Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Characterization of the chromatin accessibility in an Alzheimer’s disease (AD) mouse model

ABSTRACT: Characterization of the chromatin accessibility in an Alzheimer’s disease (AD) mouse model

PROVIDER: PRJNA608710 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11179779_1.fastq.gz	Fastqsanger.gz
	SRR11179779_2.fastq.gz	Fastqsanger.gz
	SRR11179780_1.fastq.gz	Fastqsanger.gz
	SRR11179780_2.fastq.gz	Fastqsanger.gz
	SRR11179781_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

Characterization of the chromatin accessibility in an Alzheimer’s disease (AD) mouse model (ATAC-Seq)

Project description:Characterization of the chromatin accessibility in an Alzheimer’s disease (AD) mouse model (ATAC-Seq)

| PRJNA608708 | ENA

Characterization of the chromatin accessibility in an Alzheimer’s disease (AD) mouse model (RNA-Seq)

Project description:Characterization of the chromatin accessibility in an Alzheimer’s disease (AD) mouse model (RNA-Seq)

| PRJNA608711 | ENA

Characterization of the chromatin accessibility in an Alzheimer’s disease (AD) mouse model (ATAC-Seq)

Project description:The assay for transposase-accessible chromatin by sequencing (ATAC-seq) was used to investigate the AD-associated chromatin reshaping in the APPswe/PS1dE9 (APP/PS1) mouse model. ATAC-seq data in the hippocampus of 8-month-old APP/PS1 mice were generated, and the relationship between chromatin accessibility and gene expression was analyzed in combination with RNA-sequencing.We identified 1690 increased AD-associated chromatin accessible regions in the hippocampal tissues of APP/PS1 mice and 1003 decreased chromatin accessible regions were considered to be related with declined AD-associated biological processes.In the APP/PS1 hippocampus, 1090 genes were found to be up-regulated and 1081 down-regulated. Interestingly, enhanced ATAC-seq signal was found in approximately 740 genes, with 43 exhibiting up-regulated mRNA levels.Our study reveals that alterations in chromatin accessibility may be an initial mechanism in AD pathogenesis.

2020-07-09 | GSE145906 | GEO

Characterization of the chromatin accessibility in an Alzheimer’s disease (AD) mouse model (RNA-Seq)

2020-07-09 | GSE145907 | GEO

Single-nucleus chromatin accessibility and transcriptomic characterization of Alzheimer’s Disease

Project description:Single-nucleus chromatin accessibility and transcriptomic characterization of Alzheimer’s Disease

| PRJNA729525 | ENA

Single-nucleus chromatin accessibility and transcriptomic characterization of Alzheimer’s Disease

Project description:The gene-regulatory landscape of the brain is highly dynamic in health and disease, coordinating a menagerie of biological processes across¬ distinct cell-types. Here, we present a multi-omic single-nucleus study of 191,890 nuclei in late-stage Alzheimer’s Disease (AD), accessible through our intuitive web portal, profiling chromatin accessibility and gene expression in the same biological samples and uncovering vast cellular heterogeneity. We identified cell-type specific, disease-associated candidate cis-regulatory elements and their candidate target genes, including an oligodendrocyte-associated regulatory module containing links to APOE and CLU. We describe cis-regulatory relationships in specific cell-types at AD risk loci defined by genome wide association studies (GWAS), demonstrating the utility of this multi-omic single-nucleus approach. Trajectory analysis of glial populations identified disease-relevant transcription factors, like SREBF1 and their regulatory targets. Further, we introduce scWGCNA, a co-expression network analysis strategy robust to the sparsity of single-cell data, to perform a systems-level meta-analysis of AD transcriptomics.

2021-05-12 | GSE174367 | GEO

Global Profiling of Lysine Accessibility to Evaluate Protein Structure Changes in Alzheimer’s Disease

Project description:The linear sequence of amino acids in a protein folds into a 3D structure to execute protein activity and function, but it is still challenging to profile the 3D structure at the proteome scale. Here, we present a method of native protein tandem mass tag (TMT) profiling of Lys accessibility and its application to investigate structural alterations in human brain specimens of Alzheimer’s disease (AD).

2021-03-23 | PXD024914 | Pride

Single-cell sequencing of cerebral organoids with familial Alzheimer’s disease (AD) mutation in PSEN1 and non-demented control

Project description:We set up a 3D model based on iPSCs derived from patients with familial forms of Alzheimer’s disease (AD) and healthy non-demented control. We created cerebral organoids (COs), verified their ability to mimic AD in vitro, and used it to explore early events and the progression of AD pathogenesis. Our data reveal that despite similar expression of cell-type-specific genes during CO maturation in vitro, AD-iPSCs derived COs show limited tissue patterning and altered cellular development. These findings complement unique single-cell sequencing data of AD-iPSCs derived COs confirming this observation and uncovering that a sub-set of neurons in AD-iPSCs likely differentiates prematurely while at the same time retaining the expression of progenitor marker PAX6.

2022-07-01 | E-MTAB-11438 | biostudies-arrayexpress

Alzheimer Disease (AD) and AD model detergent insoluble proteomes

Project description:Characterizing the detergent insoluble brain proteome of sporadic late-onset Alzheimer’s disease (LOAD) has identified proteins and pathways associated with disease pathogenesis. Similar studies in early onset Alzheimer’s disease cases due to presenilin-1 mutations (PS1-EOAD), along with more detailed correlations with insoluble proteomes from LOAD and AD transgenic rodents, are limited. We therefore utilized quantitative proteomics to identify proteins that were significantly changing in the PS1-EOAD insoluble proteome versus controls. Comparison with the LOAD insoluble proteome identified common pathologic AD markers in addition to unique PS1-EOAD insoluble proteins. Similarly, weighted correlation network analysis (WGCNA) identified PS1-EOAD and LOAD co-expression modules with both like and disparate expression levels. Finally, we compared the human PS1-EOAD insoluble proteome to transgenic AD mouse and rat insoluble proteomes to understand how well these models mimic the human disease. Although many common AD pathologic findings were found in the rodents, there were multiple PS1-EOAD proteome changes not well recapitulated in the animal models. These proteomic studies highlight unique PS1-EOAD proteome changes as compared to LOAD and identify limitations to using AD transgenic rodents to study some aspects of AD.

2019-06-25 | PXD005321 | Pride

The Adaptive Immune System Restrains Alzheimer’s Disease (AD) Pathogenesis by Modulating Microglial Function

Project description:Neuroinflammation and activation of innate immunity are pathological hallmarks of Alzheimer’s disease (AD). In contrast, very few studies have examined the impact of the adaptive immune system in AD pathogenesis. In this study, we find that genetic deletion of peripheral immune populations significantly accelerates amyloid pathogenesis, worsens neuroinflammation, and alters microglial activation state. We used microarray analysis to profile gene expression underlying genotype related changes at the cellular level in the context of AD .

2016-03-03 | GSE77574 | GEO

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