Jmjd3通过上调INK4a/Arf的表达来抑制重编程,并针对PHF20进行无处不在
Wei Zhao1, Qingtian Li, Stephen Ayers
1Center for Inflammation and Epigenetics, The Methodist Hospital Research Institute, Houston, TX 77030, USA.
Cell
|March 5, 2013
概括
Jmjd3负面调节细胞重编程,使其成为诱导多能干细胞 (iPSC). 它的缺席增强了iPSC的产生,而它的存在则抑制了它,揭示了一个新的Jmjd3-PHF20监管轴.
科学领域:
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
- 干细胞生物学 干细胞生物学
- 分子生物学分子生物学
背景情况:
- 身体细胞重编程以产生诱导多能干细胞 (iPSCs) 涉及显著的表观遗传变化.
- 在这个过程中表观遗传调节者的精确作用和机制尚未完全阐明.
研究的目的:
- 识别和描述调节体细胞重编程的新型表观遗传因素.
- 阐明Jmjd3影响iPSCs生成的分子机制.
主要方法:
- 产生和分析Jmjd3缺乏和野生型小鼠胚胎纤维细胞 (MEF).
- 在异胎性Jmjd3表达时对iPSC殖民地形成的评估.
- 调查Jmjd3与PHF20和Trim26的相互作用,包括无处不在的测试.
- 在重新编程实验中分析PHF20缺乏的MEF.
主要成果:
- Jmjd3 作为一个强大的负调节器的重编程; Jmjd3 缺乏 MEF 产生更多的 iPSC 殖民地.
- Jmjd3通过依赖和独立的基因组脱甲基酶机制抑制了重编程.
- Jmjd3-PHF20轴是关键的,因为PHF20缺陷即使在Jmjd3被击倒时也阻止了iPSC生成.
结论:
- Jmjd3是以前未被识别的细胞重编程的负调节器.
- Jmjd3-PHF20轴在控制iPSC发电效率方面发挥着至关重要的作用.
- 这项研究为重新编程的表观遗传调节提供了新的分子见解.
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