessed by RNA-sequencing and qPCR in monocytes of 9 and 13 CMML patients, respectively, compared with 3 and 8 control buffy coats (Ctrl), respectively (mean +/− SEM, Mann–Whitney test: *P < 0.05, **P < 0.01). c ChIP-Seq experiments showing CSF-1R peak localization on intergenic area on chromosome 1 (chr1: intergenic), upstream of CEBPA and on BCL2 genes that are conserved in control and CMML monocytes. d ChIP-Seq experiments showing CSF-1R peak localization on BPIFB1, downstream of AP1M1 and on intergenic area on chromosome 11 and 22 (chr11: intergenic and chr22: intergenic) that can be lost in CMML compared with healthy donor monocytes (CSF-1R N-ter: sc-46662 monoclonal antibody in dark blue, CSF-1R C-ter: sc-692 polyclonal antibody in light blue)