Isobavachalcone suppresses the TRIF-dependent signaling pathway of Toll-like receptors
DC Field | Value | Language |
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dc.contributor.author | Shin, Seokwon | - |
dc.contributor.author | Park, Jayeon | - |
dc.contributor.author | Lee, Ye Eun | - |
dc.contributor.author | Ko, Hanbin | - |
dc.contributor.author | Youn, Hyung-Sun | - |
dc.date.accessioned | 2022-03-17T07:40:12Z | - |
dc.date.available | 2022-03-17T07:40:12Z | - |
dc.date.issued | 2022-03 | - |
dc.identifier.issn | 0365-6233 | - |
dc.identifier.issn | 1521-4184 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/20524 | - |
dc.description.abstract | Toll-like receptors (TLRs) are integral membrane-bound receptors that are central to innate and adaptive immune responses. They are known to activate a cascade of downstream signals to induce the secretion of inflammatory cytokines, chemokines, and type I interferons. Dysregulated activation of TLR signaling pathways can induce the activation of various transcription factors, such as nuclear factor kappa B (NF-kappa B) and interferon regulatory factor 3 (IRF3). TLRs act via MyD88- and TRIF-mediated pathways to induce inflammatory responses. To evaluate the therapeutic potential of isobavachalcone (IBC), a natural chalcone component of Angelica keiskei, we examined its effects on signal transduction via TLR signaling pathways. IBC inhibited the activation of NF-kappa B and IRF3 induced by TLR agonists and their target genes. IBC also inhibited the activation of NF-kappa B and IRF3 induced by overexpression of downstream signaling components of TLR signaling pathways. These results suggest that IBC can regulate both MyD88- and TRIF-dependent signaling pathways of TLRs, resulting in a dramatic increase of new therapeutic options for various inflammatory diseases involving TLRs. | - |
dc.format.extent | 2 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | John Wiley & Sons Ltd. | - |
dc.title | Isobavachalcone suppresses the TRIF-dependent signaling pathway of Toll-like receptors | - |
dc.type | Article | - |
dc.publisher.location | 독일 | - |
dc.identifier.doi | 10.1002/ardp.202100404 | - |
dc.identifier.scopusid | 2-s2.0-85122034133 | - |
dc.identifier.wosid | 000736105300001 | - |
dc.identifier.bibliographicCitation | Archiv der Pharmazie, v.355, no.3, pp 8 - 9 | - |
dc.citation.title | Archiv der Pharmazie | - |
dc.citation.volume | 355 | - |
dc.citation.number | 3 | - |
dc.citation.startPage | 8 | - |
dc.citation.endPage | 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 | INNATE | - |
dc.subject.keywordPlus | RECOGNITION | - |
dc.subject.keywordPlus | CHALCONES | - |
dc.subject.keywordAuthor | inflammation | - |
dc.subject.keywordAuthor | isobavachalcone | - |
dc.subject.keywordAuthor | nuclear factor-kappa B | - |
dc.subject.keywordAuthor | Toll-like receptors | - |
dc.subject.keywordAuthor | TRIF | - |
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