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. 2022 Mar 31;29(5):946–960. doi: 10.1038/s41418-022-00988-z

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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. 6 — RB can form complexes with SKP2 preventing SKP2 from supporting ubiquitination and degradation of p27 (KIP1, CDKN1B). The CDK inhibitor p27 is then available to block cyclin A/E-CDK2 activity. These cyclin-CDK complexes have a preference for p130 as substrate. Inhibiting p130 phosphorylation yields hypophosphorylated p130, which then enables formation of the DREAM transcriptional repressor.