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Int J Mol Sci ; 21(5)2020 Mar 10.
Article in English | MEDLINE | ID: mdl-32164275

ABSTRACT

Traumatic brain injury is known to reprogram the epigenome. Chromatin immunoprecipitation-sequencing of histone H3 lysine 27 acetylation (H3K27ac) and tri-methylation of histone H3 at lysine 4 (H3K4me3) marks was performed to address the transcriptional regulation of candidate regeneration-associated genes. In this study, we identify a novel enhancer region for induced WNT3A transcription during regeneration of injured cortical neurons. We further demonstrated an increased mono-methylation of histone H3 at lysine 4 (H3K4me1) modification at this enhancer concomitant with a topological interaction between sub-regions of this enhancer and with promoter of WNT3A gene. Together, this study reports a novel mechanism for WNT3A gene transcription and reveals a potential therapeutic intervention for neuronal regeneration.


Subject(s)
Brain Injuries, Traumatic/genetics , Histones/metabolism , Neurons/physiology , Wnt3A Protein/genetics , Acetylation , Animals , Brain Injuries, Traumatic/metabolism , Chromatin Immunoprecipitation , Disease Models, Animal , Enhancer Elements, Genetic , Epigenesis, Genetic , Methylation , Neurons/metabolism , Promoter Regions, Genetic , Rats , Rats, Sprague-Dawley , Regeneration
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