J. Lipid Res.
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A more recent version of this article appeared on April 1, 2008

Papers In Press, published online ahead of print January 10, 2008
J. Lipid Res., doi:10.1194/jlr.M700545-JLR200
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Submitted on November 26, 2007
Revised on January 7, 2008
Accepted on January 10, 2008

TRB3 suppresses adipocyte differentiation by negatively regulating PPARgamma transcriptional activity

Yu Takahashi, Nobumichi Ohoka, Hidetoshi Hayashi, and Ryuichiro Sato

Applied Biological Chemistry, Graduate school of Agricultural and Life Sciences, The University of Tokyo, Tokyo 113-8657

Corresponding Author: aroysato{at}mail.ecc.u-tokyo.ac.jp

In the course of an effort to identify the regulators for peroxisome proliferators-activated receptor (PPAR) gamma -dependent perilipin gene expression, we have found that tribbles homolog 3 (TRB3), containing a single kinase domain without enzymatic activity, downregulates PPARgamma transcriptional activities by protein-protein interaction. We examined the role TRB3 plays in adipocyte differentiation in 3T3-L1 cells. TRB3 gene and protein expression was increased during adipocyte differentiation concomitantly with an increase in the mRNA levels of CCAAT/enhancer binding protein homologous protein (CHOP). The physical interaction between TRB3 and PPARgamma was also verified in 3T3-L1 adipocytes. Forced TRB3 expression in 3T3-L1 cells decreased the mRNA levels of PPARgamma -target genes and intracellular triglyceride levels, while knockdown of TRB3 expression by RNA interference (RNAi) elevated them. TRB3 also inhibits PPARgamma -dependent adipocyte differentiation in lentiviral mediated PPARgamma -expressing 3T3-L1 cells. These results provide evidence that TRB3 acts as a potent negative regulator of PPARgamma , a master regulator of adipocyte differentiation, and tightly controls adipogenesis.


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