Fig. 10: GrK induces tau hyperphosphorylation and alteration of signaling pathways in human neuronal cells via PAR-1. | Nature Communications

Fig. 10: GrK induces tau hyperphosphorylation and alteration of signaling pathways in human neuronal cells via PAR-1.

From: CD103–CD8+ T cells promote neurotoxic inflammation in Alzheimer’s disease via granzyme K–PAR-1 signaling

Fig. 10

a–c Bar plots and representative images showing tau phosphorylation levels on serine and threonine (AT8, AT100) (d, e) and only threonine (AT180) (f) residues in differentiated SH-SY5Y cells cultured alone (Ctrl–), in the presence of 100 nM SCH79797, in the presence of 150 nM active GrK alone, and the presence of both. Data are means ± SD of three independent experiments (two-way ANOVA-multiple comparisons). Scale bar = 5 µm. d ELISA showing the levels of phosphorylation on the pS199, pS396, and pT231 residues of tau protein in differentiated SH-SY5Y cells cultured alone (Ctrl–), in the presence of 100 nM SCH79797, in the presence of 150 nM active GrK alone, and in the presence of both. Data are means ± SD of three independent experiments. P-values are based on two-way ANOVA multiple comparisons. e, f Protein enrichment analysis from three independent proteomic experiments showing the best enriched clusters of terms (h) and terms belonging to the “Alzheimer’s/neurodegeneration” and “kinase” pathways (i) in SH-SY5Y human neuroblastoma cells cultured in the absence of GrK and SCH79797 (Ctrl–), in the presence of 100 nM SCH79797 alone, in the presence of 150 nM active GrK alone, and in the presence of both. Source data are provided as a Source Data file.

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