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Fig. 4 | Molecular Neurodegeneration

Fig. 4

From: Pathogenic LRRK2 variants are gain-of-function mutations that enhance LRRK2-mediated repression of β-catenin signaling

Fig. 4

Lrrk2 knockout mice display elevated β-catenin levels in the brain. Whole brain lysates from aged-matched Lrrk2 knockout (KO) and wild-type (WT) male mice were resolved by SDS-PAGE and blotted, as indicated, for Lrrk2, β-catenin and β-actin as a loading control. a Shows representative images for 3 wild-type and 3 knockout mice. b Mean β-catenin/β-actin ratios for ten wild-type and 11 knockout mice, ± the standard error of the mean. These calculations revealed significantly increased β-catenin levels in Lrrk2 knockout mouse brains (t-test, p = 0.015). c Graphical illustration of ECT assays. Immobilised E-cadherin cytosolic tail protein (green) bound to beads can be used to affinity purify free β-catenin (red) from complexed β-catenin in lysates. d, e ECT assays of lysates from male and female Lrrk2 knockout and heterozygous brains reveal increased free β-catenin in knockout brains with intermediate levels in heterozygotes. f Analysis of all ECT data by 2-way ANOVA followed by Bonferroni post-hoc testing reveals significant effects of Lrrk2 deficiency on free β-catenin levels in the brain

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Molecular Neurodegeneration

ISSN: 1750-1326