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REST is a hypoxia-responsive transcriptional repressor
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REST is a hypoxia-responsive transcriptional repressor TaylorC.pdf | 2.1 MB |
Author(s)
Date Issued
17 August 2016
Date Available
19T15:50:27Z December 2017
Abstract
Cellular exposure to hypoxia results in altered gene expression in a range of physiologic and pathophysiologic states. Discrete cohorts of genes can be either up- or down-regulated in response to hypoxia. While the Hypoxia-Inducible Factor (HIF) is the primary driver of hypoxia-induced adaptive gene expression, less is known about the signalling mechanisms regulating hypoxia-dependent gene repression. Using RNA-seq, we demonstrate that equivalent numbers of genes are induced and repressed in human embryonic kidney (HEK293) cells. We demonstrate that nuclear localization of the Repressor Element 1-Silencing Transcription factor (REST) is induced in hypoxia and that REST is responsible for regulating approximately 20% of the hypoxia-repressed genes. Using chromatin immunoprecipitation assays we demonstrate that REST-dependent gene repression is at least in part mediated by direct binding to the promoters of target genes. Based on these data, we propose that REST is a key mediator of gene repression in hypoxia.
Sponsorship
Science Foundation Ireland
Type of Material
Journal Article
Publisher
Springer Nature
Journal
Scientific Reports
Volume
6
Language
English
Status of Item
Peer reviewed
This item is made available under a Creative Commons License
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