Figures
In Figs 3–7, there are incorrect symbols in the labels. Please view the correct figures here.
(A) Hemizygous A53T α-syn transgenic mouse brain samples of 6, 9 and 12 months old were analyzed with in vivo biotin-switch assay for GRK6, CK2α and GAPDH. The samples were also subject to Western blot analysis of GRK6, CK2α, GAPDH, pSer129 α-syn and α-syn. (→: GRK6 band) (B) Quantification of hemizygous A53T α-syn transgenic mouse brain samples for in vivo CK2α S-nitrosylation as in (A) (* p < 0.05, ** p < 0.01; # of animals = 3 for each time point; one-way ANOVA with Bonferroni post-hoc test). (C) Quantification of hemizygous A53T α-syn transgenic mouse brain samples for in vivo GRK6 S-nitrosylation as in (A) (* p < 0.05; # of animals = 3 for each time point; one-way ANOVA with Bonferroni post-hoc test). (D) Quantification of hemizygous A53T α-syn transgenic mouse brain samples for in vivo GAPDH S-nitrosylation as in (A) (* p < 0.05; # of animals = 3 for each time point; one-way ANOVA with Bonferroni post-hoc test). (E) Quantification of hemizygous A53T α-syn transgenic mouse brain samples for protein levels of pSer129 α-syn as in (A) (# of animals = 3 for each time point). (F) Quantification of hemizygous A53T α-syn transgenic mouse brain samples for protein levels of α-syn as in (A) (# of animals = 3 for each time point).
(A) WT, and hemizygous A53T α-syn transgenic mouse brain samples of 9 months old treated with or without L-NNA were analyzed with in vivo biotin-switch assay for CK2α and GAPDH. The samples were also subject to Western blot analysis of CK2α, GAPDH, pSer129 α-syn and α-syn. (→: GRK6 band) (B) Quantification of WT and hemizygous A53T α-syn transgenic mouse brain samples for in vivo CK2α S-nitrosylation as in (A) (* p < 0.05; no. of animals = 3 in each group; two-way ANOVA with Bonferroni post-hoc test). (C) Quantification of WT and hemizygous A53T α-syn transgenic mouse brain samples for in vivo GRK6 S-nitrosylation as in (A) (* p < 0.05; # of animals = 3 in each group; two-way ANOVA with Bonferroni post-hoc test). (D) Quantification of WT and hemizygous A53T α-syn transgenic mouse brain samples for in vivo GAPDH S-nitrosylation as in (A). (E) Quantification of WT and hemizygous A53T α-syn transgenic mouse brain samples for protein levels of pSer129 α-syn as in (A) (# of animals = 3 in each group). (F) Quantification of WT and hemizygous A53T α-syn transgenic mouse brain samples for protein levels of α-syn as in (A) (# of animals = 3 in each group).
(A) Hemizygous A53T α-syn transgenic mouse brain (A53T -/+), and hemizygous A53T α-syn transgenic and nNOS heterozygous knockout (A53T -/+; nNOS -/+) double mutant mouse brain samples at 6-month-old were analyzed with in vivo biotin-switch assay for CK2α and GAPDH. The samples were also subject to Western blot analysis of CK2α, GAPDH, pSer129 α-syn and α-syn. (→: GRK6 band) (B) Quantification of CK2α, GRK6 and GAPDH S-nitrosylation and protein levels of pSer129 α-syn and α-syn as in (A) (* p<0.05; # of animals = 3 in each group; Student’s t-test).
(A) Hemizygous A53T α-syn transgenic mouse brain (A53T -/+), and hemizygous A53T α-syn transgenic and nNOS heterozygous knockout (A53T -/+; nNOS -/+) double mutant mouse brain samples at 9-month-old were analyzed with in vivo biotin-switch assay for CK2α and GAPDH. The samples were also subject to Western blot analysis of CK2α, GAPDH, pSer129 α-syn and α-syn. (→: GRK6 band) (B) Quantification of CK2α, GRK6 and GAPDH S-nitrosylation and protein levels of pSer129 α-syn and α-syn as in (A) (*** p<0.001; ** P<0.01; # of animals = 3 in each group; Student’s t-test).
(A) Hemizygous A53T α-syn transgenic mouse brain (A53T -/+), and hemizygous A53T α-syn transgenic and nNOS heterozygous knockout (A53T -/+; nNOS -/+) double mutant mouse brain samples at 12-month-old were analyzed with in vivo biotin-switch assay for CK2α and GAPDH. The samples were also subject to Western blot analysis of CK2α, GAPDH, pSer129 α-syn and α-syn. (→: GRK6 band) (B) Quantification of CK2α, GRK6 and GAPDH S-nitrosylation and protein levels of pSer129 α-syn and α-syn as in (A) (* p<0.05; ** p<0.01; # of animals = 4 in each group; Student’s t-test).
Reference
- 1. Wu W, Sung CC, Yu P, Li J, Chung KKK (2020) S-Nitrosylation of G protein-coupled receptor kinase 6 and Casein kinase 2 alpha modulates their kinase activity toward alpha-synuclein phosphorylation in an animal model of Parkinson’s disease. PLoS ONE 15(4): e0232019. https://doi.org/10.1371/journal.pone.0232019 pmid:32343709
Citation: Wu W, Sung CC, Yu P, Li J, Chung KKK (2020) Correction: S-Nitrosylation of G protein-coupled receptor kinase 6 and Casein kinase 2 alpha modulates their kinase activity toward alpha-synuclein phosphorylation in an animal model of Parkinson’s disease. PLoS ONE 15(6): e0235296. https://doi.org/10.1371/journal.pone.0235296
Published: June 18, 2020
Copyright: © 2020 Wu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.