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. 2021 Jun 12;12(6):609. doi: 10.1038/s41419-021-03895-2

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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. 7 — a–b RNA-pulldown assay verifies lincZNF337-AS1 binding to KAT5, not KAT3. c RIP-qPCR assay verifies lincZNF337-AS1 binding to KAT5, not KAT3. d Co-IP assay identifies the interaction between H2A.Z and KAT5 in HCC cell lines. e Identification of KAT5 gene knockdown effect by western blot. f, i The effect of knockdown KAT5 and lincZNF337-AS1 on H2A.Z acetylation detected by Co-IP assay. h RNA-pulldown assay verifies the binding site of lincZNF337-AS1 to KAT5 in HepG2 and MHCC-97H cell lines. The data are expressed in terms of mean ± SD (Student’s t-test used in Fig c and g; ****P < 0.0001; n = 3 in each group).