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Chromatin modification alters gene expression; therefore, scientists can add histone-modifying enzymes, histone variants, and chromatin remodeling complexes to somatic cells to aid reprogramming into pluripotent stem (iPS) cells.
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An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
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The histone proteins in the nucleosomes are post-translationally modified (PTM) to increase or decrease access to DNA. The commonly observed PTMs are methylation, acetylation, phosphorylation, and ubiquitination of lysine amino acids in the histone H3 tail region. These histone modifications have specific meaning for the cell. Hence, they are called "histone code". The protein complex involved in histone modification is termed as "reader-writer" complex.
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Chromatin is the massive complex of DNA and proteins packaged inside the nucleus. The complexity of chromatin folding and how it is packaged inside the nucleus greatly influences  access to genetic information. Generally, the nucleus' periphery is considered transcriptionally repressive, while the cell's interior is considered a transcriptionally active area. 
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Repressing Gene Transcription by Redirecting Cellular Machinery with Chemical Epigenetic Modifiers
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Targeting Chromatin Remodeling in Inflammation and Fibrosis.

J Yang1, B Tian2, A R Brasier2

  • 1University of Texas Medical Branch, Galveston, TX, United States; Sealy Center for Molecular Medicine, University of Texas Medical Branch, Galveston, TX, United States.

Advances in Protein Chemistry and Structural Biology
|February 21, 2017
PubMed
Summary

This study reveals how prolonged activation of the RelA-BRD4 pathway drives inflammation and fibrosis. Targeting this pathway and EZH2 may reverse fibrosis and restore mucosal immunity in chronic diseases.

Keywords:
Bromodomain 4Epithelial–mesenchymal transitionInnate inflammationTranscriptional elongation

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Area of Science:

  • Immunology
  • Molecular Biology
  • Epigenetics

Background:

  • Mucosal surfaces act as a barrier against pathogens.
  • Pattern recognition receptors detect viruses, initiating host responses via NFκB/RelA.
  • The RelA complex with BRD4 and P-TEFb regulates transcription and inflammation.

Purpose of the Study:

  • To explore the link between prolonged RelA-BRD4 pathway activation and epithelial-mesenchymal transition (EMT).
  • To investigate the role of EZH2 in silencing interferon response factors.
  • To highlight therapeutic targets for chronic inflammatory diseases.

Main Methods:

  • Analysis of the RelA·BRD4·P-TEFb complex's role in transcriptional regulation.
  • Investigation of EMT induction by corepressors and growth factor secretion.
  • Examination of ZEB1-mediated silencing of IRF1 by EZH2.

Main Results:

  • Prolonged RelA-BRD4 activation promotes EMT, airway fibrosis, and inflammation.
  • ZEB1 silences IRF1 expression, inhibiting type III IFN production.
  • EZH2 mediates this epigenetic silencing.

Conclusions:

  • Disrupting the RelA·BRD4·P-TEFb pathway and EZH2 offers potential for reversing fibrosis.
  • These strategies could restore mucosal immunity in chronic inflammatory conditions.
  • Small-molecule inhibitors targeting NFκB/RelA, CDK9, BRD4, and EZH2 are promising therapeutic avenues.