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. 2018 Jun 13;26(3):516–530. doi: 10.1038/s41418-018-0141-4

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© The Author(s) 2018

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 — Ubqln4 functions as a tumor suppressor by regulating p21. Ubqln4 can activate p53, which results in induction of p21. In addition, Ubqln4 can also interact with and suppress RNF114, an E3 ligase of p21, which inhibits p21 degradation via the proteasomal pathway. The activation of p21 through different mechanistic pathways ultimately induces cell cycle arrest and/or cell senescence