Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Wilson disease: intersecting DNA methylation and histone acetylation mechanisms affect gene expression regulation in a mouse model of hepatic copper accumulation [RNA-Seq]

ABSTRACT: Wilson disease: intersecting DNA methylation and histone acetylation mechanisms affect gene expression regulation in a mouse model of hepatic copper accumulation [RNA-Seq]

PROVIDER: PRJNA714118 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13956755_1.fastq.gz	Fastqsanger.gz
	SRR13956755_2.fastq.gz	Fastqsanger.gz
	SRR13956756_1.fastq.gz	Fastqsanger.gz
	SRR13956756_2.fastq.gz	Fastqsanger.gz
	SRR13956757_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 60

Similar Datasets

Wilson disease: intersecting DNA methylation and histone acetylation mechanisms affect gene expression regulation in a mouse model of hepatic copper accumulation [ChIP-Seq]

Project description:Prior investigations of DNA methylation differences in WD liver and blood and in a WD mouse model revealed an epigenetic signature of WD that included the histone deacetylase, HDAC5. To test the hypothesis that histone deacetylation and acetylation might be altered with respect to copper overload and aberrant DNA methylation in WD, we used the Jackson Laboratory toxic milk model (tx-j) of WD to study the involvement of Class IIa histone deacetylases (HDAC4 and HDAC5) and histone acetylation (H3K9ac and H3K27ac), and the effects of copper chelator D-penicillamine (PCA) and/or methyl group donor choline on histone modification. Next, we related acetylation profiles of H3K27ac to gene expression changes in wilson disease by ChIP and RNA-seq.

2021-07-09 | GSE168971 | GEO

Wilson disease: intersecting DNA methylation and histone acetylation mechanisms affect gene expression regulation in a mouse model of hepatic copper accumulation [RNA-Seq]

2021-07-09 | GSE168833 | GEO

Wilson disease: intersecting DNA methylation and histone acetylation mechanisms affect gene expression regulation in a mouse model of hepatic copper accumulation

Project description:Wilson disease: intersecting DNA methylation and histone acetylation mechanisms affect gene expression regulation in a mouse model of hepatic copper accumulation

| PRJNA714683 | ENA

Wilson disease: intersecting DNA methylation and histone acetylation mechanisms affect gene expression regulation in a mouse model of hepatic copper accumulation [ChIP-Seq]

Project description:Wilson disease: intersecting DNA methylation and histone acetylation mechanisms affect gene expression regulation in a mouse model of hepatic copper accumulation [ChIP-Seq]

| PRJNA714687 | ENA

Specific changes of liver transcriptome in the early stages of copper accumulation in the mouse model of wilson disease

Project description:Wilson disease (WD) is a severe metabolic disorder caused by genetic inactivation of copper-transporting ATPase ATP7B. In WD, copper accumulates in several tissues, particularly in the liver, inducing marked time-dependent pathological changes. To identify initial events in the copper-dependent development of liver pathology we utilized the Atp7b-/- mice, an animal model for WD. Analysis of mRNA from livers of control and Atp7b-/- 6 weeks-old mice using oligonucleotide arrays revealed specific changes of the transcriptome at this stage of copper accumulation. Few messages (29 up-regulated and 46 down-regulated) change their abundance more than 2-fold pointing to the specific effect of copper on gene expression/mRNA stability. The gene ontology analysis revealed copper effects on distinct metabolic pathways. Keywords: comparative genomic hybridization

2006-12-19 | GSE5348 | GEO

Transcription profiling of mouse model of Wilson disease reveals specific changes of liver transcriptome in the early stages of copper accumulation

2008-06-13 | E-GEOD-5348 | biostudies-arrayexpress

TRANSCRIPTIONAL REMODELLING IN RESPONSE TO CHANGING COPPER LEVELS IN WILSON DISEASE MODEL OF SACCHAROMYCES CEREVISIAE

Project description:A 3 x 2 factorial design was used to elucidate the genome-wide transcriptional response to the deletion of yeast ortholog of Wilson and Menkes disease causing gene; CCC2, at changing copper levels. Homozygous deletion mutant of CCC2, which encodes Cu+2 transporting P-type ATPase required to export copper from the cytosol into the extracytosolic compartment, and the reference strain were cultivated in fully controlled fermenters in duplicates in glucose-rich defined medium containing three different levels of copper. The three different copper concentrations were selected such that; copper deficient condition, which was prepared by excluding the CuSO4.7H2O from the defined medium, low copper or adequate copper concentration, which is the standard amount of copper in defined medium (0.04 ?M) and high copper concentration (0.5 mM), which was able to restore respiration deficiency in ccc2?/ccc2? strain.

2013-09-02 | E-MEXP-3927 | biostudies-arrayexpress

Wilson disease: intersecting DNA methylation and histone acetylation mechanisms affect gene expression regulation in a mouse model of hepatic copper accumulation

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-07-09 | GSE168972 | GEO

HF001-A: Gene expression patterns in the progression towards canine copper-associated chronic hepatitis

Project description:Copper is an essential trace element, but can become toxic when present in abundance. The severe effects of copper-metabolism imbalance are illustrated by the inherited disorders Wilson disease and Menkes disease. The Labrador retriever dog breed is a novel non-rodent model for copper-storage defects displaying identical phenotypic alterations and carrying mutations in genes known to be involved in copper transport. Besides disease initiation and progression of copper accumulation, the molecular mechanisms and pathways involved in copper accumulation and eventually progression towards copper associated chronic hepatitis still remains unclear. Using liver tissue of Labrador retrievers in different stages of copper-associated hepatitis, expression levels targeted at candidate genes as well as transcriptome microarrays, have shed light on involved molecular pathways. At the initial phase, viz. increased hepatic copper levels, transcriptomic alterations in livers revealed enrichment for cell adhesion, developmental, inflammatory, and cytoskeleton pathways. Upregulation of targeted MT1A and COMMD1 mRNA shows the livers first response to rising intrahepatic copper concentrations. In livers with copper-associated hepatitis mainly an activation of inflammatory pathways is detected. Once the hepatitis is in the chronic stage, transcriptional differences are found in cell adhesion adaptations and cytoskeleton remodelling. In view of the high similarities in hepatopathies between men and dog extrapolation of these dog data into human biomedicine seems feasible.

2017-05-02 | GSE86932 | GEO

Metallothionein immunohistochemistry has high sensitivity and specificity for detection of Wilson disease

Project description:Diagnosis of Wilson disease (WD) can be difficult because of its protean clinical presentation, but early diagnosis is important because effective treatment is available and can prevent disease progression. Using quantitative proteomics, we characterized proteins that are differentially expressed in WD compared to normal liver. Further the expression of MT1M and COX17 were validated using immunohistochemistry. We found diffuse MT immunoreactivity in all liver specimens from patients with WD (n=20), the intensity of the staining was moderate to strong. This staining pattern was distinct from that seen in specimens from the control groups which included diseases that may be in the clinical or histologic differential of WD (steatohepatitis (n=51), chronic viral hepatitis (n=40), autoimmune hepatitis (n=50), chronic biliary tract disease (n=42), and normal liver (n=20)). COX17 immunostain showed no significant difference in expression between the WD and control groups. MT had higher sensitivity than rhodanine for diagnosis of WD. While the quantitative liver copper assays also had high sensitivity, they require more tissue, have a higher cost, have longer turnaround time, and are less widely available than an immunohistochemical stain. We conclude that MT IHC is a sensitive immunohistochemical stain for the diagnosis of Wilson disease that could be widely deployed as a screening tool for liver biopsies in which Wilson disease is in the clinical or histologic differential diagnosis.

2023-04-18 | PXD029069 | Pride

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