The RNA helicase DDX6 regulates cell-fate specification in neural stem cells via miRNAs.
The RNA helicase DDX6 regulates cell-fate specification in neural stem cells via miRNAs.
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DOI：
10.1093/nar/gkv138
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发表时间：
2015-03-11
影响因子：
14.9
通讯作者：
Schwamborn JC
中科院分区：
文献类型：
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作者：
Nicklas S;Okawa S;Hillje AL;González-Cano L;Del Sol A;Schwamborn JC
在神经干细胞（NSC）中，干细胞维持和神经元分化之间的平衡取决于细胞命运决定因素，如TRIM 32。之前，我们已经证明TRIM 32与RNA诱导的沉默复合物相关，并增加了微RNA如Let-7a的活性。然而，TRIM 32在神经元分化过程中调控microRNA的确切机制尚未阐明。在这里，我们使用质谱方法来识别TRIM 32在神经元分化过程中的新型蛋白质-蛋白质相互作用伙伴。我们发现TRIM 32与参与神经发生和RNA相关过程的蛋白质相关联，例如RNA解旋酶DDX 6，它与microRNA调控有关。我们证明，DDX 6与TRIM 32在NSC和神经元中共定位，并且它增加Let-7a的活性。此外，我们提供的证据表明，DDX 6是必要的和足够的神经元分化，它的功能与TRIM 32合作。
In neural stem cells (NSCs), the balance between stem cell maintenance and neuronal differentiation depends on cell-fate determinants such as TRIM32. Previously, we have shown that TRIM32 associates with the RNA-induced silencing complex and increases the activity of microRNAs such as Let-7a. However, the exact mechanism of microRNA regulation by TRIM32 during neuronal differentiation has yet to be elucidated. Here, we used a mass spectrometry approach to identify novel protein–protein interaction partners of TRIM32 during neuronal differentiation. We found that TRIM32 associates with proteins involved in neurogenesis and RNA-related processes, such as the RNA helicase DDX6, which has been implicated in microRNA regulation. We demonstrate, that DDX6 colocalizes with TRIM32 in NSCs and neurons and that it increases the activity of Let-7a. Furthermore, we provide evidence that DDX6 is necessary and sufficient for neuronal differentiation and that it functions in cooperation with TRIM32.
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影响因子：
82.9
作者：
Eriksson, PS;Perfilieva, E;Gage, FH
通讯作者：
Gage, FH
影响因子：
64.5
作者：
Eulalio, Ana;Huntzinger, Eric;Izaurralde, Elisa
通讯作者：
Izaurralde, Elisa
DOI：
10.1073/pnas.0800803105
发表时间：
2008-07-08
影响因子：
11.1
作者：
Diederichs, Sven;Jung, Stephanie;Habert, Daniel A.
通讯作者：
Habert, Daniel A.
影响因子：
5.2
作者：
Hillje, Anna-Lena;Worlitzer, Maik M. A.;Schwamborn, Jens C.
通讯作者：
Schwamborn, Jens C.
影响因子：
9.8
作者：
通讯作者：
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