《生命科学》 2006, 18(4):

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：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: 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