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印迹的大型非编码 RNA 长距离沉默的机制。

Mechanisms of long range silencing by imprinted macro non-coding RNAs.

机构信息

CeMM Research Center for Molecular Medicine of the Austrian Academy of Science, Lazarettgasse 14, AKH-BT 25.3, 1090 Vienna, Austria.

出版信息

Curr Opin Genet Dev. 2012 Jun;22(3):283-9. doi: 10.1016/j.gde.2012.02.005. Epub 2012 Mar 3.

DOI:10.1016/j.gde.2012.02.005
PMID:22386265
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3387373/
Abstract

Non-coding (nc) RNA silencing of imprinted genes in extra-embryonic tissues provides a good model for understanding an underexamined aspect of gene regulation by macro or long ncRNAs, that is their action as long-range cis-silencers. Numerous long intergenic ncRNAs (lincRNAs) have been recently discovered that are thought to regulate gene expression, some of which have been associated with disease. The few shown to regulate protein-coding genes are suggested to act by targeting repressive or active chromatin marks. Correlative evidence also indicates that imprinted macro ncRNAs cause long-range cis-silencing in placenta by targeting repressive histone modifications to imprinted promoters. It is timely, however, to consider alternative explanations consistent with the published data, whereby transcription alone could cause gene silencing at a distance.

摘要

非编码 (nc) RNA 在胚胎外组织中对印记基因的沉默为理解长链或长 ncRNA 对基因调控的一个研究较少的方面提供了一个很好的模型,即它们作为长距离顺式沉默子的作用。最近发现了许多长基因间 ncRNA (lincRNA),它们被认为可以调节基因表达,其中一些与疾病有关。少数被证明可以调节蛋白质编码基因的 lincRNA 被认为可以通过靶向抑制性或活性染色质标记来发挥作用。相关证据还表明,印记的长链 ncRNA 通过靶向印记启动子的抑制性组蛋白修饰来引起胎盘的长距离顺式沉默。然而,现在是时候考虑与已发表数据一致的替代解释了,即转录本身就可以在远处引起基因沉默。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2463/3387373/33da09b4d5b2/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2463/3387373/018cac67736d/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2463/3387373/33da09b4d5b2/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2463/3387373/018cac67736d/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2463/3387373/33da09b4d5b2/gr2.jpg

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Tissue-specific alternative polyadenylation at the imprinted gene Mest regulates allelic usage at Copg2.组织特异性可变多聚腺苷酸化在印迹基因 Mest 调控 Copg2 的等位基因使用。
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