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. 2017 Dec 11;8(12):3201. doi: 10.1038/s41419-017-0070-z

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© The Author(s) 2017

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. 5 — a Cooperation of CACUL1 and SIRT1 to mediate PPARγ repression. HEK293 cells were transfected as indicated and were subjected to extraction for luciferase assays. Data indicate means±SD from three independent experiments (**P < 0.01). b Effect of LSD1 on PPARγ activation. Transfections and luciferase assays were performed as indicated (**P < 0.01). c Negative effect of CACUL1 on LSD1-enhanced PPARγ activity. (*P < 0.05). d Effect of CACUL1 depletion on H3K9 modifications during adipogenesis. Stable 3T3-L1 cells depleted of CACUL1 were subjected to differentiation for 8 days and chromatin IP (ChIP) assays using a primer set specific for the distal PPARγ-response site within the aP2 promoter and the indicated antibodies (H3K9ac and H3K9me, acetylation and demethylation at lysine 9 of histone H3, respectively). Data indicate means±SD from three independent experiments (*P < 0.05) (**P < 0.01). e Effect of fasting and resveratrol. After culturing undifferentiated 3T3-L1 cells in low-glucose DMEM (5.5 mm glucose; fasting condition) or treating with resveratrol (25 μm) for 24 h, ChIP assays were performed using the indicated antibodies. Data indicate means±SD from three independent experiments (*P < 0.05, **P < 0.01). CACUL1 expression is displayed by WB under these conditions. f Effect of resveratrol, SRT1720, or GSK-LSD1 treatment on adipogenesis under CACUL1-depleted conditions. CACUL1-depleted 3T3-L1 stable cells were treated with SIRT1 activators (resveratrol, 25 μm; SRT1720, 2.5 μm) or an LSD1 inhibitor (GSK-LSD1, 25 μm) and subjected to differentiation for 8 days. Lipid accumulation was visualized and measured as described (**P < 0.01)

Fig. 5 — a Cooperation of CACUL1 and SIRT1 to mediate PPARγ repression. HEK293 cells were transfected as indicated and were subjected to extraction for luciferase assays. Data indicate means±SD from three independent experiments (**P < 0.01). b Effect of LSD1 on PPARγ activation. Transfections and luciferase assays were performed as indicated (**P < 0.01). c Negative effect of CACUL1 on LSD1-enhanced PPARγ activity. (*P < 0.05). d Effect of CACUL1 depletion on H3K9 modifications during adipogenesis. Stable 3T3-L1 cells depleted of CACUL1 were subjected to differentiation for 8 days and chromatin IP (ChIP) assays using a primer set specific for the distal PPARγ-response site within the aP2 promoter and the indicated antibodies (H3K9ac and H3K9me, acetylation and demethylation at lysine 9 of histone H3, respectively). Data indicate means±SD from three independent experiments (*P < 0.05) (**P < 0.01). e Effect of fasting and resveratrol. After culturing undifferentiated 3T3-L1 cells in low-glucose DMEM (5.5 mm glucose; fasting condition) or treating with resveratrol (25 μm) for 24 h, ChIP assays were performed using the indicated antibodies. Data indicate means±SD from three independent experiments (*P < 0.05, **P < 0.01). CACUL1 expression is displayed by WB under these conditions. f Effect of resveratrol, SRT1720, or GSK-LSD1 treatment on adipogenesis under CACUL1-depleted conditions. CACUL1-depleted 3T3-L1 stable cells were treated with SIRT1 activators (resveratrol, 25 μm; SRT1720, 2.5 μm) or an LSD1 inhibitor (GSK-LSD1, 25 μm) and subjected to differentiation for 8 days. Lipid accumulation was visualized and measured as described (**P < 0.01)