Hirofumi Tachibana 교수

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

Green tea polyphenols have emerged over the past two decades as an important dietary factor for health promotion. There is considerable evidence that tea polyphenols, in particular (-)-epigallocatechin-3-gallate (EGCG) inhibit carcinogenesis. However, the mechanisms for the cancer-preventive activity of EGCG are not completely characterized and many features remain to be elucidated. Recently we have identified a cell-surface EGCG receptor and the relating molecules that confer EGCG responsivenes

Our findings suggest that metabolic profiling is a useful approach for nutraceutical evaluation of the health promotion effects of diverse tea cultivars. This may propose a novel strategy for functional food design.

Overall, our results highlight the nature of the EGCG-67LR interaction and provide novel structural insights into the understanding of 67LR-mediated functions of EGCG, and could aid in the development of potential anti-cancer compounds for chemopreventive or therapeutic uses that can mimic EGCG-67LR interactions.

The major green tea catechin, (-)-epigallocatechin-3-O-gallate (EGCG), has a suppressive effect on the expression of the high-affinity IgE receptor FcepsilonRI, which is key molecule in the IgE-mediated allergic reactions. Here we show that EGCG binds to the cell surface and highly associates with plasma membrane microdomains, lipid rafts, on the human basophilic KU812 cells. The disruption of these lipid rafts caused a reduction of the amount of raft-associated EGCG and the FcepsilonRI-suppress

For the past two decades, many researchers have been investigating the potential cancer-preventive and therapeutic effects of green tea. (-)-Epigallocatechin-3-O-gallate (EGCG) has been shown to be the most active and major polyphenolic compound from green tea. The mechanisms of action of EGCG have been extensively investigated. However, the mechanisms for the cancer-preventive activity of EGCG are not completely characterized and many features remain to be elucidated. Recently, we have identifi

The Ras/Raf/MEK/ERK pathway has been identified as a major, druggable regulator of melanoma. Mutational activation of BRAF is the most prevalent genetic alteration in human melanoma, resulting in constitutive melanoma hyperproliferation. A selective BRAF inhibitor showed remarkable clinical activity in patients with mutated BRAF. Unfortunately, most patients acquire resistance to the BRAF inhibitor, highlighting the urgent need for new melanoma treatment strategies. Green tea polyphenol (-)-epig

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-interact

We examined the constituents of tea that had an inhibitory effect on the degranulation process in the human basophilic cell line, KU812. Among the constituents purified from a extract of 'Benihomare' oolong tea by column chromatography, a methylated (-)-epigallocatechin gallate ((-)-epigallocatechin 3-O-(3-O-methyl) gallate) was found to inhibit the degranulation of KU812 cells that had been stimulated with calcium ionophore A23187. The inhibitory effect of this methylated (-)-epigallocatechin g