期刊
FEBS LETTERS
卷 585, 期 5, 页码 814-820出版社
WILEY
DOI: 10.1016/j.febslet.2011.02.010
关键词
Epigallocatechin-3-gallate; 67-kDa laminin receptor; Peptidoglycan; Toll-like receptor 2; Toll-interacting protein
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. (C) 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
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