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. 2022 Jul 8;13:3972. doi: 10.1038/s41467-022-31735-0

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© The Author(s) 2022

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. 9 — A model for the insulin–PKB–TRIM24 signalling pathway in control of hepatic lipogenesis via P-bodies. Insulin stimulates phosphorylation of TRIM24 via PKB in hepatocytes, which translocates TRIM24 from the nucleus into the cytoplasm. Cytosolic TRIM24 is targeted to Pparγ-containing P-bodies, where it interacts with P-body components such as EDC4 and AGO1/2 and ubiquitinates these proteins to stabilise Pparγ mRNA. This pathway promotes lipid accumulation in the liver, and its inhibition alleviates diet-induced hepatosteatosis.