Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

DNA methylation profiles from a transgenic sheep model of Huntington's disease

ABSTRACT: An Infinium microarray platform (HorvathMammalMethylChip40) was used to generate DNA methylation data from n=168 blood samples of a transgenic sheep model of Huntington's disease. 84 transgenic sheep and age matched control sheep.

ORGANISM(S): Rattus norvegicus Mus musculus Homo sapiens Ovis aries

PROVIDER: GSE147003 | GEO | 2020/07/02

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

DNA methylation profiles from a transgenic sheep model of Huntington's disease

Project description:DNA methylation profiles from a transgenic sheep model of Huntington's disease

| PRJNA612722 | ENA

Gene expression in the duodenum of sheep genetically resistant or susceptible to nematodes

Project description:This experiment compared gene expression in the duodenum of [1] weaned genetically resistant sheep and weaned genetically susceptible sheep (84 days old) [2] genetically resistant sheep and genetically susceptible sheep that have been naturally challenged once with nematodes (175 days old) and [3] genetically resistant sheep and genetically susceptible sheep that have been naturally challenged twice with nematodes (276 days old). At each time point (T = 84, 175, 276 days) a four factorial design was used with four resistant animals and four susceptible animals. Each animal in the resistant group was compared to each animal in the susceptible group incorporating dye swaps. At T = 84 the platform GPL4072 was used. At T = 175 days the platform GPL4076 was used and at T =276 days the platform GPL4077 was used.

2010-07-01 | E-GEOD-5492 | biostudies-arrayexpress

Gene expression in the duodenum of sheep genetically resistant or susceptible to nematodes

2006-09-06 | GSE5492 | GEO

DNA methylation profiles from a mouse model of Huntington's disease

Project description:An Infinium microarray platform (HorvathMammalMethylChip40) was used to generate DNA methylation data from mouse tissues of a heterozygous Huntingtin expansion knock-in (Q175) and wildtype (WT) controls. Mouse tissues: blood, liver, brain cortex, brain cerebellum, and striatum.

2020-07-02 | GSE147002 | GEO

Characterization of Sheep Milk Extracellular Vesicle-miRNA by Sequencing and Comparison with Cow milk

Project description:Milk can mediate maternal-neonatal signal transmission by the bioactive component-extracellular vesicles (EVs), which select specific types of miRNA to encapsulate. The miRNA profiling of sheep milk EVs was characterized by sequencing and compared with that of cow milk. Sheep milk EVs contained various small RNAs, including tRNA, Cis-regulatory element, rRNA, snRNA, other Rfam RNA, and miRNA, which held about 36% of all the small RNAs. Totally 84 types of miRNAs were annotated with Ovis aries by miRBase (version 22.0) in sheep milk EVs, with 75 shared types of miRNAs in all samples. Fourteen sheep milk EV-miRNAs in the top 20, occupying 98% of the total expression, were immune-related.

2020-01-17 | GSE143779 | GEO

Metabolic disruption identified in the Huntington's disease transgenic sheep model.

Project description: Not available

| S-EPMC4749952 | biostudies-literature

Hdac4 interactome in Huntington's Disease

Project description:Hdac4 has been found to modulate symptoms in Huntington's Disease (HD) mouse models through an uknown mechanism unrelated to any enzymatic activity. We investigated the protein-protein interactions to gain insight into the role of Hdac4 in HD.

2019-05-01 | PXD011845 | Pride

Proteomic analysis of mitochondria from Huntington's Disease patient iPSC-derived neurons

Project description:Huntington's disease is caused by an expanded CAG repeat in the huntingtin gene, yeilding a Huntingtin protein with an expanded polyglutamine tract. Patient-derived induced pluripotent stem cells (iPSCs) can help understand disease; however, defining pathological biomarkers in challanging. Here we used LC-MS/MS to determine differences in mitochondrial proteome between iPSC-derived neurons from healthy donors and Huntington's disease patients.

2023-02-10 | PXD037526 | Pride

A Multi-Omic Huntington's Disease Transgenic Sheep-Model Database for Investigating Disease Pathogenesis.

Project description: Not available

| S-EPMC8673501 | biostudies-literature

The HDAC inhibitor 4b ameliorates the disease phenotype and transcriptional abnormalities in Huntington's disease transgenic mice

Project description:Transcriptional dysregulation has emerged as a core pathologic feature of Huntington's disease (HD), one of several triplet-repeat disorders characterized by movement deficits and cognitive dysfunction. Although the mechanisms contributing to the gene expression deficits remain unknown, therapeutic strategies have aimed to improve transcriptional output via modulation of chromatin structure. Recent studies have demonstrated therapeutic effects of commercially available histone deacetylase (HDAC) inhibitors in several HD models; however, the therapeutic value of these compounds is limited by their toxic effects. Here, beneficial effects of a novel pimelic diphenylamide HDAC inhibitor, HDACi 4b, in an HD mouse model are reported. Chronic oral administration of HDACi 4b, beginning after the onset of motor deficits, significantly improved motor performance, overall appearance, and body weight of symptomatic R6/2(300Q) transgenic mice. These effects were associated with significant attenuation of gross brain-size decline and striatal atrophy. Microarray studies revealed that HDACi 4b treatment ameliorated, in part, alterations in gene expression caused by the presence of mutant huntingtin protein in the striatum, cortex, and cerebellum of R6/2(300Q) transgenic mice. For selected genes, HDACi 4b treatment reversed histone H3 hypoacetylation observed in the presence of mutant huntingtin, in association with correction of mRNA expression levels. These findings suggest that HDACi 4b, and possibly related HDAC inhibitors, may offer clinical benefit for HD patients and provide a novel set of potential biomarkers for clinical assessment. Analysis of striatum, cortex, and cerebellum from R6/2(300Q) transgenic mice before and after treatment with the HDAC inhibitor 4b

2010-12-27 | E-GEOD-26317 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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