Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Rattus norvegicus

ABSTRACT: Etiology matters - Comparing Genomic DNA Methylation Patterns in Three Rat Models of Acquired Epilepsy (TBI – MBD-seq)

PROVIDER: PRJNA302541 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR2921760.fastq.gz	Fastqsanger.gz
	SRR2921761.fastq.gz	Fastqsanger.gz
	SRR2921762.fastq.gz	Fastqsanger.gz
	SRR2921763.fastq.gz	Fastqsanger.gz
	SRR2921764.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 10

Similar Datasets

Rattus norvegicus

Project description:Etiology matters - Comparing Genomic DNA Methylation Patterns in Three Rat Models of Acquired Epilepsy (TBI – mRNA-seq)

| PRJNA302540 | ENA

Rattus norvegicus

Project description:Etiology matters - Comparing Genomic DNA Methylation Patterns in Three Rat Models of Acquired Epilepsy (Amygdala stimulation – MBD-seq)

| PRJNA304118 | ENA

Etiology matters - Comparing Genomic DNA Methylation Patterns in Three Rat Models of Acquired Epilepsy

Project description:Etiology matters - Comparing Genomic DNA Methylation Patterns in Three Rat Models of Acquired Epilepsy

| PRJNA302538 | ENA

Etiology matters - Comparing Genomic DNA Methylation Patterns in Three Rat Models of Acquired Epilepsy

Project description:Etiology matters - Comparing Genomic DNA Methylation Patterns in Three Rat Models of Acquired Epilepsy

| PRJNA304112 | ENA

Rattus norvegicus

Project description:Etiology matters - Comparing Genomic DNA Methylation Patterns in Three Rat Models of Acquired Epilepsy (Amygdala stimulation – mRNA-seq)

| PRJNA304117 | ENA

Discovery and validation of circulating microRNAs as biomarkers for epileptogenesis after experimental traumatic brain injury – the EPITARGET cohort

Project description:Purpose: Traumatic brain injury (TBI) causes 10%–20% of structural epilepsies and 5% of all epilepsies. The lack of prognostic biomarkers for post-traumatic epilepsy (PTE) is a major obstacle to the development of anti-epileptogenic treatments. In this study, we conducted high throughput small RNA-Seq analysis from tail-vein plasma samples collected from a rat model of PTE to discover miRNA biomarker candidates that could serve as prognostic biomarkers for brain damage severity and the development of PTE. Methods: Epileptogenesis was induced in adult male Sprague-Dawley rats by the lateral fluid-percussion-induced TBI. Epilepsy was defined as the occurrence of at least 1 unprovoked seizure during continuous 1-month video-electroencephalography monitoring in the sixth post-TBI month. Small RNA-seq was performed from tail-vein plasma samples collected from a subset of 20 animals (4 sham-operated controls, 7 TBI rats with epilepsy, 9 TBI rats without epilepsy) at 2 days and 9 days post-TBI. RNA was extracted from 200 μl plasma using an miRNeasy Mini Kit. Small RNA-Seq was conducted by GenomeScan (Leiden, the Netherlands). Small RNA library preparation was performed using the Illumina TruSeq Small RNA Sample Prep Kit. Single-end sequencing was performed on the Illumina HiSeq 4000.

2023-02-10 | GSE222801 | GEO

Transcriptomics but not DNA methylomics find Tp73, Cebpd, Pax6 and Spi1 transcription factors as treatment targets for traumatic brain injury

Project description:TBI was induced with lateral fluid-percussion injury in adult male rats. MBD-seq of the perilesional cortex, ipsilateral thalamus and ipsilateral hippocampus was performed at 3 months post-TBI. The data was used to identify differential methylation of gene promoter, gene body, and exons in the perilesional cortex , thalamus and hippocampus.

2018-05-22 | GSE107837 | GEO

Expression data from rat brain following ischemic stroke or undercut

Project description:Although it is well known that stroke and head trauma are one of the high risk factors for the development of acquired epilepsy, the cellular mechanisms underlying the epileptogenesis is not well understood. Using rodent models of ischemic stroke and head trauma (partial cortical isolation, undercut), we comparatively analyzed transcription profiles between two different models to explore the commonality. Despite well-known risk factors such as stroke and head trauma, it has not been clinically effective to prevent acquired epilepsy. To do so, it is crucial to understand what commonly drives neural hyperexcitability. Using comparative transcriptome analyses with different models of acquired epilepsy including stroke and head trauma (the present GEO case), as well as blood-brain barrier (BBB) disruption, albumin, and TGFβ application (GEO accession number: GSE12304), we show that TGFβ signaling activation following BBB disruption commonly occurs regardless of brain region and insult types, accompanied by the strong upregulation of genes relevant to inflammation and extracellular matrix (ECM) modulation.

2017-08-21 | GSE81302 | GEO

Dynamic changes of DNA methylome and hydroxymethylome during neural differentiation of hES cell (hMeDIP-Seq and MBD-Seq)

Project description:DNA methylation and hydroxymethylation have been implicated in normal development and differentiation, but our knowledge about the genome-wide distribution of 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC) during cellular differentiation remains limited. Using in vitro model system of gradual differentiation of human embryonic stem (hES) cells into ventral midbrain-type neural precursor (NP) cells and terminally into dopamine (DA) neurons, we explored changes in 5mC or 5hmC patterns during lineage commitment. We used three techniques, 450K DNA methylation array, MBD-seq, and hMeDIP-seq, and found combination of these methods can provide comprehensive information on the genome-wide 5mC or 5hmC patterns. We observed dramatic changes of 5mC patterns during differentiation of hES cells into NP cells. Although genome-wide 5hmC distribution was more stable than 5mC, coding exons, CpG islands and shores showed dynamic 5hmC patterns during differentiation. In addition to the role of DNA methylation as a mechanism to initiating gene silencing, we also found DNA methylation as a locking system to maintain gene silencing. More than 1,000 genes including mesoderm development related genes acquired promoter methylation during neuronal differentiation even though they were already silenced in hES cells. Finally, we found that activated genes lost 5mC in transcription start site (TSS) but acquired 5hmC around TSS and gene body during differentiation. Our findings may provide clues for elucidating the molecular mechanisms underlying lineage specific differentiation of pluripotent stem cells during human embryonic development. Examination of hMeDIP-Seq and MBD-Seq in 3 cell types (human embryonic stem, neural precursor, and dopamine neuron cells)

2013-11-04 | E-GEOD-38214 | biostudies-arrayexpress

Impact of NRSF variant over-expression in SK-N-AS human neuroblastoma cells

Project description:Neuron-restrictive silencer factor (NRSF) and its isoforms are differentially regulated in rodent models of self-sustaining status epilepticus (SSSE). NRSF isoforms regulate genes associated with SSSE, including the proconvulsant tachykinins, brain-derived neurotrophic factor and multiple ion channels. NRSF isoforms may direct distinct gene expression patterns during SSSE and the ratio of each isoform may be a causative factor in traumatic damage to the CNS. Here we analysed global gene expression changes by microarray in human SK-N-AS neuroblastoma cells following the over expression of NRSF and a truncated isoform, HZ4. We used bioinformatics software to analyse the microarray dataset and correlated these data with epilepsy candidate gene pathways. Findings were validated by RT-PCR. We demonstrated that NRSF and HZ4 direct overlapping as well as distinct gene expression patterns and that they differentially modulated gene expression patterns associated with epilepsy. Finally we revealed that NRSF gene expression may be modulated by the anticonvulsant, phenytoin. This study provides fundamental information on networks of genes that may be altered during SSSE, following altered NRSF expression, which may be important in future therapeutic research and clinical analysis of genetic variation predisposing to epilepsy. Human SK-N-AS cells were treated with expression constructs over-expressing either the full length human transcription factor, NRSF, (via the RE-EX1 construct) or a truncated variant (via the HZ4 construct). Cells were treated for either 0hrs (base line controls), 24hrs or 48hrs, before being immediately processed for RNA extraction. An affymetrix microarray was employed to investigate gene expression patterns, comparing each time point (24hrs or 48hrs) againsts its baseline ()hrs) control. This experiment was performed in triplicate samples per batch, and over three batches.

2010-07-30 | E-GEOD-22467 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data