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. 2019 Jan 24;9:737. doi: 10.1038/s41598-018-37402-z

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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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Gfi1 represses c-Fos and Egr-1 through direct binding to their promoters. (A) Gfi1 binding patterns at the c-Fos (upper panel) and Egr-1 (lower panel) based on the ChIP-seq data submitted by Möröy’s research group²¹. The pink and green arrows denote the forward and reverse primers, respectively, used to amplify the promoter regions at c-Fos (F1) and Egr-1 (E1 and E2) loci. (B) 32D/Y729F/Gfi1 cells were cultured with or without Dox for 24 hours. ChIP assays were carried out using the anti-mouse Gfi1 antibody. The indicated regions of c-Fos and Egr-1 promoters were amplified by PCR. (C) 32D/Y729F/Gfi1 cells were transfected with pGL3-basic vector containing c-Fos or Egr-1 promoter fragment and cultured in G-CSF with or without Dox. Luciferase activities were measured 24 hours later.