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Suppression of GSK3β by ERK mediates lipopolysaccharide induced cell migration in macrophage through β-catenin signaling

机译:ERK对GSK3β的抑制通过β-catenin信号传导介导脂多糖诱导的巨噬细胞迁移

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We investigate the role of β-catenin signaling in the response of macrophage to lipopolysaccharide (LPS) using RAW264.7 cells. LPS rapidly stimulated cytosolic β-catenin accumulation. β-catenin-mediated transcription was showed to be required for LPS induced gene expression and cell migration. Mechanically, ERK activation-primed GSK3β inactivation by Akt was demonstrated to mediate the LPS induced β-catenin accumulation. Overall, our findings suggest that suppression of GSK3β by ERK stimulates β-catenin signaling therefore contributes to LPS induced cell migration in macrophage activation.
机译:我们调查了使用RAW264.7细胞的巨噬细胞对脂多糖(LPS)的反应中β-catenin信号的作用。 LPS迅速刺激了胞质β-catenin的积累。已证明,LPS诱导的基因表达和细胞迁移需要β-catenin介导的转录。在机械上,由Akt引发的ERK激活引发的GSK3β失活被证明介导LPS诱导的β-catenin积聚。总体而言,我们的发现表明,ERK对GSK3β的抑制作用会刺激β-catenin信号传导,从而有助于LPS诱导的巨噬细胞活化细胞迁移。

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