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. 2020 Sep 16;11(9):763. doi: 10.1038/s41419-020-02945-5

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© The Author(s) 2020

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. 6 — a Subcellular fractionation assay for the MM2P location in RAW264.7 cells. b Pulldown assay was performed to verify the enrichment of STAT3 protein in the products pulled down by the MM2P biotin probe compared with the non-biotin probe. c RIP analysis confirmed the interaction between MM2P and STAT3. d FISH stain of MM2P and IF stain of STAT3 in M2 macrophages. Scale bar = 20 μm. e MM2P-pulldown assay for STAT3 enrichment after transfecting Flag-tagged STAT3 into IL-13/IL-4-induced M2 macrophages. f RIP analysis was used to detect the interaction between STAT3 and MM2P after adding S31–201 with indicated dose, the inhibitor of STAT3. g Co-IP assay was carried out in IL-13/IL-4-induced M2 macrophages to identify the binding of SHP2 or SHP1 with STAT3 after silencing MM2P. **P < 0.01. The error bar expressed as mean ± SD of three independent experiments in triplicates.