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. 2021 Feb 3;11(4):365–377. doi: 10.1007/s13659-021-00298-w

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© The Author(s) 2021

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/.

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Fig. 6 — HNK functions as an inhibitor of sentrin-specific protease 1 (SENP1), an essential enzyme for deSUMOylating proteins. The noncovalent structure of SENP1 in complex with SUMO2 is shown (PDB: 6NNQ) [135]. Inhibition of SENP1 by HNK leads to an increased level of six major proteins component (Sm proteins) of the U2 snRNP complex in cells. By this process, HNK induces SUMOylation of splicing factors, thus preventing the correct assembly of the spliceosome and modulating pre-mRNA splicing [89]