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. 2021 Jan 6;12(1):21. doi: 10.1038/s41419-020-03364-2

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© The Author(s) 2021

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. 7 — When TRIM21 is overexpressed in OS cells, it competitively binds to ANXA2 and thus facilitating the translocation of ANXA2 toward PM; this enables the disassociation of TFEB from the ANXA2-TFEB complex, allowing TFEB entering into the nucleus. Nuclear TFEB promotes the transcription of autophagy-related genes, including ATG9B, LC3, and P62, and inhibits OS differentiation, presumably, through regulating the Sp1/RUNX2 signaling in OS cells. TRIM21 OE: TRIM21 overexpression. ×: disassociation of ANXA2-TFEB complex.