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. 2015 Mar 20;22(9):772–784. doi: 10.1089/ars.2014.6032

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Copyright 2015, Mary Ann Liebert, Inc.

© Lisa Gasperini et al. 2015; Published by Mary Ann Liebert, Inc. This Open Access article is distributed under the terms of the Creative Commons Attribution Noncommercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited.

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FIG. 1. — In adult Prnp^0/0 hippocampus, the S-nitrosylation of GluN2A and GluN1 NMDAR subunits is lower compared to wild type. (A) Signals of S-nitrosylated fraction, controls without either biotin or ascorbate and corresponding input of GluN2A, GluN1, and β-actin resulting from the biotin switch assay of Prnp^+/+ and Prnp^0/0 hippocampus; controls without either biotin or ascorbate were done using Prnp^+/+ samples. (B) Statistical analysis of S-nitrosylated GluN2A and GluN1 signals normalized on the corresponding input and on β-actin; all error bars indicate SD; **p<0.01; ***p<0.001. NMDAR, N-methyl-d-aspartate receptors.