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Fig. 7 | Molecular Neurodegeneration

Fig. 7

From: Activation of zebrafish Src family kinases by the prion protein is an amyloid-β-sensitive signal that prevents the endocytosis and degradation of E-cadherin/β-catenin complexes in vivo

Fig. 7

Effect of Δ23-31 and ΔCR deletions on PrP activity. a. Mouse PrP deletion mutants. Protein domains are marked with different colors: SP = signal peptide, R = repetitive domain, H = hydrophobic stretch, G = globular domain; green triangles = GPI-anchor. b. Detection of mouse WT or mutant PrPs using the D18 anti-PrP antibody on 6 hpf embryo protein lysates. c. Phenotypic quantification of 7 hpf embryos co-injected with PrP-1 morpholinos and PrP mRNAs. d. Localization of mouse PrP constructs in the deep cells of 6 hpf embryos (6H4 anti-PrP antibody staining). Scale bar = 10 μm. e. Embryonic phenotypes upon expression of zebrafish (ZF) or mouse (mo) PrP mRNAs (7 hpf, lateral views); arrowheads show abnormal dorsal thickening; V = ventral, D = dorsal. f. Quantification of 7 hpf embryos with dorsoventral phenotypes upon expression of mouse PrPs. Mean values are shown in (c) and (f). g. MTT viability assay of HEK cells expressing mouse or zebrafish PrPΔCRs after Zeocin treatment. WB = Western blot; IF = immunofluorescence. Data are shown as the average percentage of A570 values in untreated cells ± SEM; statistical significance was assessed using unpaired, two-tailed t-tests, * = p ≤ 0.05, ** = p ≤ 0.01

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