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Title 

PPAR gamma partial agonist, KR-62776, inhibits adipocyte differentiation via activation of ERK

 

당뇨병 치료제와 후보물질에 의해서 조절되는 단백체분석을 통한 기전 규명연구

Authors 

Jin-A KimDong Cho HanJ M KimS Y LeeSeung Jun KimJ R WooJ W LeeSuk Gyeoung JeongKab Seog YoonH G CheonS S KimS H HongByoung-Mog Kwon

Publisher 

Springer Verlag (Germany)

Issue Date 

2009

Citation 

Cellular and Molecular Life Sciences, vol. 66, no. 10, pp. 1766-1781

Keywords 

peroxisome proliferators-activated receptor γrosiglitazoneadipocytelipolysisERKindenone

Abstract 

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.

ISSN 

1420-682X

Link 

http://dx.doi.org/10.1007/s00018-009-9169-4

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2017-04-19


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