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. 2021 Apr 14;53(4):517–527. doi: 10.1038/s12276-021-00590-2

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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. 3 — a Schematic showing that the cell cycle arrest and apoptotic functions of caspase are mediated via cleavage of MDM2 and BID following mitotic catastrophe, respectively. Figure created with BioRender.com. b An example of MDM2 cleavage by caspase-2 (Casp2) following treatment of WT or caspase-2-deficient (KO) U2OS cells with or without the AURKB inhibitor ZM447439 (ZM). c Panels showing examples of increased multinucleated (arrow) caspase-2-deficient U2OS cells following AURKB inhibition. Scale bar, 50 µm. d Examples of caspase-2-mediated BID cleavage (appearance of truncated BID, tBID) following treatment with a PLK1 inhibitor, BI2536 (BI), which induces mitotic arrest. fl.; full-length, cl.; cleaved, p33 and p18; cleaved caspase-2. The data and images in b–d were generated by Yoon Lim.