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Expression data from E12.5 NSP cells, CTL v REST shRNA

ABSTRACT: REST is a master regulator of genes that are involved in the acqusition of neuronal fate. The role of REST is not well understood so we attempted to investigate the role of REST in the development of neural cells by analysing the genes that are upregulated when REST is knocked down via shRNA We used microarrays to assess the genes which were up and down regulated after REST is knocked down

ORGANISM(S): Mus musculus

PROVIDER: GSE38538 | GEO | 2012/06/07

SECONDARY ACCESSION(S): PRJNA168167

REPOSITORIES: GEO

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Expression data from E12.5 NSP cells, CTL v REST shRNA

Project description:REST is a master regulator of genes that are involved in the acqusition of neuronal fate. The role of REST is not well understood so we attempted to investigate the role of REST in the development of neural cells by analysing the genes that are upregulated when REST is knocked down via shRNA We used microarrays to assess the genes which were up and down regulated after REST is knocked down E12.5 NSP cells were infected with either control or REST shRNA expressing lentiviruses and collected after 6 days for RNA extraction

2012-06-06 | E-GEOD-38538 | biostudies-arrayexpress

Downregulation of DDX5/DDX17 and REST

Project description:We aimed at analysing the effect of RNA helicases DDX5 and DDX17 and of the transcription factor REST on gene expression in the human SH-SY5Y neuroblastoma cell line (European Collection of Cell Cultures, ECACC), which was cultured as recommended by the supplier.

2017-12-31 | GSE98871 | GEO

Effect of hypoxia on the Represser Element-1 Silencing Transcription factor (REST) in Human

Project description:The Represser Element-1 Silencing Transcription factor (REST) was knocked-down in HEK293 cells using RNA intereference in cells exposed to 21% or 1% oxygen for 24 hours, the effects on transcript expression (poly(A)+ RNA)) were analyzed using genome wide sequencing (RNAseq).

2016-08-17 | E-MTAB-2580 | biostudies-arrayexpress

Expression analyses of E12.5 embryonic brains from Nestin Cre+, Rest GTi/GTi vs Rest GTi/GTi litermates

2015-08-01 | GSE68459 | GEO

Expression analyses of E12.5 embryonic brains from Nestin Cre+, Rest GTi/GTi, p53 fl/fl vs Rest GTi/GTi, p53 fl/fl littermates

Project description:We use mice containing a gene trap in the first intron of the Rest gene, which effectively eliminates transcription from all coding exons, to prematurely remove REST from neural progenitors. We find catastrophic DNA damage that occurs during S-phase of the cell cycle, with consequences including abnormal chromosome separation, apoptosis, and smaller brains. Further support for persistent effects is the latent appearance of proneural glioblastomas in adult mice also lacking the tumor suppressor, p53. A Rest deficient mouse line generated previously, using a conventional gene targeting approach, does not exhibit these phenotypes, likely due to a remaining C terminal peptide that still binds chromatin and recruits REST chromatin modifiers.Our results indicate that REST-mediated chromatin remodeling is required for proper S-phase dynamics, prior to its well-established role in relieving repression of neuronal genes at terminal differentiation.

2015-08-01 | GSE68368 | GEO

Expression data from H295R cells where NRSF/REST or SF-1 were knocked down

Project description:SF-1 is a nuclear receptor transcription factor playing a key role in adrenogonadal development and in adrenocortical tumorigenesis when overexpressed. NRSF/REST is a transcriptional repressor that represses expression of neuronal genes in non-neural tissues. Some data suggest that SF-1 and NRSF/REST can functionally interact in adrenocortical cancer cells. We studied gene expression profiles using Affymetrix microarrays in the H295R/TR SF-1 adrenocortical cancer cell line. In this cell line, SF-1 expression can be increased in a doxycycline-dependent manner (Mol. Endocrinol. 21: 2968–2987, 2007). The effects of a control siRNA and sRNAs specific for SF-1 and for NRSF/REST (in basal or increased SF-1 expression conditions) on gene expression were measured. In H295R/TR SF-1 cells SF-1 and NRSF/REST (in conditions of basal and increased SF-1 dosage) expression were knocked down by Amaxa nucleofection. RNA was extracted and hybridized to Human Gene 1.0 ST Affymetrix microarrays.

2013-08-01 | E-GEOD-43033 | biostudies-arrayexpress

Expression analyses of E12.5 embryonic brains from Nestin Cre+, Rest GTi/GTi vs Rest GTi/GTi litermates

2015-08-01 | E-GEOD-68459 | biostudies-arrayexpress

Expression analyses of E12.5 embryonic brains from Nestin Cre+, Rest GTi/GTi, p53 fl/fl vs Rest GTi/GTi, p53 fl/fl littermates

2015-08-01 | E-GEOD-68368 | biostudies-arrayexpress

C-terminal Domain Small Phosphatase 1 and MAP kinase reciprocally control REST stability and neuronal differentiation.

Project description:The RE1 Silencing Transcription Factor (REST) in stem cells represses hundreds of genes essential to neuronal function. During neurogenesis, REST is degraded in neural progenitors to promote subsequent elaboration of a mature neuronal phenotype. Prior studies indicate that part of the degradation mechanism involves phosphorylation of two sites in the C-terminus of REST that require activity of the E3 ubiquitin ligase, bTrCP. We identify a new proline-directed phosphorylation motif, at Serines 861/864 upstream of these sites, which is a substrate for the Peptidyl-prolyl cis-trans Isomerase, Pin1, as well as the ERK1/2 kinases. Mutation at S861/864 stabilizes REST, as does inhibition of Pin1 activity. Interestingly, we find that C-Terminal Domain Small Phosphatase1 (CTDSP1) is recruited by REST to neuronal genes, is present in REST immunocomplexes, dephosphorylates S861/864 and stabilizes REST. Expression of a REST peptide containing S861/864 in neural progenitors inhibits terminal neuronal differentiation. Together with previous work indicating that both REST and CTDSP1 are expressed to high levels in stem cells and down regulated during neurogenesis, our results suggest that CTDSP1 activity stabilizes REST in stem cells, and that ERK dependent phosphorylation combined with Pin1 activity promotes REST degradation in neural progenitors.

2014-09-15 | PXD001127 | Pride

REST knock-out ESCs: a role for REST in embryonic stem cells' cardiac lineage specification

Project description:During development, lineage specification is controlled by several signaling pathways involving various transcription factors (TFs). Here, we studied the RE1-silencing transcription factor (REST) and identified an important role of this TF in cardiac differentiation. Using mouse embryonic stem cells (ESC) to model development, we analyzed the effect of REST knock-out on the ability to these cells to differentiate into the cardiac lineage. Detailed analysis of specific lineage markers expression showed selective down-regulation of endoderm markers in REST-null cells, thus contributing to a loss of cardiogenic signals. We propose here a new role for REST in cell fate specification besides its well-known repressive role of neuronal differentiation.

2016-02-01 | GSE76580 | GEO

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