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. 2018 Jan 17;9:254. doi: 10.1038/s41467-017-02408-0

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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. 8 — Model of how the ∆133p53 isoform regulates the JAK-STAT3 and RhoA-ROCK pathways to promote inflammation and invasion. Wt p53 is activated by some (as yet undefined) stress signal, which turns on ∆133p53. ∆133p53 increases IL-6, which, then binds to its receptor and signals through the JAK-STAT pathway to amplify the IL-6 signal further. The JAK-STAT pathway, now constitutively activated by ∆133p53, drives actin polarisation, cell migration via RhoA-ROCK signalling and alters migration of immune cells