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系统地识别人类iPSC产生障碍的障碍

Han Qin¹, Aaron Diaz², Laure Blouin¹

¹Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, University of California, San Francisco, San Francisco, CA 94143, USA; Departments of Ob/Gyn and Pathology, Center for Reproductive Sciences, and Diabetes Center, University of California, San Francisco, San Francisco, CA 94143, USA.

|July 19, 2014

概括

科学家们发现了将体细胞重新编程成诱导多能干细胞 (iPSC) 的障碍. 关键因素包括转录中的基因,染色体调节和细胞粘附,特定的ADAM蛋白和内细胞分裂抑制了这一过程.

科学领域:

细胞生物学细胞生物学
干细胞生物学干细胞生物学
遗传学是一个遗传学.

背景情况:

诱导多能干细胞 (iPSCs) 为再生医学提供了重要的潜力.
了解内源性障碍对于优化体细胞重编程效率至关重要.

研究的目的:

系统地识别和描述限制人类细胞重编程的内源性障碍.
阐明这些障碍背后的分子机制和网络架构.

主要方法:

全基因组RNAi查以确定抑制基因.
路径和网络分析的计算方法.
单击验证和确定障碍物的机制性调查.
基因相互作用研究以绘制路径架构的地图.

主要成果:

确定了关键的重编程障碍,包括转录,染色体调节,无处不在,脱,囊泡运输和细胞粘附.
发现特定的ADAM蛋白质,特别是ADAM29,可以通过其分解因子域抑制重编程.
通过调节TGF-β信号传递,克拉林介导的内细胞分裂被证明可以反对重编程.
路径架构 (线性,并行,前循环) 被揭示为内细胞和无处不在的障碍物.

结论:

提供了对人类细胞重编程障碍的全面,全球视图.
突出了特定蛋白质家族 (ADAMs) 和细胞过程 (内细胞分裂,TGF-β信号传递) 在限制iPSC生成中的作用.
证明了复杂的网络相互作用,对抗重编程,为治疗干预提供了目标.

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