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TRB3通过负向调节PPARγ转录活性来抑制脂肪细胞分化。

TRB3 suppresses adipocyte differentiation by negatively regulating PPARgamma transcriptional activity.

作者信息

Takahashi Yu, Ohoka Nobumichi, Hayashi Hidetoshi, Sato Ryuichiro

机构信息

Department of Applied Biological Chemistry, Graduate School of Agricultural and Life Sciences, University of Tokyo, Tokyo 113-8657, Japan.

出版信息

J Lipid Res. 2008 Apr;49(4):880-92. doi: 10.1194/jlr.M700545-JLR200. Epub 2008 Jan 10.

Abstract

In the course of an effort to identify the regulators for peroxisome proliferator-activated receptor gamma (PPARgamma)-dependent perilipin gene expression, we 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 that 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. 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, whereas knockdown of TRB3 expression by RNA interference increased them. TRB3 also inhibits PPARgamma-dependent adipocyte differentiation in lentivirus-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.

摘要

在一项旨在鉴定过氧化物酶体增殖物激活受体γ(PPARγ)依赖性脂滴包被蛋白基因表达调控因子的研究过程中,我们发现含单个无酶活性激酶结构域的TRIB3同源物3(TRB3)通过蛋白质-蛋白质相互作用下调PPARγ转录活性。我们研究了TRB3在3T3-L1细胞脂肪生成中所起的作用。在脂肪生成过程中,TRB3基因和蛋白表达增加,同时CCAAT/增强子结合蛋白同源蛋白的mRNA水平也增加。在3T3-L1脂肪细胞中也证实了TRB3与PPARγ之间存在物理相互作用。在3T3-L1细胞中强制表达TRB3会降低PPARγ靶基因的mRNA水平和细胞内甘油三酯水平,而通过RNA干扰敲低TRB3表达则会使其升高。TRB3在慢病毒介导的表达PPARγ的3T3-L1细胞中也抑制PPARγ依赖性脂肪生成。这些结果证明TRB3作为脂肪生成主要调节因子PPARγ的有效负调节因子,严格控制脂肪生成。

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