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. 2021 Aug 4;16:11. doi: 10.1186/s13062-021-00296-5

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© The Author(s) 2021

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 2 — Mutant p53 regulates a RCan2 expression via GOF effects. a Oncoprint diagram reports mutational status of RCan2 and NUAK2 in full cohort of TCGA PanCancer Atlas. b–d mRNA level of RCan2, NUAK2 and p53 in KPC²⁷⁰ cells following p53 silencing. e ChIP-seq profile of histone post-translational modifications, transcriptional factors binding in the genomic region of mouse RCan2. f ChIP-qPCR for p53 binding on peak 1 and peak 2 in KPC²⁷⁰ cells