REST ChIP-seq in human and mouse hippocampus
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ABSTRACT:
PROVIDER: PRJNA603079 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10961908.fastq.gz | Fastqsanger.gz | |||
| SRR10961909.fastq.gz | Fastqsanger.gz | |||
| SRR10961910.fastq.gz | Fastqsanger.gz | |||
| SRR10961911.fastq.gz | Fastqsanger.gz | |||
| SRR10961912.fastq.gz | Fastqsanger.gz |
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Project description:The transcriptional repressor REST (RE1 Silencing Transcription Factor) is a master regulator of thousands of neuronal genes that together impart the terminally differentiated neuronal phenotype. Because of this unique feature, REST has been, and continues to be, a widely used model for understanding neurogenesis and neuronal cell function. These studies have focused primarily on murine embryonic development, but recent studies have pointed to distinct postnatal roles for REST in stroke, epilepsy, aging and cognitive decline. The function of REST in healthy human brain tissue, however, still remains poorly characterized. Here, we present deep sequencing chromatin immunoprecipitation evidence for divergent REST function in normal mouse and human postmortem adult hippocampus. In mouse, REST occupies only 221 peaks that are divided between prototypical REST target genes shared with non-neuronal cells, as well as peaks unique to the hippocampus. Surprisingly, the mouse hippocampal-unique sites are not conserved in human, which contains 1886 REST peaks unique to the hippocampus. Further, the REST peaks unique to the hippocampus represent a potentially new category of target genes encoding proteins important in the immune response. Our results suggest the possibility that REST protects against aberrant immunological responses during normal human aging and that mouse may not model this aging function.
2020-07-24 | GSE144226 | GEO
Project description:Multiple protein complexes and histone marks have been implicated and/or associated with gene repression in ES cells. To gain insights into repressive complexes present at repressed genes and their associated chromatin state, we profiled REST, MCAF1, Ring1b and H4K20me3 in mouse ES cells. DNA was enriched by chromatin immunoprecipitation (ChIP) and analyzed by Solexa sequencing. ChIP was performed using an antibody against REST, MCAF1, Ring1b and H4K20me3.
2011-01-19 | E-GEOD-26680 | biostudies-arrayexpress
Project description:In this experiment, we exposed mice to ethanol injections on postnatal days 4 and 7. We then extracted whole-hippocampus on postnatal day 70. We performed MeDIP-chip using an antibody against 5mC. We also perfomed MEDME anaylsis using a chip with fully methylated DNA to act as a control. We found alterations in both modifications at many sites, including oxidative stress genes and imprinted loci. We also found many affect lipid metabolism pathways. Comparision of neonatal ethanol-injected with saline injected C57BL/6J mouse hippocampus in adulthood (day 70)
2015-07-25 | E-GEOD-71313 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE28141: Genome-wide analysis of REST knockdown responsive gene expression in mouse ES cells GSE28233: Genome-wide maps of REST and its cofactors in mouse E14 cells Refer to individual Series
2011-03-31 | E-GEOD-28289 | biostudies-arrayexpress
Project description:We performed ChIP-seq to identify genome-wide REST (NRSF) binding in the human CD4+ T cells. The data were compared to REST occupancy in additional 15 human cell types analyzed by the ENCODE project (GSE32465) in order to study the dynamics and context-dependent functions of REST-chromatin interaction.
2014-08-06 | GSE49570 | GEO
Project description:We performed ChIP-seq to identify genome-wide REST (NRSF) binding in the human CD4+ T cells. The data were compared to REST occupancy in additional 15 human cell types analyzed by the ENCODE project (GSE32465) in order to study the dynamics and context-dependent functions of REST-chromatin interaction. Identification of REST binding by ChIP-seq in human CD4+ T cells.
2014-08-06 | E-GEOD-49570 | biostudies-arrayexpress
Project description:ENCODE ChIP-chip study using 8 diverse human cell lines; 4 of neural origin (NB69, KELLY, SHSY-5Y, U373) and 4 of non-neural origin (HeLa, HepG2, HEK293 and K562) and anti-REST/NRSF antibody (Santa Cruz Biotech; sc-25398 aka H290) to asses REST-genome interactions across 1% of the human genome used in the pilot phase of the ENCODE project. Additionally the REST binding profile in K562 cells that had been transfected with REST specific siRNA oligos (72h and 96h) were determined revealing genomic in vivo binding affinity hierarchies for REST. Additionally the REST binding profile in K562 cells that had been transfected with REST specific siRNA oligos (72h and 96h) were determined
2009-03-31 | E-TABM-660 | biostudies-arrayexpress
Project description:We report the application of single-molecule-based sequencing technology for REST and its cofactors genome wide binding sites in E14 cells.We then combine these binding sirtes with REST regulating gene profiling, to understand REST binding and regulation in E14 cells. Examination of REST and 5 cofactors(RCOR1, RCOR2,RCOR3,SIN3A,SIN3B) in E14 cells, REST and SIN3A endogenous antibody were used for ChIP experiment. The stable E14 cells expressing low level exogenous RCOR1, RCOR2, RCOR3,and SIN3B with V5 tag were used for ChIP experiment with V5 antibody to obtain individual ChIP DNA.
2011-04-01 | E-GEOD-28233 | biostudies-arrayexpress
Project description:Overexpression of REST has been implicated in brain tumors, ischemic insults, epilepsy, and movement disorders such as Huntington’s disease. However, owing to the lack of a conditional REST overexpression animal model, the mechanism of action of REST overexpression in these disorders has not been established in vivo. We created a REST overexpression mouse model using the human REST (hREST) gene. Our results using these mice confirm that hREST expression parallels endogenous REST expression in embryonic mouse brains. Further analyses indicate that REST represses the dopamine receptor 2 (Drd2) gene, which encodes a critical nigrostriatal receptor involved in regulating movement, in vivo. Overexpression of REST using Drd2-Cre in adult mice results in increased REST and decreased DRD2 expression in the striatum, a major site of DRD2 expression, and phenocopies the spontaneous locomotion deficits seen upon global DRD2 deletion or specific DRD2 deletion from indirect-pathway medium spiny neurons. Thus, our studies using this mouse model not only reveal a new function of REST in regulating spontaneous locomotion but also suggest that REST overexpression in DRD2-expressing cells results in spontaneous locomotion deficits.
2022-10-07 | GSE214743 | GEO