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Fig. 7 | Acta Neuropathologica Communications

Fig. 7

From: CK2 alpha prime and alpha-synuclein pathogenic functional interaction mediates synaptic dysregulation in Huntington’s disease

Fig. 7

CK2α’ regulates phosphorylation of S129-α-syn and nuclear accumulation in symptomatic zQ175 mice. A, pS129-α-syn (EP1536Y antibody) IB in the striatum of 12-month-old WT, zQ175 and SNCAKO (n = 4 mice/genotype). B, pS129-α-syn (81A antibody) IB in the striatum of patients with HD (Vonsattel grade 3 and 4, Harvard Brain Tissue Resource Center) compared to age and sex matched controls. GAPDH is used as loading control. C, pS129-α-syn protein levels (combined grades 3 and 4) analyzed by Image J from images in (B). D, pS129-α-syn IF (81A antibody) in the dorsal striatum of 12-month-old WT, zQ175 and zQ175:CK2α’(±) (n = 3 mice/genotype), Scale bar, 20 μm. E, pS129-α-syn fluorescence signal was calculated using Image J from images in D (n = 3 mice/genotype, at least 3 images averaged/mouse). F, Magnification of images in D, pS129-α-syn and EM48 colocalization in zQ175 and zQ175:CK2α’(±). G, Quantification of pS129-α-syn and EM48 colocalized puncta using Image J puncta plug in (n = 3 mice/group, at least 3 images averaged/mouse). All data are mean ± SEM. Statistical analyses were conducted by one-way ANOVA. H, Working model for the role of CK2α’ in the regulation of pS129-α-syn and HD-like phenotype

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