Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mus musculus

ABSTRACT: Epigenetic correction of defective plasticity in a tauopathy mouse model with an acetyltransferase activator [ChIP-Seq]

PROVIDER: PRJNA401662 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR5996660.fastq.gz	Fastqsanger.gz
	SRR5996651.fastq.gz	Fastqsanger.gz
	SRR5996661.fastq.gz	Fastqsanger.gz
	SRR5996652.fastq.gz	Fastqsanger.gz
	SRR5996662.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 15

Similar Datasets

Epigenetic correction of defective plasticity in a tauopathy mouse model with an acetyltransferase activator

Project description:Epigenetic correction of defective plasticity in a tauopathy mouse model with an acetyltransferase activator

| PRJNA400914 | ENA

Mus musculus

Project description:Epigenetic correction of defective plasticity in a tauopathy mouse model with an acetyltransferase activator [RNA-Seq]

| PRJNA401661 | ENA

Epigenetic correction of defective plasticity in a tauopathy mouse model with an acetyltransferase activator [RNA-Seq]

Project description:In the adult brain, histone acetylation is associated with activity-regulated transcriptional changes that are required for synaptic plasticity and memory. These processes are dismantled in neurodegenerative diseases. Here, we demonstrate that synaptic plasticity and memory deficiencies can be restored in a mouse model of tauopathy following treatment with CSP-TTK21, a small molecule activator of CBP/p300 histone acetyltransferases (HAT). CSP-TTK21 normalized the H2B acetylation levels in many genes, including a series of super-enhancer –regulated genes, associated with plasticity and neuronal function in resting tauopathic mice. CSP-TTK21 re-established part of the learning-induced hippocampal transcriptome, including the induction of immediate early genes and memory-related genes, and the down-regulation of neuronal identity genes that bear super-enhancers. This study is the first to provide in vivo proof-of-concept evidence that direct activation of CBP/p300 HAT efficiently and selectively reverses epigenetic, transcriptional, synaptic plasticity, and behavioral deficits associated to Alzheimer’s disease lesions in mice.

2018-11-05 | GSE103359 | GEO

Epigenetic correction of defective plasticity in a tauopathy mouse model with an acetyltransferase activator [ChIP-Seq]

2018-11-05 | GSE103358 | GEO

RNA-seq and TRAP-seq of astrocytes and brain tissue in mouse models of Alzheimer's pathology

Project description:Alzheimer’s disease is known to alter astrocytes, but the effect of Aß and Tau pathology on these cells remains poorly understood. We investigated the transcriptomic behaviour of astrocytes (via translating ribosome affinity purification (TRAP)), and bulk brain tissue, in mouse models of APP/PS1 ß-amyloidopathy and MAPT-P301S tauopathy, in a mouse model overexpressing cytoprotective Nrf2 specifically in astrocytes (GFAP-Nrf2 model), and in crosses between the amyloidopathy and tauopathy models with the GFAP-Nrf2 mouse.

2021-12-02 | E-MTAB-10985 | biostudies-arrayexpress

Epigenetic Treatment of Behavioral and Physiological Deficits in a Tauopathy Mouse Model

Project description:Epigenetic Treatment of Behavioral and Physiological Deficits in a Tauopathy Mouse Model

| PRJNA755255 | ENA

Mouse transcriptome changes by Adrb1 mutation in PS19 mice

Project description:To investigate effects of the FNSS mutation Adrb1-A187V on the gene expression profile in a mouse model of tauopathy.

2023-04-05 | GSE205558 | GEO

LncRNA/mRNA sequencing analysis on cerebral cortex of P301S mutant Tau transgenic mice (PS19).

Project description:Aggregation of the microtubule-associated protein, tau, can lead to neurofibrillary tangle formation in neurons and glia, the hallmark of tauopathy. The cellular damages induced by the tau overexpression and aggregation may lead to multiple pathologic features of tauopathy. However, the effect of aging on tauopathy has not been elucidated yet. Here, we conducted lncRNA/mRNA sequencing analysis on P301S mutant Tau transgenic mouse model (PS19) with different ages to track the genetic changes occurred by the aging and progression of tau overexpression.

2019-06-23 | GSE118473 | GEO

Increase genome editing efficiency by Cas9 transcriptional activator and histone acetyltransferase activator

Project description:Increase genome editing efficiency by Cas9 transcriptional activator and histone acetyltransferase activator

| PRJNA827683 | ENA

Human Dorsal Root Ganglion RNA Seq Profiling

Project description:RNA sequencing was performed on human DRGs and relative gene abundances were calculated. Various analyses were performed: <ol> <li>Human DRG gene expression profiles were contrasted with a panel of gene expression profiles of relevant tissues in human and mouse ( integrating, among other sources, datasets from ENCODE and GTex ) in order to identify.</li> <ol type="a"> <li>DRG-enriched gene expression, co-expression modules of DRG-expressed genes, and key transcriptional regulators in humans.</li> <li>Contrasting the human and mouse DRG transcriptomes to identify DRG-enriched gene expression patterns that were conserved between human and mouse, identifying putative cell types of expression of these genes, and potential known drugs that might target the corresponding gene products.</li> <li>Characterization of non-coding RNA profile of human and mouse DRGs.</li> <li>Characterization of DRG-enriched alternative splicing and alternative transcription start site usage based transcript variants in humans and mouse, and the overlap between these two species.</li> <li>Contrasting of human DRG and GTex human tibial nerve samples to identify putative axonally transported mRNAs in sensory neurons.</li> </ol> <li>Human DRG transcriptomes from donors suffering from neuropathic and/or chronic pain were contrasted with controls to identify.</li> <ol type="a"> <li>Differentially expressed genes, pathways and regulators path play a potential role in neuronal plasticity, electrophysiological activity, immune signaling and response.</li> <li>Predictive models (Random Forests) were built to jointly predict the sex and pain state of samples based on information contained solely in autosomal gene expression profile.</li> <li>Gene co-expression modules were identified and gene set enrichment analysis performed.to identify sample - pathway associations, and to broadly characterize plasticity in human DRG cell types.</li> </ol> </ol>

| phs001158 | dbGaP

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