ERK 通过抑制 GSK3β 介导脂多糖诱导的巨噬细胞迁移及β-catenin 信号通路。
Suppression of GSK3β by ERK mediates lipopolysaccharide induced cell migration in macrophage through β-catenin signaling.
机构信息
Department of Biological Sciences and Biotechnology, Tsinghua University, Beijing, China.
出版信息
Protein Cell. 2012 Oct;3(10):762-8. doi: 10.1007/s13238-012-2058-x. Epub 2012 Sep 15.
Abstract
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.
摘要
我们使用 RAW264.7 细胞研究了β-连环蛋白信号在巨噬细胞对脂多糖（LPS）反应中的作用。LPS 迅速刺激细胞质β-连环蛋白的积累。研究表明，β-连环蛋白介导的转录对于 LPS 诱导的基因表达和细胞迁移是必需的。从机制上讲，我们证明 Akt 激活的 ERK 导致 GSK3β失活，从而介导 LPS 诱导的β-连环蛋白积累。总的来说，我们的发现表明 ERK 通过抑制 GSK3β 刺激β-连环蛋白信号，从而有助于 LPS 诱导的巨噬细胞激活中的细胞迁移。
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