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. 2019 Nov 26;5:57. doi: 10.1038/s41421-019-0126-6

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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. 5 — Both WT and mutant HA-tagged VAV2 (a) and myc-tagged IQGAP1 (b) were expressed in HEK293 and HeLa cells, as indicated. The activation status of MAPK and PI3K/AKT pathways were determined by detecting the levels of phosphorylated ERK (p-ERK) and AKT (p-AKT). The relative fold change of p-ERK and p-AKT in the VAV2- and IQGAP1-expressed cells to that in the cells expressing empty vectors were calculated by normalizing to the total ERK and AKT expression levels respectively