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. 2023 Jan 9;21:3. doi: 10.1186/s12959-022-00443-6

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© The Author(s) 2023

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. 5 — Prediction of structures of antithrombin (AT) protein mutants. (a) Schematic representation of functional domains of AT proteins and their variants. (b) Three-dimensional crystal structure diagram of AT protein versus coagulation factor IX (FIX) in Swiss-model database; red represents AT protein, green FIX protein, and yellow Asn460 (https://swissmodel.expasy.org/repository/uniprot/P00740?template=3kcg). (c) Swiss-model prediction of the three-dimensional structure of the Asn460Thrfs*20 mutant, with the yellow site represents Asn460 and the green sequence as the amino acid sequence missing from the frameshift mutation. (d) The three-dimensional structure of the Asn460Thrfs*20 mutant was predicted by Alphafold2 software, and the green sequence was the amino acid sequence that was generated after frameshift. (e) The sequence in green is the sequence deleted by the nonsense mutation Arg229*. (f) The deletion protein structure of the nonsense mutation Arg229* resulted in the loss of the domain interacting with FIX (Ala414 site). (g) Alphafold2 predicts the tertiary structure of a truncated protein with the nonsense mutation Arg229*