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. 2022 Mar 22;12:36. doi: 10.1186/s13578-022-00770-1

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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. 3 — SARS-CoV-2 NSP13 suppresses type I and II IFN signaling by preventing STAT1 phosphorylation. HEK293T cells were transfected with an expression plasmid for V5-tagged NSP13. A At 48 h post transfection, cells were stimulated by 1000 U/mL of IFN-β. B Cells were treated with 100 ng/mL of IFN-γ. At 10- and 20-min post IFN treatment, cell lysates were collected and analyzed by Western blotting with the indicated antibodies. C Experiment in A was repeated with FLAG-tagged NSP13. At 30 and 45 min post IFN-β treatment, cell lysates were collected and analyzed by Western blotting. Relative ratios of pSTAT1 versus total STAT1, pSTAT2 versus total STAT2 and pJAK1 versus total JAK1 were determined by densitometry and are indicated below the blots. pSTAT1: phospho-STAT1. pSTAT2: phospho-STAT2. pJAK1: phospho-JAK1. Results were representative of three independent experiments