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. 2024 Feb 13;8(4):bvae029. doi: 10.1210/jendso/bvae029

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© The Author(s) 2024. Published by Oxford University Press on behalf of the Endocrine Society.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 3. — KDM5 modulates H3K4 methylation at the Dlk1 promoter and Ucp1 enhancer. H3K4 methylation status was determined by ChIP-qPCR at promoters/enhancers indicated with antibodies against total histone H3, lysine 4 trimethylated H3 (H3K4me3) and lysine 4 monomethylated H3 (H3K4me1). A control IgG antibody was used in tandem to assess nonspecific antibody binding and data are expressed as the fold-enrichment of H3 antibodies relative to the IgG control. (A) ChIP-qPCR of total H3 and H3K4 methylation status near the Dlk1 transcription start site (+605 bp) in 3T3-L1 and brown adipocytes treated with KDM5 inhibitor C70 or vehicle (Veh) at day −2 and harvested for ChIP-qPCR at day 2 (3T3-L1) or treated with C70 at day −1 and harvested for ChIP-qPCR at day 8 (brown adipocytes). (B) ChIP-qPCR to assess total H3 and H3K4 methylation at Ucp1 enhancer (−2550 bp) in brown adipocytes treated with C70 or Veh at day −1 and harvested for ChIP-qPCR at day 8. Comparison of Veh and C70-treated cells by t test; * P < .05.