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

Cited 57 time in scopus
Metadata Downloads
Title
β-Arrestin 2 mediates G protein-coupled receptor 43 signals to Nuclear Factor-kappaB = 베타어레스틴 2에 의한 GPR43-NFkB 신호전달계의 조절
Author(s)
Su Ui Lee; H J In; M S Kwon; Bi-oh Park; M Jo; Mun-Ock KimSungchan ChoSangku LeeHyun Jun Lee; Y S Kwak; Sunhong Kim
Bibliographic Citation
Biological & Pharmaceutical Bulletin, vol. 36, no. 11, pp. 1754-1759
Publication Year
2013
Abstract
G-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
Keyword
G protein-coupled receptor 43InflammationNuclear factor-κBβ-arrestin
ISSN
0918-6158
Publisher
Pharmaceutical Soc Japan
DOI
http://dx.doi.org/10.1248/bpb.b13-00312
Type
Article
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
Files in This Item:
  • There are no files associated with this item.


Items in OpenAccess@KRIBB are protected by copyright, with all rights reserved, unless otherwise indicated.