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. 2017 Aug 29;7:9584. doi: 10.1038/s41598-017-09489-3

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© The Author(s) 2017

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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Spontaneous generation of human misfolded recombinant proteins. Graphical representation of the emergence of spontaneous protein misfolding evaluated through Western blot analysis in SDS-PAGE for each round of recPMCA (outlined as R01–R30). Different human recombinant proteins were grouped according to the substitution and the polymorphism at codon 129 and according to the disease [genetic Creutzfeldt-Jakob disease (gCJD), Gerstmann-Sträussler-Scheinker syndrome (GSS) and Fatal Familial Insomnia (FFI)] with which they are associated. Every experiment contained 4–5 tubes (intra-experimental replicates) and was performed in duplicate as shown. The percentage of positive tubes (tubes showing a protease resistant signal after digestion with 80 μg/ml of PK) after each round of recPMCA was noted with different intensities of grey, as shown in the legend below the figure. WT: wild type human rec-PrPs.