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. 2019 Jun 28;10:2854. doi: 10.1038/s41467-019-10786-w

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© The Author(s) 2019

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 — SETD1A maintains the balance between proliferation and senescence. Suppression of SETD1A leads to mitotic defects and simultaneous repression of SKP2 in these cells causes the defective daughter cells to enter senescence with increased levels of p21 and p27. SETD1A-KD cells escaping senescence re-enter the cell cycle through upregulation of SKP2 as well as other mechanisms. The inset summarizes the pivotal role SETD1A expression in maintaining the balance between mitosis and senescence