Suppression of the TRIF-dependent signaling pathway of toll-like receptors by (E)-isopropyl 4-oxo-4-(2-oxopyrrolidin-1-yl)-2-butenoate
- Authors
- Park, Se-Jeong; Park, Hye-Jeong; Kim, Soo-Jung; Shin, Hwa-Jeong; Min, In Soon; Koh, Kwang Oh; Kim, Dae Young; Youn, Hyung-Sun
- Issue Date
- 31-Jul-2011
- Publisher
- 생화학분자생물학회
- Keywords
- Fumaryl pyrrolidinone; Lipopolysaccharide; Polyinosinic-polycytidylic acid; Toll-like receptor; TRIF
- Citation
- BMB Reports, v.44, no.7, pp 468 - 472
- Pages
- 5
- Journal Title
- BMB Reports
- Volume
- 44
- Number
- 7
- Start Page
- 468
- End Page
- 472
- URI
- https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/16335
- DOI
- 10.5483/BMBRep.2011.44.7.468
- ISSN
- 1976-6696
1976-670X
- Abstract
- Toll-like receptors (TLRs) are pattern recognition receptors that recognize molecular structures derived from microbes and initiate innate immunity. TLRs have two downstream signaling pathways, the MyD88- and TRIF-dependent pathways. Dysregulated activation of TLRs is closely linked to increased risk of many chronic diseases. Previously, we synthesized fumaryl pyrrolidinone, (E)-isopropyl 4-oxo-4-(2-oxopyrrolidin-1-yl)-2-butenoate (IPOP), which contains a fumaric acid isopropyl ester and pyrrolidinone, and demonstrated that it inhibits the activation of nuclear factor kappa B by inhibiting the MyD88-dependent pathway of TLRs. However, the effect of IPOP on the TRIF-dependent pathway remains unknown. Here, we report the effect of IPOP on signal transduction via the TRIF-dependent pathway of TLRs. IPOP inhibited lipopolysaccharide- or polyinosinic-polycytidylic acid-induced interferon regulatory factor 3 activation, as well as interferon-inducible genes such as interferon inducible protein-10. These results suggest that IPOP can modulate the TRIF-dependent signaling pathway of TLRs, leading to decreased inflammatory gene expression. [BMB reports 2011; 44(7): 468-472]
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Collections - College of Medical Sciences > Department of Biomedical Laboratory Science > 1. Journal Articles
- College of Natural Sciences > Department of Chemistry > 1. Journal Articles
- College of Medical Sciences > Department of Health Administration and Management > 1. Journal Articles
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