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"EGCG inhibited the activation of IRF3 induced by TRIF as determined by IRF3 binding site (IFNβ PRDIII-I)-reporter gene assay while catechin did not ( Fig. 4 A )."
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"EGCG inhibited the activation of IRF3 induced by overexpression of TBK1 as determined by IRF3 binding site (IFNβ PRDIII-I) reporter gene assay ( Fig. 4 C)."
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"Our results showed that EGCG inhibited the activation of IRF3 induced by the transfection of TBK1 expression plasmid."
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"Youn and colleagues [XREF_BIBR] reported that EGCG could inhibit LPS- or PolyI : C mediated activation of interferon regulatory factor 3."
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"Furthermore, EGCG has been reported to inhibit the activation of transcription factor, NF-kappaB (possibly through the suppression of IkappaB kinase) and IRF3 (via suppression of kinase activity of TBK1) XREF_BIBR - XREF_BIBR."
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"EGCG suppressed activation of IRF3 induced by LPS (TLR4 agonist) or poly[I:C] (TLR3 agonist) as determined by reporter gene assay using IFNβ promoter domain containing IRF3 binding site (IFNβ PRDIII-I[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"However, catechin did not affect the activation of IRF3.To investigate the consequence of the inhibition of IRF3 by EGCG, we determined the expression of IRF3-target genes such as IFNβ."
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"The results from our previous studies showed that resveratrol, (-)-epigallocatechin-3-gallate (EGCG), 6-shogaol, and isoliquiritigenin, which are well-known anti-inflammatory agents, inhibit IRF3 acti[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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