Mystery of Trbp, tale of a RBP in the miRNA pathway.
Mystery of Trbp, tale of a RBP in the miRNA pathway.
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Trbp 之谜，miRNA 通路中 RBP 的故事。
DOI：
10.1080/15384101.2015.1084202
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发表时间：
2015
期刊：
影响因子：
--
通讯作者：
Wang,Da-Zhi
中科院分区：
文献类型：
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作者：
Ding,Jian;Wang,Da-Zhi
RNA 结合蛋白 (RBP) 是与双链或单链 RNA 分子结合的蛋白质。一般来说，RBP 被认为在 RNA 转录后控制中发挥着重要作用，例如：mRNA 定位、mRNA 稳定、聚腺苷酸化、剪接和翻译。在哺乳动物中已发现数百种 RBP。然而，迄今为止，仅对这些 RBP 的一小部分进行了机械和功能表征，这就留下了一个问题：为什么细胞要投入如此大量的资源来生产如此多的 RBP。答案之一可能来自最近发现的非编码RNA；现在人们认识到，我们的基因组大部分用于编码非编码RNA (ncRNA)，包括微小RNA (miRNA) 和长非编码RNA (lncRNA)。预计细胞中需要许多 RBP 来调节这些大量 ncRNA 的生物发生、修饰和功能作用。 Trbp 最初被确定为与 HIV RNA 结合的 RBP，随后有报道称其参与许多细胞和分子事件。在之前的几项研究中，Trbp 被认为是细胞生长和侵袭的关键调节因子，但其功能结果在不同条件下显得不同，甚至存在争议。 1-4 我们最近使用心肌细胞特异性 Trbp 敲除小鼠进行的研究表明，Trbp 的缺失不会影响心肌细胞的生长或增殖。相反，正常心脏收缩需要 Trbp
RNA-Binding Proteins (RBPs) are proteins that bind to double or single stranded RNA molecules. In general, RBPs are thought to play a major role in post-transcriptional control of RNAs, such as: mRNA localization, mRNA stabilization, polyadenylation, splicing and translation. Hundreds of RBPs have been discovered in mammals. However, only a small fraction of these RBPs was mechanistically and functionally characterized thus far, leaving the question of why the cell has invested such a huge amount of resource to produce so many RBPs. One of the answers may come from the recently identified non-coding RNAs; it is now recognized that majority of our genome is used to code for non-coding RNAs (ncRNAs), including microRNAs (miRNAs) and long non-coding RNAs (lncRNAs). It is anticipated that many RBPs will be needed to modulate the biogenesis, modification and functional action of these large amount of ncRNAs in a cell.Trbp was initially identified as a RBP binding to HIV RNA and has subsequently been reported to participate in numerous cellular and molecular events. In several previous studies, Trbp has been characterized as a key regulator of cell growth and invasion, but the functional outcomes appear distinct, even controversial under different conditions. 1-4 Our recent study, using cardiomyocyte-specific Trbp knockout mice demonstrated that loss of Trbp did not affect cardiomyocyte growth or proliferation. Instead, Trbp is required for normal cardiac contraction