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YY1的作用原理:阴阳1蛋白的转录调控机制

The Why of YY1: Mechanisms of Transcriptional Regulation by Yin Yang 1.

作者信息

Verheul Thijs C J, van Hijfte Levi, Perenthaler Elena, Barakat Tahsin Stefan

机构信息

Department of Cell Biology, Erasmus MC University Medical Center, Rotterdam, Netherlands.

Department of Neurology, Erasmus MC University Medical Center, Rotterdam, Netherlands.

出版信息

Front Cell Dev Biol. 2020 Sep 30;8:592164. doi: 10.3389/fcell.2020.592164. eCollection 2020.

DOI:10.3389/fcell.2020.592164
PMID:33102493
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7554316/
Abstract

First described in 1991, Yin Yang 1 (YY1) is a transcription factor that is ubiquitously expressed throughout mammalian cells. It regulates both transcriptional activation and repression, in a seemingly context-dependent manner. YY1 has a well-established role in the development of the central nervous system, where it is involved in neurogenesis and maintenance of homeostasis in the developing brain. In neurodevelopmental and neurodegenerative disease, the crucial role of YY1 in cellular processes in the central nervous system is further underscored. In this mini-review, we discuss the various mechanisms leading to the transcriptional activating and repressing roles of YY1, including its role as a traditional transcription factor, its interactions with cofactors and chromatin modifiers, the role of YY1 in the non-coding genome and 3D chromatin organization and the possible implications of the phase-separation mechanism on YY1 function. We provide examples on how these processes can be involved in normal development and how alterations can lead to various diseases.

摘要

阴阳1(YY1)于1991年首次被描述,是一种在哺乳动物细胞中普遍表达的转录因子。它以一种看似依赖于上下文的方式调节转录激活和抑制。YY1在中枢神经系统发育中具有既定作用,参与发育中大脑的神经发生和内环境稳态的维持。在神经发育和神经退行性疾病中,YY1在中枢神经系统细胞过程中的关键作用进一步得到强调。在本综述中,我们讨论了导致YY1转录激活和抑制作用的各种机制,包括其作为传统转录因子的作用、与辅因子和染色质修饰剂的相互作用、YY1在非编码基因组和三维染色质组织中的作用以及相分离机制对YY1功能的可能影响。我们提供了这些过程如何参与正常发育以及改变如何导致各种疾病的实例。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53af/7554316/c12a9c70a33f/fcell-08-592164-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53af/7554316/16d3cf908c8b/fcell-08-592164-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53af/7554316/c12a9c70a33f/fcell-08-592164-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53af/7554316/16d3cf908c8b/fcell-08-592164-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53af/7554316/c12a9c70a33f/fcell-08-592164-g002.jpg

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2
Long noncoding RNA SNHG17 induced by YY1 facilitates the glioma progression through targeting miR-506-3p/CTNNB1 axis to activate Wnt/β-catenin signaling pathway.由YY1诱导的长链非编码RNA SNHG17通过靶向miR-506-3p/CTNNB1轴激活Wnt/β-连环蛋白信号通路促进胶质瘤进展。
Cancer Cell Int. 2020 Jan 28;20:29. doi: 10.1186/s12935-019-1088-3. eCollection 2020.
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The Two Sides of YY1 in Cancer: A Friend and a Foe.
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