Please use this identifier to cite or link to this item:
Title: Epigenetics in ENS development and Hirschsprung disease.
Authors: Torroglosa, A
Alves, M M
Fernández, R M
Antiñolo, G
Hofstra, R M
Borrego, S
Keywords: Enteric nervous system;Epigenetics;Hirschsprung disease;Neural crest cells
metadata.dc.subject.mesh: DNA Methylation
Enteric Nervous System
Epigenesis, Genetic
Gastrointestinal Tract
Hirschsprung Disease
Neural Crest
RNA Processing, Post-Transcriptional
Signal Transduction
Issue Date: 16-Jun-2016
Abstract: Hirschsprung disease (HSCR, OMIM 142623) is a neurocristopathy caused by a failure of the enteric nervous system (ENS) progenitors derived from neural crest cells (NCCs), to migrate, proliferate, differentiate or survive to and within the gastrointestinal tract, resulting in aganglionosis in the distal colon. The formation of the ENS is a complex process, which is regulated by a large range of molecules and signalling pathways involving both the NCCs and the intestinal environment. This tightly regulated process needs correct regulation of the expression of ENS specific genes. Alterations in the expression of these genes can have dramatic consequences. Several mechanisms that control the expression of genes have been described, such as DNA modification (epigenetic mechanisms), regulation of transcription (transcription factor, enhancers, repressors and silencers), post-transcriptional regulation (3'UTR and miRNAs) and regulation of translation. In this review, we focus on the epigenetic DNA modifications that have been described so far in the context of the ENS development. Moreover we describe the changes that are found in relation to the onset of HSCR.
metadata.dc.identifier.doi: 10.1016/j.ydbio.2016.06.017
Appears in Collections:Producción 2020

Files in This Item:
There are no files associated with this item.

This item is protected by original copyright

Except where otherwise noted, Items on the Andalusian Health Repository site are licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives License.