13024_2017_153_MOESM1_ESM.pdf (46.74 kB)

Additional file 1: Figure S10. of Pathogenic LRRK2 variants are gain-of-function mutations that enhance LRRK2-mediated repression of β-catenin signaling

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journal contribution
posted on 19.01.2017, 05:00 by Daniel Berwick, Behzad Javaheri, Andrea Wetzel, Mark Hopkinson, Jonathon Nixon-Abell, Simone Grannò, Andrew Pitsillides, Kirsten Harvey
Kinase-dead but not GTP-non-binding mutations weaken basal Wnt signalling. Lrrk2 knockout (KO) cells were transfected with TOPflash or FOPflash plus wild-type LRRK2 or the indicated LRRK2 mutant. 1-way ANOVA (n = 12–15, F = 7.449, p < 0.001) followed by 2-sided Dunnett’s post-hoc analysis indicate that kinase-dead mutations significantly weaken canonical Wnt signalling relative to wild-type LRRK2 (1994, p < 0.05; 2017, p < 0.05). Mutations used: kinase-dead: 1994 = D1994A, 2017 = D2017A; guanyl nucleotide-non-binding: KA = K1347A, TN = T1348N. (PDF 46 kb)


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