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地塞米松可下调 3T3-L1 前脂肪细胞分化过程中的 TAZ。

TAZ is downregulated by dexamethasone during the differentiation of 3T3-L1 preadipocytes.

机构信息

Key Laboratory of Molecular Medicine, The Ministry of Education, Department of Biochemistry and Molecular Biology, Fudan University Shanghai Medical College, PR China.

出版信息

Biochem Biophys Res Commun. 2012 Mar 16;419(3):573-7. doi: 10.1016/j.bbrc.2012.02.074. Epub 2012 Feb 20.

DOI:10.1016/j.bbrc.2012.02.074
PMID:22374070
Abstract

TAZ (transcriptional co-activator with PDZ binding motif) is a transcriptional modulator of mesenchymal stem cell differentiation. We have found that TAZ was expressed in postconfluent 3T3-L1 preadipocytes and downregulated during differentiation. Downregulation of TAZ was specifically mediated by dexamethasone (DEX), one component of induction cocktails routinely used in adipocyte differentiation. DEX repressed the transcription of TAZ by direct binding of the glucocorticoid receptor (GR) to the GR binding element in its promoter. More importantly, overexpression of TAZ inhibited adipogenesis and promoted the trans-differentiation of preadipocytes into osteocytes. This establishes a new functional interaction between DEX and TAZ that contributes to the mechanism of adipogenesis.

摘要

TAZ(含 PDZ 结合基序的转录共激活因子)是间充质干细胞分化的转录调节剂。我们发现,TAZ 在汇合后的 3T3-L1 前脂肪细胞中表达,并在分化过程中下调。TAZ 的下调是由诱导鸡尾酒中的一种成分地塞米松(DEX)特异性介导的,DEX 通过糖皮质激素受体(GR)直接结合其启动子中的 GR 结合元件来抑制 TAZ 的转录。更重要的是,TAZ 的过表达抑制脂肪生成,并促进前脂肪细胞向成骨细胞的转分化。这确立了 DEX 和 TAZ 之间新的功能相互作用,有助于脂肪生成的机制。

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