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Fig. 5 | Epigenetics & Chromatin

Fig. 5

From: Ethionine-mediated reduction of S-adenosylmethionine is responsible for the neural tube defects in the developing mouse embryo-mediated m6A modification and is involved in neural tube defects via modulating Wnt/β-catenin signaling pathway

Fig. 5

Ethionine suppresses Wnt/β-catenin signaling pathway by deleting Mettl3 gene and overexpressing Alkbh5 gene. A, B Western blot analysis of the protein levels of total β-catenin, Axin-2, and TCF-4 in E10.5 embryos. Bar graphs for protein abundance were quantitative data from three independent experiments. β-Tubulin was used as a loading control. C, D Western blot analysis of the protein levels of total CyclinD1 and C-myc in E10.5 embryos. Bar graphs for protein abundance were quantitative data from three independent experiments. β-Tubulin was used as a loading control. EH Representative micrographs of immunofluorescent staining for β-catenin (green), TCF-4 (green), and CyclinD1 (red) to determine whether SAM activated Wnt/β-catenin signaling pathway (E). Nuclei stained blue with DAPI. The percentage of β-catenin-positive cells (F), TCF-4-positive cells (G), CyclinD1-positive cells (H) in each region is shown. I, J Western blot analysis of the protein levels of total β-catenin, CyclinD1 and C-myc in HT-22 cells treated with SiMettl3 and SiNc. Bar graphs for protein abundance were quantitative data from three independent experiments. K, L Western blot analysis of the protein levels of total β-catenin, CyclinD1 and C-myc in HT-22 cells treated with control OE and Alkbh5 OE. Bar graphs for protein abundance were quantitative data from three independent experiments. * indicated significant differences (p < 0.05) and ** indicated significant differences (p < 0.01) compared to the other groups in one-way ANOVA followed by Tukey tests

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