Epigenetic Regulation of Gene Expression in the Inflammatory Response and Relevance to Common Diseases

2008 ◽  
Vol 79 (8s) ◽  
pp. 1514-1519 ◽  
Author(s):  
Anthony G. Wilson
Leukemia ◽  
2015 ◽  
Vol 30 (6) ◽  
pp. 1436-1440 ◽  
Author(s):  
C Song ◽  
X Pan ◽  
Z Ge ◽  
C Gowda ◽  
Y Ding ◽  
...  

2014 ◽  
Vol 5 (3) ◽  
pp. 183-194 ◽  
Author(s):  
Reuben M. Buckley ◽  
David L. Adelson

AbstractTransposable elements (TEs) make up a large proportion of mammalian genomes and are a strong evolutionary force capable of rewiring regulatory networks and causing genome rearrangements. Additionally, there are many eukaryotic epigenetic defense mechanisms able to transcriptionally silence TEs. Furthermore, small RNA molecules that target TE DNA sequences often mediate these epigenetic defense mechanisms. As a result, epigenetic marks associated with TE silencing can be reestablished after epigenetic reprogramming – an event during the mammalian life cycle that results in widespread loss of parental epigenetic marks. Furthermore, targeted epigenetic marks associated with TE silencing may have an impact on nearby gene expression. Therefore, TEs may have driven species evolution via their ability to heritably alter the epigenetic regulation of gene expression in mammals.


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