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. 2018 Mar 19;9(4):423. doi: 10.1038/s41419-018-0462-8

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© The Author(s) 2018

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. 4 — a, b Hela and HepG2 cells were transfected with PIWIL2, shPIWIL2 or control vectors, respectively, followed by western blotting with antibody against P-HDAC3. c Treatment with CK2 inhibitor TBB abolishes the up-regulation of P-HDAC3 by PIWIL2. Hela cells transfected with PIWIL2 vector or control vector were treated with CK2 inhibitor TBB, PI3K inhibitor LY294002 or GSK3β inhibitor TWS119 for 6 h. d Knockdown of CK2 (shCK2α and shCK2α’) blocks PIWIL2 from upregulating P-HDAC3