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. 2021 Jun 23;4:777. doi: 10.1038/s42003-021-02337-1

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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. 3 — a Schematic representation of PI-PLC activity against GPI-APs. The remodeled mature GPI-APs on the cell surface in WT cells are cleaved by PI-PLC and released from the plasma membrane. On the other hand, the inositol-acylated GPI-APs in PGAP1-KO cells show resistance to PI-PLC. b PI-PLC sensitivity of CD55, CD59, and prion. WT and KO cell lines were treated with and without PI-PLC. The residual amounts of CD55, CD59, and prion on the cell surface after PL-PLC treatment were analyzed by flow cytometry. The ratio of remaining GPI-APs was calculated and is shown as the mean ± SD from three independent experiments.