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. 2023 Apr 18;9:131. doi: 10.1038/s41420-023-01399-w

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© The Author(s) 2023

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. 2 — A HDAC3 is recruited to interact with NCoR or SMRT, forming nuclear receptor co-repressors complexes with G protein pathway suppressor 2 (GPS2), transducin β-like 1 (TBL1X), and TBL1-related protein 1 (TBL1XR). Co-repressors complexes binds to NR that have bound chromatin to perform transcriptional regulation dependent on its deacetylation function. B HDAC3 mutated in deacetylation sites directly binds to ATF2 to regulate transcription of inflammation-related genes independently of deacetylase activity. HDAC3 also can interact with PRC2 or SOX30 to regulates heart development and male fertility.