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. 2019 Jan 31;294(13):5198–5207. doi: 10.1074/jbc.RA118.006601

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© 2019 Frossi et al.

Published under exclusive license by The American Society for Biochemistry and Molecular Biology, Inc.

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Figure 3. — Re-expression of APE1^WT but not APE1^C65S or APE1^E96A mutant forms restores the ability of APE1-null CH12F3 cells to undergo isotype switching. A–C, representative dot plots (A), percentages of CD19/IgA double-positive cells (B), and amounts of released IgA (C) by switching CH12F3 APE1^+/+/Δ and CH12F3 APE1^Δ/Δ/Δ cells under CIT(−) and CIT(+) conditions. D–F, representative dot plots (D), percentages of GFP/IgA double-positive cells (E), and amounts of released IgA (F) by CH12F3 APE1^+/+/Δ transfected with empty vector or with GFP-APE1^WT, APE1^C65S, or APE1^E96A mutant forms and induced toward IgA switching. G–I, representative dot plots (G), percentages of GFP/IgA double-positive cells (H), and amounts of released IgA (I) by CH12F3 APE1^Δ/Δ/Δ transfected with empty vector, GFP-APE1^WT, APE1^C65S, or APE1^E96A mutant forms and induced toward IgA switching. The data are representative of four independent experiments. *, p < 0.05; **, p < 0.005; ***, p < 0.001; ns, not significant.