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Trichostatin A and vorinostat promote adipogenic differentiation through H3K9 acetylation and dimethylation

机译:Trichostatin A和Vorinostat通过H3K9乙酰化和二甲基化促进脂肪切征

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To explore the effect of epigenetic modification on the differentiation of goat adipose-derived stem cells in vitro, we used two common epigenetic modification inhibitors, trichostatin A and vorinostat, to treat cashmere goat adipose-derived stem cells and induce adipocyte differentiation. The results showed that trichostatin A and vorinostat changed the relative amounts of H3K9 acetylation and dimethylation in the upstream sequence of PPARG, increased peroxisome proliferator-activated receptor gamma (PPARG) transcription before differentiation and then promoted adipocyte differentiation, and regulated the expression of adipocyte-specific genes. We conclude that adipocyte differentiation is regulated dynamically by different histone modifications. The areas of acetylation and demethylation changed by trichostatin A and vorinostat are the basis for further research on the mechanism of PPARG promoter to regulate adipocytes differentiation and provide research theroies for using adipose-derived stem cells as donor to produce transgenic animals to improve meat quality improvement.
机译:为了探讨表观遗传改性对体外山羊脂肪衍生干细胞的分化的影响,我们使用了两种常见的表观遗传修饰抑制剂,Trichostatin A和Vorinostat,治疗羊绒山羊脂肪衍生的干细胞并诱导脂肪细胞分化。结果表明,在分化之前,颅骨蛋白A和vorinostat在PPARG的上游序列中改变了H3K9乙酰化和二甲基化的相对量,增加了过氧化物体增殖物激活的受体γ(PPARG)转录,然后促进了脂肪细胞分化,并调节了脂肪细胞的表达 - 特定基因。我们得出结论,脂肪细胞分化通过不同的组蛋白修饰动态调节。甲状腺素A和vorinostat改变的乙酰化和去甲基化的区域是进一步研究PPARG启动子调节脂肪细胞分化的机制的基础,并提供使用脂肪衍生的干细胞作为供体的研究,以产生转基因动物以改善肉质改善。

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