CAJ | 학술논문

背景细菌脂多糖(lipopolysaccharide,LPS)可激活细胞合成和释放多种细胞因子,导致全身炎症反应.LPS识别及跨膜信号转导是引起细胞效应的关键,成为近年的研究热点.目的对新近提出的“LPS受体簇”理论和大电导Ca2+激活K+通道(MaxiK)在LPS信号识别中的作用研究进展进行综述.内容 LPS与CD14结合后,不同的信号分子在脂质筏内聚集,LPS被释放到脂质双分子层,并与由多种受体分子组成的受体簇相互作用.根据不同的细胞类型和细菌刺激,形成了不同的LPS受体簇.MaxiK通道在LPS诱导的巨噬细胞信号转导过程的早期即被激活.并且以IκB-α/NF-κB为中心的促炎症反应依赖MaxiK的功能.趋向需要进一步研究来阐明LPS受体簇在细胞膜特定区域内形成的确切分子机制,以及组成受体簇的几种蛋白分子在刺激识别和信号转导过程中的作用.
배경 세균지다당(lipopolysaccharide,LPS)가격활세포합성화석방다충세포인자,도치전신염증반응.LPS식별급과막신호전도시인기세포효응적관건,성위근년적연구열점.목적 대신근제출적“LPS수체족”이론화대전도Ca2+격활K+통도(MaxiK)재LPS신호식별중적작용연구진전진행종술.내용 LPS여CD14결합후,불동적신호분자재지질벌내취집,LPS피석방도지질쌍분자층,병여유다충수체분자조성적수체족상호작용.근거불동적세포류형화세균자격,형성료불동적LPS수체족.MaxiK통도재LPS유도적거서세포신호전도과정적조기즉피격활.병차이IκB-α/NF-κB위중심적촉염증반응의뢰MaxiK적공능.추향 수요진일보연구래천명LPS수체족재세포막특정구역내형성적학절분자궤제,이급조성수체족적궤충단백분자재자격식별화신호전도과정중적작용.
Background Bacterial lipopolysaccharide(LPS) induces cytokine synthesis and secretion in cells,subsequently resulting in systemic inflammatory response.The LPS receptor recognition and transmembrane signal transduction play a key role in LPS-induced cell activation. Objective To review a novel theory of LPS receptor activation cluster and the role of largeconductance Ca2+-activated potassium channel (MaxiK) in LPS recognition.Content Following ligation of CD14 by LPS,different signaling molecules are recruited at the site of the ligation within lipid rafts,where LPS is then briefly released into the lipid bilayer and finally interacts with a complex of receptors.Depending on the cell type and the bacterial stimulus,different LPS receptor clusters can be formed.The activation of the MaxiK channel is an early step in LPS-induced transmembrane signal transduction in macrophages.And the central IκB-α/NF-κB-dependent proinflammatory pathway depends on the function of MaxiK channel in macrophages.Trend The molecular mechanism of LPS receptor recruitment to specific membrane domains is not well understood.The signaling complex appears to recruit several accessory proteins with yet mostly unknown functions for the process of stimulus recognition and signal transduction.