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Brd4 is on the move during inflammation.在炎症过程中，Brd4处于动态变化中。
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2
NF-κB directs dynamic super enhancer formation in inflammation and atherogenesis.NF-κB 指导炎症和动脉粥样硬化形成中的动态超级增强子形成。
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Re-place your BETs: the dynamics of super enhancers.替换你的 BET 蛋白：超级增强子的动力学
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Efficacy of Novel Highly Specific Bromodomain-Containing Protein 4 Inhibitors in Innate Inflammation-Driven Airway Remodeling.新型高特异性溴结构域蛋白 4 抑制剂在先天炎症驱动的气道重塑中的疗效。
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本文引用的文献

1
NF-κB directs dynamic super enhancer formation in inflammation and atherogenesis.NF-κB 指导炎症和动脉粥样硬化形成中的动态超级增强子形成。
Mol Cell. 2014 Oct 23;56(2):219-231. doi: 10.1016/j.molcel.2014.08.024. Epub 2014 Sep 25.
2
Enhancer biology and enhanceropathies.增强子生物学与增强子病。
Nat Struct Mol Biol. 2014 Mar;21(3):210-9. doi: 10.1038/nsmb.2784.
3
A high-resolution map of the three-dimensional chromatin interactome in human cells.人类细胞三维染色质互作组的高分辨率图谱。
Nature. 2013 Nov 14;503(7475):290-4. doi: 10.1038/nature12644. Epub 2013 Oct 20.
4
Remodeling of the enhancer landscape during macrophage activation is coupled to enhancer transcription.在巨噬细胞激活过程中，增强子景观的重塑与增强子转录相偶联。
Mol Cell. 2013 Aug 8;51(3):310-25. doi: 10.1016/j.molcel.2013.07.010.
5
Selective inhibition of tumor oncogenes by disruption of super-enhancers.通过破坏超级增强子选择性抑制肿瘤癌基因。
Cell. 2013 Apr 11;153(2):320-34. doi: 10.1016/j.cell.2013.03.036.
6
Latent enhancers activated by stimulation in differentiated cells.受分化细胞刺激激活的潜伏增强子。
Cell. 2013 Jan 17;152(1-2):157-71. doi: 10.1016/j.cell.2012.12.018.
7
Transcription factors: from enhancer binding to developmental control.转录因子：从增强子结合到发育控制。
Nat Rev Genet. 2012 Sep;13(9):613-26. doi: 10.1038/nrg3207. Epub 2012 Aug 7.
8
Suppression of inflammation by a synthetic histone mimic.通过合成组蛋白类似物抑制炎症。
Nature. 2010 Dec 23;468(7327):1119-23. doi: 10.1038/nature09589. Epub 2010 Nov 10.
9
Simple combinations of lineage-determining transcription factors prime cis-regulatory elements required for macrophage and B cell identities.转录因子的简单组合为巨噬细胞和 B 细胞特性所需的顺式调控元件提供了启动条件。
Mol Cell. 2010 May 28;38(4):576-89. doi: 10.1016/j.molcel.2010.05.004.
10
Brd4 coactivates transcriptional activation of NF-kappaB via specific binding to acetylated RelA.Brd4通过与乙酰化的RelA特异性结合，共激活NF-κB的转录激活。
Mol Cell Biol. 2009 Mar;29(5):1375-87. doi: 10.1128/MCB.01365-08. Epub 2008 Dec 22.

在炎症过程中，Brd4处于动态变化中。

Brd4 is on the move during inflammation.

作者信息

Xu Yali, Vakoc Christopher R

机构信息

Cold Spring Harbor Laboratory, One Bungtown Road, Cold Spring Harbor, NY 11724, USA; Molecular and Cellular Biology Program, Stony Brook University, Stony Brook, NY 11794, USA.

Cold Spring Harbor Laboratory, One Bungtown Road, Cold Spring Harbor, NY 11724, USA.

出版信息

Trends Cell Biol. 2014 Nov;24(11):615-6. doi: 10.1016/j.tcb.2014.09.005. Epub 2014 Oct 3.

DOI:10.1016/j.tcb.2014.09.005
PMID:25288306
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4252248/
Abstract

Enhancer landscapes are shaped by the integrated functions of lineage-specific and signal-dependent transcription factors. A new study by Brown et al. suggests that the signal-dependent transcription factor NF-kB can modulate global enhancer activities by altering the occupancy of Brd4, a BET bromodomain coactivator protein, across the genome. This work reveals new principles of enhancer dynamics and insights into the therapeutic modulation of enhancer function with BET bromodomain inhibitors.

摘要

增强子景观由谱系特异性和信号依赖性转录因子的综合功能塑造。布朗等人的一项新研究表明，信号依赖性转录因子NF-κB可通过改变全基因组范围内BET溴结构域共激活蛋白Brd4的占据情况来调节整体增强子活性。这项工作揭示了增强子动态变化的新原理，并为使用BET溴结构域抑制剂对增强子功能进行治疗性调节提供了见解。