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. 2021 Oct 1;12:5779. doi: 10.1038/s41467-021-26049-6

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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 — a SPOP-CUL3-RBX1 functions as an E3 ubiquitin ligase that binds to Geminin and catalyzes K27-linked poly-ubiquitination of Geminin at Lys100 and Lys127. b SPOP-dependent Geminin poly-ubiquitination blocks Cdt1 binding to MCM proteins. Poly-ubiquitination keeps the licensing-competent state in check and prevents DNA replication over-firing. c Cancer-associated SPOP mutations impair DNA replication surveillance and cause replication origin over-firing and re-replication. d SPOP mutations trigger replication catastrophe and cancer cell death upon ATR inhibition.