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题目:: ChIP-Seq of mouse Ago-1 and TRIM32-bound small RNAs from E14.5 brain
ID:
状态:: 发布时间Aug. 29, 2009 , 更新时间 June 2, 2014 , 提交时间 Sept. 1, 2008,
物种:: Mus musculus
摘要:: In the mouse neocortex, neural progenitor cells generate neurons through repeated rounds of asymmetric cell division. How distinct fates are established in their daughter cells is unclear. We show here that the TRIM-NHL protein TRIM32 segregates asymmetrically during progenitor division and induces neuronal differentiation in one of the two daughter cells. TRIM32 is highly expressed in differentiating neurons. In both horizontally and vertically dividing progenitor cells, TRIM32 distribution becomes polarized in mitosis so that the protein is enriched in one of the two daughter cells. While TRIM32 overexpression induces cell cycle exit and neuronal differentiation, TRIM32 RNAi causes both daughter cells to proliferate and prevents the initiation of a neuronal differentiation program . TRIM32 ubiquitinates and degrades the transcription factor c-Myc but also binds Argonaute-1 and thereby increases the activity of specific micro-RNAs. We show that Let-7 is one of the TRIM32 targets and is required and sufficient for neuronal differentiation. Our data suggest that the asymmetric segregation of a micro RNA regulator controls self renewal in the mammalian brain. Experiment Overall Design: small RNA from total mouse brain, Ago-1 and TRIM32 IPs were cloned and sequenced using 454 GS FLX system.
实验种类:: ChIP-seq
样本量:: 4
实验设计:
: 无设计数据
数据号:: E-GEOD-12633, GSE12633
数据状态:: 无法自动分析，您可以尝试手动分析数据。

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