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. 2019 Dec 4;10(12):911. doi: 10.1038/s41419-019-2141-9

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© The Author(s) 2019

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. 2 — a GSEA indicated that genes, which are downregulated upon 17-AAG treatment are enriched in siUSP22 HCT116 and b HCC1954 cells. c Venn diagram displaying the overlap of HSP90i- and USP22 knockdown-responsive genes in HCT116 and HCC1954 cells. d The dependency of ABCE1, CYCS and EIF4A1 on HSP90 as well as USP22 was verified by treating HCT116 USP22^+/+ and USP22^−/− cells with the HSP90i Ganetespib or DMSO as a negative control. Mean ± SEM, one-way ANOVA. e ChIP-qPCR revealed in two independent experiments that the H3K9ac occupancy on the HSP90AB1 gene is significantly reduced upon the deletion of USP22 in HCT116 cells (n = 4). An adjacent H3K9ac-negative site was analyzed as a control. The average signal for the negative control IgG is represented by dotted lines. Mean ± SEM, t-test. f siRNA-mediated silencing of the acetyltransferase GCN5 reduced HSP90AB1 mRNA levels in HCT116 cells (n = 3). Mean ± SEM, t-test.