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. 2018 Feb 21;9(3):303. doi: 10.1038/s41419-018-0291-9

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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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Fig. 6 — a The predicted NFYA binding sites in the promotor of SATB1 and the designed mutant sequence are indicated. A luciferase assay of NFYA and SATB1 was carried out. b ChIP assays were performed in Ishikawa and RL-95-2 cells followed by qRT-PCR. c Results of qRT-PCR confirmed that NFYA regulated SATB1 expression in Ishikawa and RL-95-2 cells. d The results of western blots showed that NFYA regulated SATB1 expression in Ishikawa and RL-95-2 cells. Data are presented as the means ± SD from three independent experiments. *P < 0.05