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. 2025 Feb 7;44(6):1608–1640. doi: 10.1038/s44318-025-00366-8

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© The Author(s) 2025

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. Creative Commons Public Domain Dedication waiver http://creativecommons.org/publicdomain/zero/1.0/ applies to the data associated with this article, unless otherwise stated in a credit line to the data, but does not extend to the graphical or creative elements of illustrations, charts, or figures. This waiver removes legal barriers to the re-use and mining of research data. According to standard scholarly practice, it is recommended to provide appropriate citation and attribution whenever technically possible.

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Figure EV6 — (A) ACC1 immunofluorescence with transfection markers of mCit-PRD-overexpressing HepG2 cells, without (PRD) or with treatment by COP1-KD shRNA (PRD + COP1-KD). Scale bars, 20 μm. Note that COP1 deficiency increased the ACC1 level. (B) Statistics of (A). Error bars, mean ± SEM. One-sided nonpaired Welch’s t test. Biological replicates, mouse individuals. Corresponds to Fig. 6H,I.