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. 2021 May 24;7:37. doi: 10.1038/s41421-021-00279-w

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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. 6 — Our data support a model in which: (Left) at the cell surface, SARS-CoV-2 entry relies on LSD1-dependent demethylation of ACE2, which is required for ACE2/SARS-CoV-2 spike binding. LSD1 inhibition therefore reduces viral entry via ACE2, especially LSD1 catalytic inhibitors such as GSK. In addition, our novel ACE2 peptide inhibitors, which compete with binding to SARS-CoV-2 spike protein, also block viral replication. (Right) Intracellularly, NACE2i blocks LSD1/ACE2 binding at cytoplasmic tail, and this change in protein–protein interactions might consequently inhibit LSD1’s demethylation activity. IMPα binds to the cytoplasmic tail of non-methylated ACE2 to mediate nuclear translocation and Pol II association to regulate gene expression. Therefore, NACE2i blocking IMPα/ACE2 binding impact ACE2-Pol II nuclear co-localization, which is required for SARS-CoV-2-related transcription, to reduce viral replication.