Ligand-dependent Toll-like receptor 4 (TLR4)-oligomerization is directly linked with TLR4-signaling.

Saitoh S; Akashi S; Yamada T; Tanimura N; Matsumoto F; Fukase K; Kusumoto S; Kosugi A; Miyake K

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Ligand-dependent Toll-like receptor 4 (TLR4)-oligomerization is directly linked with TLR4-signaling.

机译：配体依赖性的Toll样受体4（TLR4）寡聚化与TLR4信号直接相关。

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Toll-like receptor 4 (TLR4) and MD-2 recognize lipid A, the active moiety of microbial lipopolysaccharide (LPS). Little is known about mechanisms for LPS recognition by TLR4/MD-2. We here showed, by using in vitro transfectants, ligand-induced TLR4-oligomerization, which required both membrane CD14 and MD-2. We previously reported that lipid IVa, a lipid A precursor, is agonistic on mouse TLR4/MD-2 but antagonistic on human TLR4/MD-2 and chimeric mouse TLR4/human MD-2. Lipid IVa triggered oligomerization of mouse TLR4/MD-2 but not human TLR4/MD-2 or chimeric mouse TLR4/human MD-2. Further, lipid IVa inhibited lipid A-dependent oligomerization of chimeric mouse TLR4/human MD-2. These results demonstrate that ligand-induced TLR4-oligomerization is directly linked with TLR4-signaling and suggest that MD-2 has an important role in regulating TLR4-oligomerization.

机译：Toll样受体4（TLR4）和MD-2识别脂质A，即微生物脂多糖（LPS）的活性部分。关于TLR4 / MD-2识别LPS的机制知之甚少。我们在这里通过使用体外转染子显示了配体诱导的TLR4-寡聚，这需要膜CD14和MD-2。我们先前曾报道脂质IVa（脂质A的前体）对小鼠TLR4 / MD-2具有拮抗作用，但对人TLR4 / MD-2和嵌合小鼠TLR4 /人MD-2具有拮抗作用。脂质IVa触发了小鼠TLR4 / MD-2的寡聚，但未引发人TLR4 / MD-2或嵌合小鼠TLR4 /人MD-2的寡聚。此外，脂质IVa抑制了嵌合小鼠TLR4 /人MD-2的脂质A依赖性寡聚。这些结果证明配体诱导的TLR4-寡聚化与TLR4-信号化直接相关，并且表明MD-2在调节TLR4-寡聚化中具有重要作用。

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《Journal of endotoxin research》 |2004年第4期|共4页
作者
Saitoh S; Akashi S; Yamada T; Tanimura N; Matsumoto F; Fukase K; Kusumoto S; Kosugi A; Miyake K;
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正文语种 eng
中图分类内科学;
关键词
Medial Dorsal Nucleus; Laboratory mice; Lipids; Toll-like receptor; Lipopolysaccharides; 脂类; 脂多糖类;

机译：Medial Dorsal Nucleus;Laboratory mice;Lipids;Toll-like receptor;Lipopolysaccharides;脂类;脂多糖类;

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专利

1. Ligand-dependent Toll-like receptor 4 (TLR4)-oligomerization is directly linked with TLR4-signaling. [J] . Saitoh S, Akashi S, Yamada T, Journal of endotoxin research . 2004,第4期

机译：配体依赖性的Toll样受体4（TLR4）寡聚化与TLR4信号直接相关。
2. Lipid A antagonist, lipid IVa, is distinct from lipid A in interaction with Toll-like receptor 4 (TLR4)-MD-2 and ligand-induced TLR4 oligomerization. [J] . Saitoh S, Akashi S, Yamada T, International immunology. . 2004,第7期

机译：脂质A拮抗剂脂质IVa在与Toll样受体4（TLR4）-MD-2和配体诱导的TLR4寡聚的相互作用中不同于脂质A。
3. Synthesis of anti-inflammatory alpha-and beta-linked acetamidopyranosides as inhibitors of toll-like receptor 4 (TLR4) [J] . Wipf Peter, Eyer Benjamin R., Yamaguchi Yukihiro, Tetrahedron letters: The International Journal for the Rapid Publication of Preliminary Communications in Organic Chemistry . 2015,第23期

机译：合成抗炎性α-和β-连接的乙酰氨基吡喃糖苷作为toll样受体4（TLR4）的抑制剂
4. Models of SIGIRR inhibiting the Toll-like receptor TLR4 signaling pathway [C] . Jing Gong, Tiandi Wei, Robert W.Stark, International Workshop on Computational amp; Integrative Biology,2009(CIB'09)(2009年计算与整合生物学国际研讨会） . 2009

机译：SIGIRR抑制Toll样受体TLR4信号通路的模型
5. Porphyromonas gingivalis major and minor fimbria-induced interleukin-8 production by human aortic endothelial cells: The role of Toll-like receptors (TLR)2 and TLR4. [D] . Davey, Michael Thomas. 2007

机译：人主动脉内皮细胞牙龈卟啉单胞菌主要和次要的菌毛诱导白细胞介素8的产生：Toll样受体（TLR）2和TLR4的作用。
6. Synthesis of anti-inflammatory α-and β-linked acetamidopyranosides as inhibitors of toll-like receptor 4 (TLR4) [O] . Peter Wipf, Benjamin R. Eyer, Yukihiro Yamaguchi, -1

机译：合成抗炎性α-和β-连接的乙酰氨基吡喃糖苷作为toll-like受体4（TLR4）的抑制剂
7. Lipid A antagonist, lipid IVa, is distinct from lipid A in interaction with Toll-like receptor 4 (TLR4)-MD-2 and ligand-induced TLR4 oligomerization [O] . S.-i. Saitoh 2004

机译：脂质是抗脂肪剂，脂质IVA不同于与Toll样受体4（TLR4）-MD-2和配体诱导的TLR4低聚相互作用的脂质A.
8. Novel Approach for Effectively Treating SCI Pain, Improving Opioid Efficacy, and Preventing Opioid Induced Constipation: Key Role of Toll-Like Receptor 4 (TLR4). [R] . Watkins, L. 2016

机译：有效治疗sCI疼痛，提高阿片类药物功效，预防阿片类药物引起的便秘的新方法：Toll样受体4（TLR4）的关键作用。

Ligand-dependent Toll-like receptor 4 (TLR4)-oligomerization is directly linked with TLR4-signaling.

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