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. 2021 Apr 29;12(5):422. doi: 10.1038/s41419-021-03703-x

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© The Author(s) 2021

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. 4 — A In vitro interactions between POU1F1 and HMGA1B or HMGA2 were determined by GST pull-down assay. B In vivo interactions between POU1F1 and HMGA1B or HMGA2 were determined by co-IP. Whole-cell lysates served as an input control. C The enrichment of HMGA1 or HMGA2 at POU1F1 promoter was assessed by ChIP assay. Normal IgG served as a negative control. The non-immunoprecipitated chromatin served as an input control. D POU1F1 promoter region containing sequence between nt −1321 and +15 was cloned into pGL-3 Basic vector. Luciferase activity was determined by dual luciferase reporter assay. Renilla luciferase activity served as an internal control. E The protein level of POU1F1 was determined by western blot. GAPDH served as a loading control. F The correlations between POU1F1 and HMGA1B or HMGA2 in GC were determined by Pearson correlation analysis. Data were expressed as the mean ± SD of n = 3 experiments. *P < 0.05, **P < 0.01, ***P < 0.001.