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本文引用的文献

1
"Stripe" transcription factors provide accessibility to co-binding partners in mammalian genomes."Stripe" 转录因子为哺乳动物基因组中的共结合伴侣提供了可及性。
Mol Cell. 2022 Sep 15;82(18):3398-3411.e11. doi: 10.1016/j.molcel.2022.06.029. Epub 2022 Jul 20.
2
Prioritization of autoimmune disease-associated genetic variants that perturb regulatory element activity in T cells.优先考虑自身免疫性疾病相关的遗传变异,这些变异会干扰 T 细胞中调节元件的活性。
Nat Genet. 2022 May;54(5):603-612. doi: 10.1038/s41588-022-01056-5. Epub 2022 May 5.
3
ChIP-Atlas 2021 update: a data-mining suite for exploring epigenomic landscapes by fully integrating ChIP-seq, ATAC-seq and Bisulfite-seq data.ChIP-Atlas 2021 更新:通过全面整合 ChIP-seq、ATAC-seq 和 Bisulfite-seq 数据,用于探索表观基因组景观的数据挖掘套件。
Nucleic Acids Res. 2022 Jul 5;50(W1):W175-W182. doi: 10.1093/nar/gkac199.
4
JASPAR 2022: the 9th release of the open-access database of transcription factor binding profiles.JASPAR 2022:转录因子结合谱开放获取数据库的第 9 个版本。
Nucleic Acids Res. 2022 Jan 7;50(D1):D165-D173. doi: 10.1093/nar/gkab1113.
5
Factorbook: an updated catalog of transcription factor motifs and candidate regulatory motif sites.Factorbook:转录因子基序和候选调控基序位点的更新目录。
Nucleic Acids Res. 2022 Jan 7;50(D1):D141-D149. doi: 10.1093/nar/gkab1039.
6
ReMap 2022: a database of Human, Mouse, Drosophila and Arabidopsis regulatory regions from an integrative analysis of DNA-binding sequencing experiments.ReMap 2022:一个整合了 DNA 结合测序实验分析的人类、小鼠、果蝇和拟南芥调控区域数据库。
Nucleic Acids Res. 2022 Jan 7;50(D1):D316-D325. doi: 10.1093/nar/gkab996.
7
Cooperative binding between distant transcription factors is a hallmark of active enhancers.远距离转录因子之间的协同结合是活跃增强子的一个标志。
Mol Cell. 2021 Apr 15;81(8):1651-1665.e4. doi: 10.1016/j.molcel.2021.02.014. Epub 2021 Mar 10.
8
GTRD: an integrated view of transcription regulation.GTRD:转录调控的综合视图。
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9
Seven myths of how transcription factors read the cis-regulatory code.转录因子如何解读顺式调控密码的七个误区。
Curr Opin Syst Biol. 2020 Oct;23:22-31. doi: 10.1016/j.coisb.2020.08.002. Epub 2020 Sep 4.
10
ATACdb: a comprehensive human chromatin accessibility database.ATACdb:一个全面的人类染色质可及性数据库。
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TFSyntax:哺乳动物基因组中转录因子结合语法的数据库。

TFSyntax: a database of transcription factors binding syntax in mammalian genomes.

机构信息

Lymphocyte Nuclear Biology, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA.

出版信息

Nucleic Acids Res. 2023 Jan 6;51(D1):D306-D314. doi: 10.1093/nar/gkac849.

DOI:10.1093/nar/gkac849
PMID:36200824
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9825613/
Abstract

In mammals, transcriptional factors (TFs) drive gene expression by binding to regulatory elements in a cooperative manner. Deciphering the rules of such cooperation is crucial to obtain a full understanding of cellular homeostasis and development. Although this is a long-standing topic, there is no comprehensive database for biologists to access the syntax of TF binding sites. Here we present TFSyntax (https://tfsyntax.zhaopage.com), a database focusing on the arrangement of TF binding sites. TFSyntax maps the binding motif of 1299 human TFs and 890 mouse TFs across 382 cells and tissues, representing the most comprehensive TF binding map to date. In addition to location, TFSyntax defines motif positional preference, density and colocalization within accessible elements. Powered by a series of functional modules based on web interface, users can freely search, browse, analyze, and download data of interest. With comprehensive characterization of TF binding syntax across distinct tissues and cell types, TFSyntax represents a valuable resource and platform for studying the mechanism of transcriptional regulation and exploring how regulatory DNA variants cause disease.

摘要

在哺乳动物中,转录因子(TFs)通过协同结合调控元件来驱动基因表达。解析这种协同作用的规则对于全面了解细胞内稳态和发育至关重要。尽管这是一个长期存在的话题,但生物学家并没有一个全面的数据库来访问 TF 结合位点的语法。在这里,我们介绍 TFSyntax(https://tfsyntax.zhaopage.com),这是一个专注于 TF 结合位点排列的数据库。TFSyntax 绘制了 1299 个人类 TF 和 890 个小鼠 TF 在 382 种细胞和组织中的结合基序,这是迄今为止最全面的 TF 结合图谱。除了位置外,TFSyntax 还定义了可及元件中 motif 位置偏好、密度和共定位。基于一系列基于网络界面的功能模块,用户可以自由搜索、浏览、分析和下载感兴趣的数据。TFSyntax 对不同组织和细胞类型的 TF 结合语法进行了全面描述,是研究转录调控机制和探索调控 DNA 变异如何导致疾病的宝贵资源和平台。