Bidirectional regulation of neutrophil migration by mitogen-activated protein kinases.
Bidirectional regulation of neutrophil migration by mitogen-activated protein kinases.
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DOI：
10.1038/ni.2258
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发表时间：
2012-03-25
影响因子：
30.5
通讯作者：
中科院分区：
文献类型：
--
作者：
为了杀死入侵的细菌，中性粒细胞必须解释空间线索，迁移并到达目标部位。尽管趋化性迁移的启动已经被广泛研究，但对其终止知之甚少。在这里，我们报告说，两个丝裂原活化蛋白激酶在中性粒细胞运输中发挥了相反的作用。细胞外信号调节激酶（Erk）增强G蛋白偶联受体激酶GRK2活性并抑制中性粒细胞迁移，而p38 MAPK作为非经典GRK，磷酸化甲酰肽受体FPR 1并通过阻断GRK2功能促进中性粒细胞迁移。因此，Erk和p38 MAPK之间的动态平衡控制着中性粒细胞的“停止”和“前进”行为，确保中性粒细胞精确地到达其最终目的地作为宿主防御的第一道防线。
To kill invading bacteria, neutrophils must interpret spatial cues, migrate, and reach target sites. Although initiation of chemotactic migration has been extensively studied, little is known about its termination. Here we report that two mitogen-activated protein kinases played opposing roles in neutrophil trafficking. The extracellular signal-regulated kinase (Erk) potentiated G protein-coupled receptor kinase GRK2 activity and inhibited neutrophil migration, whereas p38 MAPK acted as a non-canonical GRK that phosphorylated the formyl peptide receptor FPR1 and facilitated neutrophil migration by blocking GRK2 function. Therefore, the dynamic balance between Erk and p38 MAPK controls neutrophil “stop” and “go” behaviors, ensuring neutrophils precisely reach their final destination as the first line of host-defense.
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影响因子：
56.9
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通讯作者：
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