β-Arrestin 2 mediates G protein-coupled receptor 43 signals to Nuclear Factor-kappaB = 베타어레스틴 2에 의한 GPR43-NFkB 신호전달계의 조절

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dc.contributor.authorSu Ui Lee-
dc.contributor.authorH J In-
dc.contributor.authorM S Kwon-
dc.contributor.authorBi-oh Park-
dc.contributor.authorM Jo-
dc.contributor.authorMun-Ock Kim-
dc.contributor.authorSungchan Cho-
dc.contributor.authorSangku Lee-
dc.contributor.authorHyun Jun Lee-
dc.contributor.authorY S Kwak-
dc.contributor.authorSunhong Kim-
dc.date.accessioned2017-04-19T09:44:10Z-
dc.date.available2017-04-19T09:44:10Z-
dc.date.issued2013-
dc.identifier.issn0918-6158-
dc.identifier.uri10.1248/bpb.b13-00312ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/11571-
dc.description.abstractG-protein coupled receptor 43 (GPR43) serves as a receptor for short-chain fatty acids (SCFAs), implicated in neutrophil migration and inflammatory cytokine production. However, the intracellular signaling pathway mediating GPR43 signaling remains unclear. Here, we show that β-arrestin 2 mediates the internalization of GPR43 by agonist. Agonism of GPR43 reduced the phosphorylation and nuclear translocation of nuclear factor-eB (NF-eB), which was relieved by short interfering RNA (siRNA) of β-arrestin 2. Subsequently, mRNA expression of proinflammatory cytokines, interleukin (IL)-6 and IL-1β, was downregulated by activation of GPR43 and knockdown of β-arrestin 2 recovered the expression of the cytokines. Taken together, these results suggest that GPR43 may be a plausible target for a variety of inflammatory diseases-
dc.publisherPharmaceutical Soc Japan-
dc.titleβ-Arrestin 2 mediates G protein-coupled receptor 43 signals to Nuclear Factor-kappaB = 베타어레스틴 2에 의한 GPR43-NFkB 신호전달계의 조절-
dc.title.alternativeβ-Arrestin 2 mediates G protein-coupled receptor 43 signals to Nuclear Factor-kappaB-
dc.typeArticle-
dc.citation.titleBiological & Pharmaceutical Bulletin-
dc.citation.number11-
dc.citation.endPage1759-
dc.citation.startPage1754-
dc.citation.volume36-
dc.contributor.affiliatedAuthorSu Ui Lee-
dc.contributor.affiliatedAuthorBi-oh Park-
dc.contributor.affiliatedAuthorMun-Ock Kim-
dc.contributor.affiliatedAuthorSungchan Cho-
dc.contributor.affiliatedAuthorSangku Lee-
dc.contributor.affiliatedAuthorHyun Jun Lee-
dc.contributor.affiliatedAuthorSunhong Kim-
dc.contributor.alternativeName이수의-
dc.contributor.alternativeName인현주-
dc.contributor.alternativeName권미소-
dc.contributor.alternativeName박비오-
dc.contributor.alternativeName조민미-
dc.contributor.alternativeName김문옥-
dc.contributor.alternativeName조성찬-
dc.contributor.alternativeName이상구-
dc.contributor.alternativeName이현준-
dc.contributor.alternativeName곽영신-
dc.contributor.alternativeName김선홍-
dc.identifier.bibliographicCitationBiological & Pharmaceutical Bulletin, vol. 36, no. 11, pp. 1754-1759-
dc.identifier.doi10.1248/bpb.b13-00312-
dc.subject.keywordβ-arrestin-
dc.subject.keywordG protein-coupled receptor 43-
dc.subject.keywordInflammation-
dc.subject.keywordNuclear factor-κB-
dc.subject.localβ-arrestin-
dc.subject.localG protein-coupled receptor 43-
dc.subject.localInflammation-
dc.subject.localinflammation-
dc.subject.localnflammation-
dc.subject.localNFkappaB-
dc.subject.localNFκB-
dc.subject.localNf-κB-
dc.subject.localNf-κb-
dc.subject.localNuclear factor (NF)-κB-
dc.subject.localNuclear factor kappa B-
dc.subject.localNuclear factor kappaB-
dc.subject.localNuclear factor κB-
dc.subject.localNuclear factor κB (NF-κB)-
dc.subject.localNuclear factor-kappa B-
dc.subject.localNuclear factor-kappa B (NF-κB)-
dc.subject.localNuclear factor-kappaB-
dc.subject.localNuclear factor-κB-
dc.subject.localNuclear factor-κb-
dc.subject.localNF-kB-
dc.subject.localNF-kappa B-
dc.subject.localNF-kappaB-
dc.subject.localNF-ΚB-
dc.subject.localNF-κ B-
dc.subject.localNF-κB-
dc.subject.localNF-κB (nuclear factor kappa-B)-
dc.subject.localnuclear factor kappa B-
dc.subject.localnuclear factor κB-
dc.subject.localnuclear factor-kappaB-
dc.subject.localnuclear factor-kappaB (NF-κB)-
dc.subject.localnuclear factor-κB-
dc.subject.localnuclear factorκB-
dc.description.journalClassY-
Appears in Collections:
Ochang Branch Institute > Natural Product Research Center > 1. Journal Articles
Ochang Branch Institute > Nucleic Acid Therapeutics Research Center > 1. Journal Articles
Ochang Branch Institute > Chemical Biology Research Center > 1. Journal Articles
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