Toll‐like receptor 2 (TLR2) mediates activation of stress‐activated MAP kinase p38
Toll‐like receptor 2 (TLR2) mediates activation of stress‐activated MAP kinase p38
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DOI：
10.1189/jlb.71.3.503
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发表时间：
2002-03
影响因子：
5.5
通讯作者：
T. Vasselon;W. Hanlon;S. Wright;P. Detmers
中科院分区：
文献类型：
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作者：
T. Vasselon;W. Hanlon;S. Wright;P. Detmers
细胞对脂多糖（LPS）反应的早期事件包括NF-κB和应激激活的MAP激酶p38的激活。最近的研究表明，人Toll样受体2（TLR 2）介导NF-κB活化，以响应LPS（comLPS）、膜脂蛋白和革兰氏阳性细菌产物的商业制剂。在这里，我们表明，TLR 2在人胚肾293细胞中的表达使p38磷酸化，以响应comLPS，一种合成的细菌脂蛋白，和B。枯草杆菌。通过使用ATF 2作为底物的体外激酶试验和测量细胞中p38下游效应物MAP激酶活化蛋白激酶的活化的试验证实了p38的活化。因此，TLR 2启动了p38的信号通路，以响应细菌产物。
Early events in the response of cells to lipopolysaccharide (LPS) include activation of NF‐κB and stress‐activated MAP kinase p38. Recent studies have shown that the human Toll‐like receptor 2 (TLR2) mediates activation of NF‐κB in response to commercial preparations of LPS (comLPS), membrane lipoproteins, and Gram‐positive bacterial products. Here, we show that expression of TLR2 in human embryonic kidney 293 cells enabled p38 phosphorylation in response to comLPS, a synthetic bacterial lipoprotein, and B. subtilis. Activation of p38 was confirmed by an in vitro kinase assay using ATF2 as substrate and by an assay measuring activation of the downstream effector of p38, MAP kinase‐activated protein kinase in cells. Thus, TLR2 initiated the signaling pathway for p38 in response to bacterial products.