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Fig. 1 | Acta Neuropathologica Communications

Fig. 1

From: C1q-targeted inhibition of the classical complement pathway prevents injury in a novel mouse model of acute motor axonal neuropathy

Fig. 1

Comparison of ganglioside expression and localisation in wild type and novel GalNAcT−/−(Tg-neuronal) mice that exclusively express complex gangliosides in neurons. a Enzyme activity assays showed a restoration of GalNAcT activity to ~50 % in 2 different GalNAcT −/− -Tg(neuronal) lines compared to wild type (n = 3/genotype). The dashed line represents the threshold level of activity for the assay therefore GalNAcT −/− falls below this and is essentially zero despite minimal value. b Ganglioside biosynthetic pathway. The GalNAcT enzyme is necessary for generation of complex gangliosides (surrounded by the green box). c Brain extracts from wild type, GalNAcT −/− and 2 strains of GalNAcT −/− -Tg(neuronal) were probed with anti-GM1 IgG antibody, DG2. This antibody bound all genotype extracts except for GalNAcT −/− which lack complex gangliosides including GM1. GM1 lipid was printed on the left and provided a positive control for anti-GM1 antibody binding. d Axonal binding can be observed in the GalNAcT −/− -Tg(neuronal) mice treated with anti-GM1 antibody (arrows), while it bound to the terminal kranocyte (asterisk) in wild type mice and was absent in GalNAcT−/− tissue. Anti-GQ1b/GD3 antibody bound similarly in both strains along the axons and on the perisynaptic Schwann cell membranes (arrowheads) that are simple ganglioside GD3 positive. Scale bar = 10 μm

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