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组蛋白去乙酰化酶 1 和 2 对脂肪生成的冗余控制。

Redundant control of adipogenesis by histone deacetylases 1 and 2.

机构信息

Department of Molecular Biology, The University of Texas Southwestern Medical Center, Dallas, Texas 75390-9148, USA.

出版信息

J Biol Chem. 2010 May 7;285(19):14663-70. doi: 10.1074/jbc.M109.081679. Epub 2010 Feb 26.

Abstract

Adipocyte differentiation is a well defined process that is under the control of transcriptional activators and repressors. We show that histone deacetylase (HDAC) inhibitors efficiently block adipocyte differentiation in vitro. This effect is specific to adipogenesis, as another mesenchymal differentiation process, osteoblastogenesis, is enhanced upon HDAC inhibition. Through the systematic genetic deletion of HDAC genes in cultured mesenchymal precursor cells, we show that deletion of HDAC1 and HDAC2 leads to reduced lipid accumulation, revealing redundant and requisite roles of these class I HDACs in adipogenesis. These findings unveil a previously unrecognized role for HDACs in the control of adipogenesis.

摘要

脂肪细胞分化是一个明确的过程,受转录激活因子和转录抑制因子的控制。我们表明,组蛋白去乙酰化酶 (HDAC) 抑制剂能有效地阻断体外脂肪细胞分化。这种作用是特异性的,因为另一种间充质分化过程,成骨细胞分化,在 HDAC 抑制时被增强。通过在培养的间充质前体细胞中系统地遗传删除 HDAC 基因,我们表明,HDAC1 和 HDAC2 的缺失导致脂质积累减少,揭示了这些 I 类 HDAC 在脂肪生成中的冗余和必需作用。这些发现揭示了 HDAC 在控制脂肪生成中的一个以前未被认识到的作用。

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