中国科技核心期刊
CN:31-1600/Q
ISSN:1004-0374
“健康与疾病的免疫”国际学术研讨会通知      关于有网站冒充本刊网站的声明
《生命科学》 2006, 18(4): 391-
选择性剪接在Toll样受体4信号转导通路中的作用
李洪忠,万敬员*,周岐新
重庆医科大学重庆市生物化学与分子药理学重点实验室, 重庆 400010
摘 要:Toll样受体4(Toll-like receptor4,TLR4)属于模式识别受体,可识别来自G-细菌细胞壁的脂多糖(lipopoly-saccharides,LPS),并通过MyD88依赖途径或MyD88非依赖途径进行信号转导,引发核因子-kB(NF-kB)和其他转录因子的表达,从而诱导细胞因子、化学趋化因子的产生,引起系统性炎症反应。选择性剪接是真核生物控制基因表达的一种重要机制,在TLR4通路中很多信号分子都存在着选择性剪接产生的异构体,且这些剪接异构体分子大都可负性调控TLR4信号转导通路。本文针对这方面的研究进展作一综述。
关键词:TLR4;脂多糖;信号转导;选择性剪接
 
The role of alternative splicing in the Toll-like receptor 4 signal transduction
LI Hong-Zhong, WAN Jing-Yuan*, ZHOU Qi-Xin
Chongqing Key Laboratory of Biochemistry and Molecular Pharmacology, Chongqing Unversity of Medical Sciences, Chongqing 400010, China
Abstract: Toll-like receptor4 (TLR4) is the primary recognition molecule for inflammatory responses initiated by bacterial lipopolysaccharides(LPS). After LPS is recognized by TLR4, the transcription factors such as nuclear factor-kB (NF-kB) can be expressed through MyD88-dependent pathway or MyD88-independent pathway subsequently, which can induce the cytokines production provoking systematical inflammatory reaction. Alternative splicing plays important roles in the eucaryotic gene expression, and a great deal of signaling molecules in the TLR4 passageway can be alternative spliced naturally. Furthermore, a majority of the isomerides can negatively modulate TLR4 signal transduction.
Key words: TLR4;lipopolysaccharides;signal transduction;alternative splicing
 
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