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在基因调控与基因组组织的交叉路口:ATP依赖的染色质重塑因子在CTCF介导的三维结构调控中的潜在作用

At the Crossroad of Gene Regulation and Genome Organization: Potential Roles for ATP-Dependent Chromatin Remodelers in the Regulation of CTCF-Mediated 3D Architecture.

作者信息

Alpsoy Aktan, Sood Surbhi, Dykhuizen Emily C

机构信息

Purdue University Interdisciplinary Life Science Graduate Program (PULSe), Department of Medicinal Chemistry and Molecular Pharmacology, Purdue University, West Lafayette, IN 47907, USA.

Purdue University Center for Cancer Research, Department of Medicinal Chemistry and Molecular Pharmacology, Purdue University, West Lafayette, IN 47907, USA.

出版信息

Biology (Basel). 2021 Mar 27;10(4):272. doi: 10.3390/biology10040272.

DOI:10.3390/biology10040272
PMID:33801596
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8066914/
Abstract

In higher order organisms, the genome is assembled into a protein-dense structure called chromatin. Chromatin is spatially organized in the nucleus through hierarchical folding, which is tightly regulated both in cycling cells and quiescent cells. Assembly and folding are not one-time events in a cell's lifetime; rather, they are subject to dynamic shifts to allow changes in transcription, DNA replication, or DNA damage repair. Chromatin is regulated at many levels, and recent tools have permitted the elucidation of specific factors involved in the maintenance and regulation of the three-dimensional (3D) genome organization. In this review/perspective, we aim to cover the potential, but relatively unelucidated, crosstalk between 3D genome architecture and the ATP-dependent chromatin remodelers with a specific focus on how the architectural proteins CTCF and cohesin are regulated by chromatin remodeling.

摘要

在高等生物中,基因组组装成一种名为染色质的蛋白质密集结构。染色质通过分级折叠在细胞核中进行空间组织,这种折叠在循环细胞和静止细胞中都受到严格调控。组装和折叠并非细胞生命周期中的一次性事件;相反,它们会发生动态变化,以允许转录、DNA复制或DNA损伤修复发生改变。染色质在多个层面受到调控,最近的技术工具使我们能够阐明参与三维(3D)基因组组织维持和调控的特定因子。在这篇综述/观点文章中,我们旨在探讨3D基因组结构与ATP依赖的染色质重塑因子之间潜在但相对未被阐明的相互作用,特别关注结构蛋白CTCF和黏连蛋白如何受到染色质重塑的调控。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/873b/8066914/a0a8d3517caa/biology-10-00272-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/873b/8066914/c97056599870/biology-10-00272-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/873b/8066914/ed3e46d6ebbd/biology-10-00272-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/873b/8066914/4d1ef39f338d/biology-10-00272-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/873b/8066914/1581a1f1e072/biology-10-00272-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/873b/8066914/a0a8d3517caa/biology-10-00272-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/873b/8066914/c97056599870/biology-10-00272-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/873b/8066914/ed3e46d6ebbd/biology-10-00272-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/873b/8066914/4d1ef39f338d/biology-10-00272-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/873b/8066914/1581a1f1e072/biology-10-00272-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/873b/8066914/a0a8d3517caa/biology-10-00272-g005.jpg

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本文引用的文献

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Multi-level remodelling of chromatin underlying activation of human T cells.人类 T 细胞激活相关染色质的多层次重塑。
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Promoter-proximal CTCF binding promotes distal enhancer-dependent gene activation.启动子近端 CTCF 结合促进远端增强子依赖的基因激活。
长链非编码RNA SLC7A11-AS1通过抑制CTCF的泛素连接酶E3A(UBE3A)介导的泛素化来稳定CTCF,从而促进黑色素瘤转移。
Am J Cancer Res. 2023 Dec 15;13(12):6256-6269. eCollection 2023.
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The Conserved Chromatin Remodeler SMARCAD1 Interacts with TFIIIC and Architectural Proteins in Human and Mouse.保守的染色质重塑因子 SMARCAD1 在人和小鼠中与 TFIIIC 和结构蛋白相互作用。
Genes (Basel). 2023 Sep 13;14(9):1793. doi: 10.3390/genes14091793.
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Loss of PBAF promotes expansion and effector differentiation of CD8 T cells during chronic viral infection and cancer.PBAF 的缺失促进慢性病毒感染和癌症期间 CD8 T 细胞的扩增和效应分化。
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