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Fig. 6 | Journal of Neuroinflammation

Fig. 6

From: Interleukin-1β drives NEDD8 nuclear-to-cytoplasmic translocation, fostering parkin activation via NEDD8 binding to the P-ubiquitin activating site

Fig. 6

IL-1β increases P-Parkin in a GSK3β-dependent manner. IL-1β-treated NT2 cells have increased levels of GSK3β (a, p = 4.6 × 10− 9) and elevated GSK3β-activation, demonstrated (b) via decrease in P-GSK3β (p = 1.2 × 10− 8) and quantified in (c). Western immunoblot analysis of NT2 cells treated with a recognized inhibitor of GSK3β attenuates IL-1β-induced parkin phosphorylation (d). Western immunoblot quantification shows a significant decrease in P-parkin levels in NT2 cells treated with GSK3β inhibitor before IL-1β treatment compared with IL-1β treatment alone (p = 0.003, one-way ANOVA, significance determined with Bonferroni-corrected α = 0.016), quantified in (e). siRNA inhibition of GSK3β in NT2 cells attenuated IL-1β-induced parkin phosphorylation (f). Quantification of P-parkin levels demonstrates that GSK3β knockdown attenuates IL-1β upregulation of parkin activation (p = 0.046, one-way ANOVA, significance determined with Bonferroni-corrected α = 0.016) quantified in (g)

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