首页> 外文期刊>FEBS letters. >Green tea polyphenol epigallocatechin-3-gallate inhibits TLR2 signaling induced by peptidoglycan through the polyphenol sensing molecule 67-kDa laminin receptor.
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Green tea polyphenol epigallocatechin-3-gallate inhibits TLR2 signaling induced by peptidoglycan through the polyphenol sensing molecule 67-kDa laminin receptor.

机译:绿茶多酚表没食子儿茶素-3-没食子酸酯通过多酚感测分子67-kDa层粘连蛋白受体抑制肽聚糖诱导的TLR2信号传导。

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摘要

Here we show the molecular basis for the inhibition of peptidoglycan (PGN)-induced TLR2 signaling by a major green tea polyphenol epigallocatechin-3-gallate (EGCG). Recently, we identified the 67-kDa laminin receptor (67LR) as the cell-surface EGCG receptor. Anti-67LR antibody treatment or silencing of 67LR resulted in abrogation of the inhibitory action of EGCG on PGN-induced production of pro-inflammatory mediators and activation of mitogen-activated protein kinases. Silencing of Toll-interacting protein (Tollip), a negative regulator of TLR signaling impaired the TLR2 signaling inhibitory activity of EGCG, suggesting that TLR2 response could be inhibited by EGCG via 67LR and Tollip.
机译:在这里,我们显示了主要绿茶多酚表没食子儿茶素-3-没食子酸酯(EGCG)抑制肽聚糖(PGN)诱导的TLR2信号传导的分子基础。最近,我们确定67 kDa层粘连蛋白受体(67LR)为细胞表面EGCG受体。抗67LR抗体治疗或67LR沉默导致废除了EGCG对PGN诱导的促炎性介质产生和丝裂原激活的蛋白激酶活化的抑制作用。 Toll相互作用蛋白(Tollip)的沉默,TLR信号的负调节剂削弱了EGCG的TLR2信号抑制活性,这表明EGCG可以通过67LR和Tollip抑制TLR2反应。

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