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. 2015 Nov 10;3:69. doi: 10.1186/s40478-015-0248-5

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© Makarava et al. 2015

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 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.

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Fig. 4 — 2D analysis of sialylation status of PrP^Sc and atypical PrPres. 2D analysis of charge distribution of S05 brain-derived PrP^Sc (a) and atypical PrPres from animals inoculated with F^0.5 fibrils (b, upper panel), atypical PrPres induced in animals by inoculating brain-derived atypical PrPres amplified in dgPMCAb (b, middle panel), or asymptomatic S05 animals that lacked PrP^Sc (b, lower panel). Black triangles, white triangles and arrows mark di-, mono-, and unglycosylated glycoforms, respectively. The distributions of all three glycoforms of atypical PrPres are shifted toward acidic pH relative to those of PrP^Sc due to differences in number of charged amino acid residues and, accordingly, pIs between atypical PrPres and PrP^Sc. All samples were treated with PK. Western blots were stained with 3F4 (a) and SAF-84 (b)