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. 2017 May 19;7:2155. doi: 10.1038/s41598-017-02204-2

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© The Author(s) 2017

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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CXCR4 interactions with FAK were inhibited by ASK1. Panel A Cell lysates were collected from MLE-12 cells with control shRNA, ASK1-shRNA, or PP5-shRNA, immunoprecipitated with a FAK antibody, and immunoblotted for CXCR4 or FAK. Decreased expression of ASK1 caused a significant increase in CXCR4 associated with FAK as indicated by densitometry analysis (right panel), but decreased expression of PP5 did not affect the interaction (n = 3). Panel B CXCR4 interaction with FAK was significantly increased in cell lysates from ATII cells from ASK1−/− mice compared with cells from wild type (wt) mice (n = 5). Asterisks (*) indicate a significant difference compared to control (control-shRNA or wild type); p < 0.05. Total FAK was immunoblotted as a loading control. Each set of bands shown was cropped from the same blot, and the full-length blots were provided in supplemental data.