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. 2017 Aug 11;9:82. doi: 10.1186/s13148-017-0382-y

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© The Author(s). 2017

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 2 — a Immunoprecipitation (IP) and western blotting (WB) data showing that LSD1 and VDR belong to the same transcriptional complex. IP was performed from nuclear lysate in samples treated with vehicle control or 1,25-D₃ using the same LSD1 antibody described for IHC and WB. In post-IP, the samples were probed for LSD1 and VDR. The same double band visible in Fig. 1 was also detected in this sample. b, c Effect of LSD1 knockdown and 1,25-D₃ treatment on gene expression of VDR target genes. Every graph compares the effect of vitamin D in control (CTR) cells and LSD1 knockdown (siLSD1) cells. Each bar is the mean of at least three biological replicates with SEM, showing the fold changes of treated (+ D3) vs. vehicle-treated (− Veh) samples. The columns indicate, from left to right, siCTR + Veh, siCTR + 1,25-D₃, siLSD1 + Veh, and siLSD1 + 1,25-D₃. Transcript levels were measured for b E2f1 and Cdkn1a and c Cyp24a1 and S100g. Statistical significance was evaluated with one-way ANOVA and Tukey post hoc correction (***p < 0.001, **p < 0.01, *p < 0.05)