摘要
最近研究显示Toll样受体 4 (TLR4 )及其附属蛋白MD2介导内毒素 (LPS)信号 :LPS首先与LPS结合蛋白(LBP)结合 ,再传递给CD14分子 ,形成LPS/LBP/CD14复合物。该复合物与TLR4 MD2相互作用 ,激活胞内的几种信号通路 ,包括NF κB通路和 3种丝裂原活化蛋白激酶通路〔胞外信号调节激酶 (ERK)、c jun氨基末端激酶 (JNK)和p38〕 ,最后导致NF κB和AP 1(c fos/c jun)活化 ,诱导炎性细胞因子表达。
Recent evidence suggests Toll like receptor 4 (TLR4) and its accessory protein MD2 mediate endotoxin/lipopolysaccharide (LPS) signaling. LPS binds to LPS binding protein (LBP) in plasma and is delivered to CD14. Next, LPS is transferred to TLR4 MD2 complex. LPS activates several intracellular signaling pathways that include the NF κB pathway and three mitogen activated peotein kinase (MAPK) pathway: extracellular signal regulated kinase (ERK), c Jun N terminal kinase (JNK) and p38. These signaling pathways in turn activate NF κB and AP 1 (c fos/c jun), which coordinate the induction of many genes encoding inflammatory mediators. Targeting the signaling molecule in the pathway will develop new remedies for treatment of inflammatory disorder.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2002年第2期121-125,共5页
Chinese Pharmacological Bulletin
基金
国家自然科学基金资助重点项目 No 3 973 0 2 10