PPAR gamma partial agonist, KR-62776, inhibits adipocyte differentiation via activation of ERK = 당뇨병 치료제와 후보물질에 의해서 조절되는 단백체분석을 통한 기전 규명연구
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- PPAR gamma partial agonist, KR-62776, inhibits adipocyte differentiation via activation of ERK = 당뇨병 치료제와 후보물질에 의해서 조절되는 단백체분석을 통한 기전 규명연구
- Jin-A Kim; Dong Cho Han; J M Kim; S Y Lee; Seung Jun Kim; J R Woo; J W Lee; Suk Gyeoung Jeong; Kab Seog Yoon; H G Cheon; S S Kim; S H Hong; Byoung-Mog Kwon
- Bibliographic Citation
- Cellular and Molecular Life Sciences, vol. 66, no. 10, pp. 1766-1781
- Publication Year
- Indenone KR-62776 acts as an agonist of PPARγ without inducing obesity in animal models and cells. X-ray crystallography reveals that the indenone occupies the binding pocket in a different manner than rosiglitazone. 2-Dimensional gel-electrophoresis showed that the expression of 42 proteins was altered more than 2.0-fold between KR-62776- or rosiglitazone-treated adipocyte cells and control cells. Rosiglitazone down-regulated the expression of ERK1/2 and suppressed the phosphorylation of ERK1/2 in these cells. However, the expression of ERK1/2 was up-regulated in KR-62776-treated cells. Phosphorylated ERK1/2, activated by indenone, affects the localization of PPARγ, suggesting a mechanism for indenone-inhibition of adipogenesis in 3T3- L1 preadipocyte cells. The preadipocyte cells are treated with ERK1/2 inhibitor PD98059, a large amount of the cells are converted to adipocyte cells. These results support the conclusion that the localization of PPARγ is one of the key factors explaining the biological responses of the ligands.
- peroxisome proliferators-activated receptor γrosiglitazonelipolysisERKindenoneadipocyte
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- Division of Biomedical Research > Personalized Genomic Medicine Research Center > 1. Journal Articles
Critical Diseases Diagnostics Convergence Research Center > 1. Journal Articles
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