β-Arrestin 2 Mediates G Protein-Coupled Receptor 43 Signals to Nuclear Factor-κB

DOI Web Site Web Site PubMed 被引用文献3件 参考文献7件
  • Lee Su Ui
    Targeted Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology
  • In Hyun Ju
    Targeted Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology
  • Kwon Mi So
    Targeted Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology Biomolecular Science Major, University of Science and Technology
  • Park Bi-oh
    Targeted Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology
  • Jo Minmi
    College of Pharmacy, Korea University
  • Kim Mun-Ock
    Targeted Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology
  • Cho Sungchan
    Targeted Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology Biomolecular Science Major, University of Science and Technology
  • Lee Sangku
    Targeted Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology
  • Lee Hyun-Jun
    Targeted Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology
  • Kwak Young Shin
    College of Pharmacy, Korea University
  • Kim Sunhong
    Targeted Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology Biomolecular Science Major, University of Science and Technology

この論文をさがす

抄録

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-κB (NF-κB), 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.

収録刊行物

被引用文献 (3)*注記

もっと見る

参考文献 (7)*注記

もっと見る

キーワード

詳細情報 詳細情報について

問題の指摘

ページトップへ