Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

E-GEOD-3866

ABSTRACT: Transcription profiling by array of left ventricle tissues from rat with overexpression of constitutively active upstream kinase mitogen-activated protein kinase kinase 3b (MKK3bE) and wild-type p38? in the heart

OTHER RELATED OMICS DATASETS IN: PRJNA94101

PROVIDER: E-GEOD-3866 | ExpressionAtlas | 2014-10-10

REPOSITORIES: ExpressionAtlas

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	E-GEOD-3866-analysis-methods.tsv	Tabular
	E-GEOD-3866-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-3866-configuration.xml	Xml
	E-GEOD-3866-percentile-ranks.tsv	Tabular
	E-GEOD-3866.condensed-sdrf.tsv	Tabular

Items per page:

1 - 5 of 59

Similar Datasets

Transcription profiling by array of left ventricle tissues from rat with overexpression of constitutively active upstream kinase mitogen-activated protein kinase kinase 3b (MKK3bE) and wild-type p38? in the heart

Project description:Mitogen-activated protein kinases (MAPKs) regulate cardiomyocyte growth and apoptosis in response to extracellular stimulation, but the downstream effectors that mediate their pathophysiological effects remain poorly understood. We determined the targets and role of p38 MAPK in the heart in vivo by using local adenovirus-mediated gene transfer of constitutively active upstream kinase mitogen-activated protein kinase kinase 3b (MKK3bE) and wild-type p38Î± in rats. DNA microarray analysis of animals with cardiac-specific overexpression of p38 MAPK revealed that 264 genes were upregulated more than 2-fold including multiple genes controlling cell division, cell signaling, inflammation, adhesion and transcription. Several previously unknown p38 target genes were found. Using gel mobility shift assays we identified several cardiac transcription factors that were directly activated by p38 MAPK. Finally, we determined the functional significance of the altered cardiac gene expression profile by histological analysis and echocardiographic measurements, which indicated that p38 MAPK overexpression induced gene expression results in cell proliferation, myocardial inflammation and fibrosis. In conclusion, we defined the novel target genes and transcription factors as well as the functional effects of p38 MAPK in the heart. Expression profiling of p38 MAPK overexpression identified cell cycle regulatory and inflammatory genes critical for pathological processes in the adult heart. Experiment Overall Design: Left ventricular gene expression profiles three days after MKK3bE + WT p38Î± gene transfer were compared with those of Lac Z âtreated animals by screening Affymetrix Rat Expression Set 230_2.0 Arrays (there are 5 samples in both group).

2009-04-25 | E-GEOD-3866 | biostudies-arrayexpress

p38 MAPK overexpression in heart in vivo.

Project description:Mitogen-activated protein kinases (MAPKs) regulate cardiomyocyte growth and apoptosis in response to extracellular stimulation, but the downstream effectors that mediate their pathophysiological effects remain poorly understood. We determined the targets and role of p38 MAPK in the heart in vivo by using local adenovirus-mediated gene transfer of constitutively active upstream kinase mitogen-activated protein kinase kinase 3b (MKK3bE) and wild-type p38α in rats. DNA microarray analysis of animals with cardiac-specific overexpression of p38 MAPK revealed that 264 genes were upregulated more than 2-fold including multiple genes controlling cell division, cell signaling, inflammation, adhesion and transcription. Several previously unknown p38 target genes were found. Using gel mobility shift assays we identified several cardiac transcription factors that were directly activated by p38 MAPK. Finally, we determined the functional significance of the altered cardiac gene expression profile by histological analysis and echocardiographic measurements, which indicated that p38 MAPK overexpression induced gene expression results in cell proliferation, myocardial inflammation and fibrosis. In conclusion, we defined the novel target genes and transcription factors as well as the functional effects of p38 MAPK in the heart. Expression profiling of p38 MAPK overexpression identified cell cycle regulatory and inflammatory genes critical for pathological processes in the adult heart. Keywords: Gene transfer

2006-12-19 | GSE3866 | GEO

E-MTAB-6460

Project description:RNA-seq of heart left ventricle during myocardial ischemia in TAB-1 knock-in mice compared to wild type controls

2018-09-17 | E-MTAB-6460 | ExpressionAtlas

ChIP-on-chip experiments of normal and failed hearts of Dahl rat

2009-02-19 | GSE8341 | GEO

ChIP-chip profiling of rat normal and failed hearts of Dahl strain

Project description:Left ventricle myocytes from Dahl rats with a normal or failed heart was subjected to mRNA quantitation or ChIP-on-chip experiments with Affymetrix Rat Genome 230 2.0 microarrays. Experiment Overall Design: One left venctricle specimen was used for each mRNA quantitation/ChIP-on-chip experiment with a normal or failed heart.

2009-03-01 | E-GEOD-8341 | biostudies-arrayexpress

Heart ventricles proteomic profile in pulmonary arterial hypertension

Project description:Arterial pulmonary hypertension is a rare disease, with little knowledge regarding its etiology, and high mortality. Development of right and later on also left ventricular heart insufficiency, secondary to pulmonary hypertension, is a negative predictive factor. Genetic and molecular processes underlying left heart ventricle remodeling over the course of pulmonary hypertension remain unknown. In particular, there is no knowledge regarding the mechanisms of left heart ventricle atrophy which was completely avoided by researchers until recently.The aim of this study was to assess changes in protein abundance in left and right heart ventricle free wall of rats in monocrotaline model of PAH.

2020-09-07 | PXD015896 | Pride

RNA-seq of heart left ventricle

Project description:RNA-seq of heart left ventricle

| PRJNA549694 | ENA

Whole genome transcriptomics reveal distinct atrial versus ventricular responses to neonatal hyperoxia

Project description:Preterm infants exposed to supplemental oxygen (hyperoxia) are at risk for developing heart failure later in life. Rodent studies show that exposure to hyperoxia in early postnatal life causes heart failure later in life that resembles heart failure in humans who were born preterm. Neonatal hyperoxia exposure affected the left atrium and left ventricle differently, inhibiting the proliferation and survival of atrial cardiomyocytes while enhancing cardiomyocyte differentiation in the ventricle. In this study, whole genome transcriptomics revealed the left atria of neonatal mice are more responsive to hyperoxia than the left ventricle, with the expression of 4,285 genes affected in the atrium and 1,743 in the ventricle. While hyperoxia activated p53 target genes in both chambers, it caused greater DNA damage, phosphorylation of the DNA damage responsive ataxia telangiectasia mutated (ATM) kinase, mitochondrial stress, and apoptosis in the atrium. In contrast, hyperoxia induced the expression of DNA repair and growth arrest genes in the ventricle. Atrial cells also showed a greater loss of extracellular matrix and superoxide dismutase 3 (SOD3) expression, possibly contributing to the enlargement of the left atrium and reduced velocity of blood flow across the mitral valve seen in hyperoxia exposed mice. Diastolic dysfunction and heart failure in hyperoxia exposed mice may thus stem from its effects on the left atrium, suggesting chamber-specific therapies may be needed to address diastolic dysfunction and heart failure in people who were born preterm.

2025-02-25 | GSE282365 | GEO

Does high fibre diet or acetate supplementation cause changes to DNA methylation in the heart or spleen?

Project description:Mice were fed either a control diet, high fibre diet or a diet supplemented with acetate for 3 weeks. Heart (left ventricle) and spleen tissues were harvested for DNA methylation analysis.

2019-03-26 | GSE128817 | GEO

Transcription profiling of BXH/HXB rat recombinant inbred strains derived from the spontaneously hypertensive rat (SHR/Ola) and the Brown Norway congenic strains carrying the polydactylyl-luxate mutation (BN-Lx)

Project description:BXH/HXB rat recombinant inbred (RI) strains are derived from the spontaneously hypertensive rat (SHR/Ola) and the Brown Norway congenic strains carrying the polydactylyl-luxate mutation (BN-Lx). Tissue from the apex of left ventricle of the heart was disected from 128 RI SHR/Ola and BN-Lx parental strains, RNA was extracted and labelled and hybridised to Affymetrix Rat Genome 230 2.0 Arrays.

2008-04-01 | E-MIMR-222 | 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