摘要
Toll样受体 (TLR)介导着绝大部分哺乳动物、昆虫及植物的宿主防御 .TLR4与配体结合涉及膜抗原CD14和分泌蛋白MD 2的调节并一起形成受体复合物 ,然后与接头分子MyD88结合 ,使IRAK磷酸化 ,再使TRAF6寡聚化 ,随后激活控制着各种效应基因表达的转录因子NF κB .
The most ancient host defense system found in mammals, insects and plants are mediated by Toll-like receptors (TLRs) and its associated signaling pathways of NK-kappaB. Signaling pathways of downstream of TLR2 or TLR4 complex which includes ligands (LPS or another), CD14 or/and MD-2 and receptor itself recruit MyD88 to activate the autophosphorylation of IRAK. The oligomerization of TNF receptor-associated factor 6 (TRAF6) is necessary to initiate the activation of NF-kappaB-inducing kinase (NIK) which finally leads to the activation of NF-kappaB via the Toll/IL-1-receptor homologous region (TIR) domain.
出处
《生物化学与生物物理进展》
SCIE
CAS
CSCD
北大核心
2001年第3期304-308,共5页
Progress In Biochemistry and Biophysics
基金
国家自然科学基金资助项目 (39970 0 4 1 )&&
关键词
病原识别
TOLL样受体
信号转导
pathogen recognition
TLRs
IL-1R1
signaling transduction
