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Mediators of Inflammation - Volume 2017 2017, Article ID 7848591, 6 pages - https:-doi.org-10.1155-2017-7848591

Review ArticleInstitute of Interdisciplinary Research Complex, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China

Correspondence should be addressed to Jin-Wen Xu

Received 20 October 2016; Accepted 21 March 2017; Published 9 April 2017

Academic Editor: Soh Yamazaki

Copyright © 2017 Jin-Wen Xu et al. 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.


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.

Author: Jin-Wen Xu, Shuang Ling, and Jun Liu

Source: https://www.hindawi.com/


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