MyD88 is a mediator for the activation of Nrf2 = MyD88에 의한 Nrf2 활성화

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dc.contributor.authorK H Kim-
dc.contributor.authorJ H Lyu-
dc.contributor.authorS T Koo-
dc.contributor.authorSei Ryang Oh-
dc.contributor.authorHyeong Kyu Lee-
dc.contributor.authorKyung Seop Ahn-
dc.contributor.authorR T Sadikot-
dc.contributor.authorM Joo-
dc.date.accessioned2017-04-19T09:21:13Z-
dc.date.available2017-04-19T09:21:13Z-
dc.date.issued2011-
dc.identifier.issn0006-291X-
dc.identifier.uri10.1016/j.bbrc.2010.11.051ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/9937-
dc.description.abstractIf not controlled properly, inflammatory response is often detrimental. However, in many cases, it can be self-limited and subsides without inflicting tissue damage. In this study, we tested the hypothesis that inflammatory stimuli can trigger anti-inflammatory response, which may contribute to limiting tissue damage induced by excessive inflammation. We found that treatment of bone marrow-derived macrophages with lipopolysaccharide (LPS) activated NF-E2-related factor 2 (Nrf2), a basic leucine zipper transcription factor that regulates inflammation, leading to expression of Nrf2-regulated genes including NAD(P)H:quinine oxidoreductase 1,glutamyl cysteine ligase catalytic unit and heme oxygenase-1. Suppression of Nrf2 by siRNA significantly diminished the expression of the Nrf2-regulated genes induced by LPS. By using pharmacological, genetic and epigenetic analyses, we found that activation of Nrf2 in response to LPS is dependent on MyD88 but independent of the production of reactive oxygen species. Together, our results show that activation of Nrf2 by MyD88 dependent signaling induced by LPS is an important intrinsic mechanism that limits excessive inflammation.-
dc.publisherElsevier-
dc.titleMyD88 is a mediator for the activation of Nrf2 = MyD88에 의한 Nrf2 활성화-
dc.title.alternativeMyD88 is a mediator for the activation of Nrf2-
dc.typeArticle-
dc.citation.titleBiochemical and Biophysical Research Communications-
dc.citation.number1-
dc.citation.endPage51-
dc.citation.startPage46-
dc.citation.volume404-
dc.contributor.affiliatedAuthorSei Ryang Oh-
dc.contributor.affiliatedAuthorHyeong Kyu Lee-
dc.contributor.affiliatedAuthorKyung Seop Ahn-
dc.contributor.alternativeName김균하-
dc.contributor.alternativeName류지효-
dc.contributor.alternativeName구성태-
dc.contributor.alternativeName오세량-
dc.contributor.alternativeName이형규-
dc.contributor.alternativeName안경섭-
dc.contributor.alternativeNameSadikot-
dc.contributor.alternativeName주명수-
dc.identifier.bibliographicCitationBiochemical and Biophysical Research Communications, vol. 404, no. 1, pp. 46-51-
dc.identifier.doi10.1016/j.bbrc.2010.11.051-
dc.subject.keywordGene regulation-
dc.subject.keywordInflammation-
dc.subject.keywordMacrophages-
dc.subject.keywordNrf2-
dc.subject.keywordSiRNA-
dc.subject.keywordTLR4 signaling-
dc.subject.localgene regulation-
dc.subject.localGene regulation-
dc.subject.localinflammation-
dc.subject.localInflammation-
dc.subject.localmacrophages-
dc.subject.localmacrophage-
dc.subject.localMacrophages-
dc.subject.localMacrophage-
dc.subject.localNRF2-
dc.subject.localNrf2-
dc.subject.localNrf-2-
dc.subject.localsiRNA-
dc.subject.localSiRNA-
dc.subject.localTLR4 signaling-
dc.description.journalClassY-
Appears in Collections:
Ochang Branch Institute > 1. Journal Articles
Ochang Branch Institute > Natural Product Research Center > 1. Journal Articles
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