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. 2021 Aug 13;12:4917. doi: 10.1038/s41467-021-25203-4

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© The Author(s) 2021

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 — Viral infection triggers the host pattern recognition receptors RIG-I and MDA5 to promote A3A expression through the stimulation of MAVS, IRF3, and STAT2. Alternatively, genotoxic stresses lead to the activation of the canonical NF-κB pathway to transiently upregulate A3A expression.