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. 2018 Jan 19;9(2):63. doi: 10.1038/s41419-017-0094-4

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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. 3 — a, b Co-IP assay showed the interaction between exogenous PPIL2 and SNAI1 in T47D cells. c,d Co-IP assay showed the interaction between endogenous PPIL2 and SNAI1 in T47D cells. e Co-IP assay showed that PPIL2 interacted with SNAI1 via its U-box domain in T47D cells. f Co-IP assay showed that SNAI1 interacted with PPIL2 via its N terminal in T47D cells. g The direct interaction between PPIL2 and SNAI1 was observed using mammalian two-hybrid system. h GST pull-down assay showed the interaction between GST-SNAI1 and endogenous PPIL2 in MCF cells. i Immunofluorescence showed that PPIL2 (red) and SNAI1 (green) colocalized in the nucleus of MCF-7 cells (20×)