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Suppression of the TRIF-dependent signaling pathway of TLRs by epoxomicin

Authors
Kim, Su Y.Shin, SeokwonKwon, MinjiYoun, DanielSung, Nam J.Kim, Na H.Park, Sin-AyeYoun, Hyung-Sun
Issue Date
Sep-2021
Publisher
WILEY-V C H VERLAG GMBH
Keywords
epoxomicin; IRF3; MyD88; Toll-like receptor; TRIF
Citation
ARCHIV DER PHARMAZIE, v.354, no.9
Journal Title
ARCHIV DER PHARMAZIE
Volume
354
Number
9
URI
https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/19319
DOI
10.1002/ardp.202100130
ISSN
0365-6233
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.
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의료과학대학 (Department of Biomedical Laboratory Science)
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