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. 2021 Aug 12;11:16427. doi: 10.1038/s41598-021-95941-4

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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 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/.

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Interaction between p300 and Api5 stabilises Api5. (a) MCF7 cells treated with varying concentrations of CBP/p300 inhibitor C646 for 4 h were lysed and Api5 levels were analysed using western blotting. (b) Quantification showing the fold change in Api5 protein levels after normalisation with GAPDH. (a–d) Acetyl p53 and E2F1 were used as positive control for p300 inhibition. (e) API5 transcript levels upon C646 treatment was analysed using semi-quantitative PCR. (f) Quantification of transcript levels after normalising to GAPDH. MCF7 cells stably expressing mCherry-Api5 were lysed and immunoprecipitations were performed using (g) GFP and (h) p300-specfic antibodies.