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. 2022 Nov 11;29:95. doi: 10.1186/s12929-022-00877-0

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© The Author(s) 2022

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 9 — Schematic summary of thrombin-induced IL-8/CXCL8 expression signaling pathway involving DCLK1 in lung epithelial cells. It has previously been revealed that thrombin-induced ERK activation increases IKKα/β phosphorylation, which promotes p65 to translocate to the nucleus from the cytosol, resulting in IL-8/CXCL8 expression. In this report, DCLK1 is involved in thrombin-induced IL-8/CXCL8 expression via ERK and then mediates the activation of RhoA and YAP. Once YAP is activated, it moves to nucleus from cytosol, where it binds to the transcription factor p65, increasing IL-8/CXCL8 expression in human lung epithelial cells. This image was created with BioRender (https://biorender.com/)