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. 2021 Aug 31;36(2):370–382. doi: 10.1038/s41375-021-01392-1

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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. 8 — In JAK3^M511I-induced leukemia, PHF6 could bind to ADGRB1 (BAI1) gene, increase its expression, upregulate BAI1 level, prevent MDM2-mediated P53 ubiquitination, stabilize the P53 protein, and suppress leukemia development (Left panel). In the same leukemia model, loss of PHF6 could downregulate the expression of BAI1, lead to increased MDM2-P53 binding and P53 degradation, and accelerate JAK3^M511I-induced T-ALL progression (Right panel).