Cargando…

Higher-Order Chromatin Regulation of Inflammatory Gene Expression

Whether it is caused by viruses and bacteria infection, or low-grade chronic inflammation of atherosclerosis and cellular senescence, the transcription factor (TF) NF-κB plays a central role in the inducible expression of inflammatory genes. Accumulated evidence has indicated that the chromatin envi...

Descripción completa

Detalles Bibliográficos
Autores principales: Xu, Jin-Wen, Ling, Shuang, Liu, Jun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5401750/
https://www.ncbi.nlm.nih.gov/pubmed/28490839
http://dx.doi.org/10.1155/2017/7848591
_version_ 1783231103929155584
author Xu, Jin-Wen
Ling, Shuang
Liu, Jun
author_facet Xu, Jin-Wen
Ling, Shuang
Liu, Jun
author_sort Xu, Jin-Wen
collection PubMed
description Whether it is caused by viruses and bacteria infection, or low-grade chronic inflammation of atherosclerosis and cellular senescence, the transcription factor (TF) NF-κB plays a central role in the inducible expression of inflammatory genes. Accumulated evidence has indicated that the chromatin environment is the main determinant of TF binding in gene expression regulation, including the stimulus-responsive NF-κB. Dynamic changes in intra- and interchromosomes are the key regulatory mechanisms promoting the binding of TFs. When an inflammatory process is triggered, NF-κB binds to enhancers or superenhancers, triggering the transcription of enhancer RNA (eRNA), driving the chromatin of the NF-κB-binding gene locus to construct transcriptional factories, and forming intra- or interchromosomal contacts. These processes reveal a mechanism in which intrachromosomal contacts appear to be cis-control enhancer-promoter communications, whereas interchromosomal regulatory elements construct trans-form relationships with genes on other chromosomes. This article will review emerging evidence on the genome organization hierarchy underlying the inflammatory response.
format Online
Article
Text
id pubmed-5401750
institution National Center for Biotechnology Information
language English
publishDate 2017
publisher Hindawi
record_format MEDLINE/PubMed
spelling pubmed-54017502017-05-10 Higher-Order Chromatin Regulation of Inflammatory Gene Expression Xu, Jin-Wen Ling, Shuang Liu, Jun Mediators Inflamm Review Article Whether it is caused by viruses and bacteria infection, or low-grade chronic inflammation of atherosclerosis and cellular senescence, the transcription factor (TF) NF-κB plays a central role in the inducible expression of inflammatory genes. Accumulated evidence has indicated that the chromatin environment is the main determinant of TF binding in gene expression regulation, including the stimulus-responsive NF-κB. Dynamic changes in intra- and interchromosomes are the key regulatory mechanisms promoting the binding of TFs. When an inflammatory process is triggered, NF-κB binds to enhancers or superenhancers, triggering the transcription of enhancer RNA (eRNA), driving the chromatin of the NF-κB-binding gene locus to construct transcriptional factories, and forming intra- or interchromosomal contacts. These processes reveal a mechanism in which intrachromosomal contacts appear to be cis-control enhancer-promoter communications, whereas interchromosomal regulatory elements construct trans-form relationships with genes on other chromosomes. This article will review emerging evidence on the genome organization hierarchy underlying the inflammatory response. Hindawi 2017 2017-04-09 /pmc/articles/PMC5401750/ /pubmed/28490839 http://dx.doi.org/10.1155/2017/7848591 Text en Copyright © 2017 Jin-Wen Xu et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Xu, Jin-Wen
Ling, Shuang
Liu, Jun
Higher-Order Chromatin Regulation of Inflammatory Gene Expression
title Higher-Order Chromatin Regulation of Inflammatory Gene Expression
title_full Higher-Order Chromatin Regulation of Inflammatory Gene Expression
title_fullStr Higher-Order Chromatin Regulation of Inflammatory Gene Expression
title_full_unstemmed Higher-Order Chromatin Regulation of Inflammatory Gene Expression
title_short Higher-Order Chromatin Regulation of Inflammatory Gene Expression
title_sort higher-order chromatin regulation of inflammatory gene expression
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5401750/
https://www.ncbi.nlm.nih.gov/pubmed/28490839
http://dx.doi.org/10.1155/2017/7848591
work_keys_str_mv AT xujinwen higherorderchromatinregulationofinflammatorygeneexpression
AT lingshuang higherorderchromatinregulationofinflammatorygeneexpression
AT liujun higherorderchromatinregulationofinflammatorygeneexpression