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. 2023 Sep 4;21:227. doi: 10.1186/s12964-023-01247-5

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© The Author(s) 2023

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. 4 — Binding of different death receptors to ligands and downstream signal transduction. Fas and FasL combine to activate downstream FADD and cause caspase activation. TNFR binds to TNFR1 to recruit TRADD, and post-translational modification of RIPK1 determines cell apoptosis. DR4 and DR5 are involved in an external pathway mediating caspase-8 activation