| http://purl.uniprot.org/citations/20511545 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/20511545 | http://www.w3.org/2000/01/rdf-schema#comment | "Epigallocatechin-3-gallate (EGCG), a major active polyphenol of green tea, has been shown to downregulate inflammatory responses in macrophages; however, the underlying mechanism has not been understood. Recently, we identified the 67-kDa laminin receptor (67LR) as a cell-surface EGCG receptor that mediates the anticancer action of EGCG at physiologically relevant concentrations (0.1-1 microM). In this study, we show the molecular basis for the downregulation of TLR4 signal transduction by EGCG at 1 microM in macrophages. Anti-67LR Ab treatment or RNA interference-mediated silencing of 67LR resulted in abrogation of the inhibitory action of EGCG on LPS-induced activation of downstream signaling pathways and target gene expressions. Additionally, we found that EGCG reduced the TLR4 expression through 67LR. Interestingly, EGCG induced a rapid upregulation of Toll-interacting protein (Tollip), a negative regulator of TLR signaling, and this EGCG action was prevented by 67LR silencing or anti-67LR Ab treatment. RNA interference-mediated silencing of Tollip impaired the TLR4 signaling inhibitory activity of EGCG. Taken together, these findings demonstrate that 67LR plays a critical role in mediating anti-inflammatory action of a physiologically relevant EGCG, and Tollip expression could be modulated through 67LR. These results provide a new insight into the understanding of negative regulatory mechanisms for the TLR4 signaling pathway and consequent inflammatory responses that are implicated in the development and progression of many chronic diseases."xsd:string |
| http://purl.uniprot.org/citations/20511545 | http://purl.org/dc/terms/identifier | "doi:10.4049/jimmunol.0903742"xsd:string |
| http://purl.uniprot.org/citations/20511545 | http://purl.uniprot.org/core/author | "Yamada K."xsd:string |
| http://purl.uniprot.org/citations/20511545 | http://purl.uniprot.org/core/author | "Tachibana H."xsd:string |
| http://purl.uniprot.org/citations/20511545 | http://purl.uniprot.org/core/author | "Fujimura Y."xsd:string |
| http://purl.uniprot.org/citations/20511545 | http://purl.uniprot.org/core/author | "Hong Byun E."xsd:string |
| http://purl.uniprot.org/citations/20511545 | http://purl.uniprot.org/core/date | "2010"xsd:gYear |
| http://purl.uniprot.org/citations/20511545 | http://purl.uniprot.org/core/name | "J Immunol"xsd:string |
| http://purl.uniprot.org/citations/20511545 | http://purl.uniprot.org/core/pages | "33-45"xsd:string |
| http://purl.uniprot.org/citations/20511545 | http://purl.uniprot.org/core/title | "TLR4 signaling inhibitory pathway induced by green tea polyphenol epigallocatechin-3-gallate through 67-kDa laminin receptor."xsd:string |
| http://purl.uniprot.org/citations/20511545 | http://purl.uniprot.org/core/volume | "185"xsd:string |
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