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Fig. 6 Working model for how Cu2+ induces myofibrillogenesis defects. Cu2+ overload in the embryonic cells of Cu2+-stressed embryos and larvae led to the downregulation of the smyd1b-H3K4me3 signaling axis and changed the promoter methylation level of gene smyd5. The downregulated expression of smyd1b and the up-regulated expression of smyd5 might contribute jointly to the occurrence of muscle fiber specification defects in Cu2+-stressed embryos and larvae
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Full text @ FASEB J.