Suppression of the TRIF-dependent signaling pathway of TLRs by epoxomicin
DC Field | Value | Language |
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dc.contributor.author | Kim, Su Y. | - |
dc.contributor.author | Shin, Seokwon | - |
dc.contributor.author | Kwon, Minji | - |
dc.contributor.author | Youn, Daniel | - |
dc.contributor.author | Sung, Nam J. | - |
dc.contributor.author | Kim, Na H. | - |
dc.contributor.author | Park, Sin-Aye | - |
dc.contributor.author | Youn, Hyung-Sun | - |
dc.date.accessioned | 2021-09-10T06:45:03Z | - |
dc.date.available | 2021-09-10T06:45:03Z | - |
dc.date.issued | 2021-09 | - |
dc.identifier.issn | 0365-6233 | - |
dc.identifier.issn | 1521-4184 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/19319 | - |
dc.description.abstract | Toll-like receptors (TLRs) can recognize specific signatures of invading microbial pathogens and activate a cascade of downstream signals to induce the secretion of inflammatory cytokines, chemokines, and type I interferons. The activation of TLRs triggers two downstream signaling pathways: the MyD88- and the TRIF-dependent pathways. To evaluate the therapeutic potential of epoxomicin, a member of the linear peptide alpha',beta'-epoxyketone first isolated from an actinomycetes strain, we examined its effects on signal transduction via TLR signaling pathways. Epoxomicin inhibited the activation of NF-kB and IRF3 induced by TLR agonists, decreased the expression of interferon-inducible protein-10, and inhibited the activation of NF-kB and IRF3 induced by overexpression of downstream signaling components of TLR signaling pathways. These results suggest that epoxomicin can regulate both the MyD88- and TRIF-dependent signaling pathways of TLRs. Thus, it might have potential as a new therapeutic drug for a variety of inflammatory diseases. | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | John Wiley & Sons Ltd. | - |
dc.title | Suppression of the TRIF-dependent signaling pathway of TLRs by epoxomicin | - |
dc.type | Article | - |
dc.publisher.location | 독일 | - |
dc.identifier.doi | 10.1002/ardp.202100130 | - |
dc.identifier.scopusid | 2-s2.0-85107317746 | - |
dc.identifier.wosid | 000656501400001 | - |
dc.identifier.bibliographicCitation | Archiv der Pharmazie, v.354, no.9 | - |
dc.citation.title | Archiv der Pharmazie | - |
dc.citation.volume | 354 | - |
dc.citation.number | 9 | - |
dc.type.docType | Article | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Pharmacology & Pharmacy | - |
dc.relation.journalResearchArea | Chemistry | - |
dc.relation.journalWebOfScienceCategory | Chemistry, Medicinal | - |
dc.relation.journalWebOfScienceCategory | Chemistry, Multidisciplinary | - |
dc.relation.journalWebOfScienceCategory | Pharmacology & Pharmacy | - |
dc.subject.keywordPlus | TOLL-LIKE RECEPTOR | - |
dc.subject.keywordPlus | RECOGNITION | - |
dc.subject.keywordAuthor | epoxomicin | - |
dc.subject.keywordAuthor | IRF3 | - |
dc.subject.keywordAuthor | MyD88 | - |
dc.subject.keywordAuthor | Toll-like receptor | - |
dc.subject.keywordAuthor | TRIF | - |
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