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. 2024 Jul 23;22:372. doi: 10.1186/s12964-024-01727-2

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© The Author(s) 2024

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 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. 2 — IAV infection activates TAK1. L929 (A) and LET1 (B) cells were infected with various MOI of H1N1 (PR8 strain) or H5N1 (SY strain) viruses for 18 h or with H1N1 virus (2 MOI) for the indicated lengths of time. Cell lysates were analyzed for the levels of TAK1, RIPK1^S321, and p38 phosphorylation and their corresponding total proteins by Western blot. The levels of NS1 and β-actin as a loading control were also detected