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. 2020 Apr 22;17:56. doi: 10.1186/s12985-020-01323-z

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© The Author(s) 2020

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. 1 — TMPRSS2 cleaves H2-HA. Human embryonic kidney 293 T cells were cotransfected with plasmids encoding H2-HA and plasmids encoding TMPRSS2 of murine origin or empty plasmid (Mock) as negative control. At 48 h post transfection, cells were harvested and treated with either PBS or TPCK trypsin followed by analysis of HA expression by immunoblot, using antiserum raised against H2-HA. Detection of β-actin (ACTB) served as loading control. The results were confirmed in an independent experiment. The black arrow indicates uncleaved HA₀ (HA0), the grey arrow indicates cleaved HA₁ (HA1)