Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

12 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcription profiling of transcription factor CREM deficient mice to assess its role in beta1-aderenoceptor-mediated detrimental cardiac effects

ABSTRACT: To assess a potential role of transcription factor CREM in the long-term detrimental effects of beta1-adrenoceptor overexpression, four mouse lines were generated and studied: wild-type mice (WT), Crem-normal beta1AR-transgenic mice (beta1ARTG), Crem-deficient non-transgenic mice (Crem-/-) and Crem-deficient beta1AR-transgenic mice (beta1ARTG/Crem-/-). We focused on genes up- or down-regulated in transgenic mice due to the lacking of CREM (beta1ARTG/Crem-/- vs. beta1ARTG).

ORGANISM(S): Mus musculus

SUBMITTER: Frank Müller

PROVIDER: E-MEXP-582 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

mRNA expression data from BCR-ABL, MYC and CD22DE12 transgenic mouse models

Project description:Leukemic splenocytes from these commercial transgenic mice that developed fatal leukemia with massive splenomegaly were isolated at the time of the necropsy and subjected to gene expression profiling and phosphoprotein profiling in side by side comparison with CD22DE12-Tg BPL or CD22DE12_BCR-ABL double transgenic cells. Mouse leukemia cells were isolated from markedly enlarged spleens of CD22DE12-Tg (N=2), BCR-ABL-Tg (N=2), Eµ-MYC Tg mice (N=2) and Splenocytes from wildtype healthy C57BL/6 mice served as controls (N=4).

2015-06-25 | E-GEOD-58872 | biostudies-arrayexpress

The effect of Crem absence on gene expression in mouse testis.

Project description:CREM (cAMP responsive element modulator) together with CREB and ATF-1 belong to the CREB family of transcriptional factors, that respond to cyclic AMP signaling and bind to cAMP responsive element (CRE) sites in promoters of selected genes. CREM can produce isoforms that have either activating or repressing functions, depending on the transcription of specific exons. In testis, it is involved in the regulation of spermatogenesis. In this dataset, we include the expression data obtained from wild-type and Crem knock-out mouse testis. 2 condition experiment: 2 strains (WT, Crem-/-). 5 biological replications per condition.

2012-04-10 | E-GEOD-29593 | biostudies-arrayexpress

The effect of Crem absence on gene expression in mouse adrenal glands.

Project description:CREM (cAMP responsive element modulator) together with CREB and ATF-1 belong to the CREB family of transcriptional factors, that respond to cyclic AMP signaling and bind to cAMP responsive element (CRE) sites in promoters of selected genes. CREM can produce isoforms that have either activating or repressing functions, depending on the transcription of specific exons. In adrenal glands it is involved in the regulation of expression of genes for steroid hormone synthesis. In this dataset, we include the expression data obtained from wild-type and Crem knock-out mouse adrenal glands. 2 condition experiment: 2 strains (WT, Crem-/-). 5 biological replications per condition.

2014-05-25 | E-GEOD-29592 | biostudies-arrayexpress

The effect of Crem absence on gene expression in mouse liver.

Project description:CREM (cAMP responsive element modulator) together with CREB and ATF-1 belong to the CREB family of transcriptional factors, that respond to cyclic AMP signaling and bind to cAMP responsive element (CRE) sites in promoters of selected genes. CREM can produce isoforms that have either activating or repressing functions, depending on the transcription of specific exons. In this dataset, we include the expression data obtained from wild-type (WT) and Crem knock-out (KO) mouse liver. Several comparisons were made. KO<WT at 0h, KO<WT at 12 h, 0h<12h in WT and 0h<12h in KO. 4 condition experiment: 2 strains (WT, Crem-/-), 2 time points (0h and 12h). 5 biological replications per condition.

2014-05-25 | E-GEOD-29594 | biostudies-arrayexpress

Microarray gene expression profiling of cardiac genes at the onset of heart failure

Project description:Atherosclerosis and pressure overload are major risk factors for the development of heart failure in patients. Cardiac hypertrophy often precedes the development of heart failure. However, underlying mechanisms are incompletely understood. To investigate pathomechanisms underlying the transition from cardiac hypertrophy to heart failure we used experimental models of atherosclerosis- and pressure overload-induced cardiac hypertrophy and failure, i.e. apolipoprotein E (apoE)-deficient mice, which develop heart failure at an age of 18 months, and non-transgenic C57BL/6J (B6) mice with heart failure triggered by 6 months of pressure overload induced by abdominal aortic constriction (AAC). The development of heart failure was monitored by echocardiography, invasive hemodynamics and histology. The microarray gene expression study of cardiac genes was performed with heart tissue from failing hearts relative to hypertrophic and healthy heart tissue, respectively. The microarray study revealed that the onset of heart failure was accompanied by a strong up-regulation of cardiac lipid metabolism genes involved in fat synthesis, storage and oxidation. Microarray gene expression profiling was performed with heart tissue isolated from (i) 18 month-old apoE-deficient mice relative to age-matched non-transgenic C57BL/6J (B6) mice, (ii) 6 month-old apoE-deficient mice with 2 months of chronic pressure overload induced by abdominal aortic constriction (AAC) relative to sham-operated apoE-deficient mice and nontransgenic B6 mice, (iii) 10 month-old B6 mice with 6 months of AAC relative to sham-operated B6 mice, and (iv) 5 month-old B6 mice with 1 month of AAC relative to age-matched B6 mice.

2010-12-03 | E-GEOD-25765 | biostudies-arrayexpress

Model of heart failure induced by mild thiol-blocking with cystamine

Project description:Depletion of cardiac ATP content is a characteristic feature of heart failure in patients and experimental animal models. To analyze the impact of insufficient ATP supply on heart function we inhibited cellular respiration by disulfide poisoning with the mild thiol-blocking agent, cystamine. We chose 4 month-old apolipoprotein E (apoE)-deficient mice, which are highly vulnerable to increased oxygen and ATP demands. After 4 weeks of cystamine treatment (300 mg/kg in drinking water), echocardiography and histology analyses demonstrated that apoE-deficient mice had developed heart failure with cardiac dilation. The microarray gene expression study of heart tissue from cystamine-treated apoE-deficient mice relative to untreated mice confirmed the development of heart failure showing up-regulation heart failure-specific genes by mild thiol-blocking with cystamine. Microarray gene expression profiling was performed with heart tissue isolated from three study groups: (i) cystamine-treated 5 month-old apolipoprotein- (apoE)- deficient mice with symptoms of heart failure, (ii) untreated 5 month-old apoE- deficient mice, and (iii) age-matched, untreated, non-transgenic B6 control mice.

2010-12-03 | E-GEOD-25768 | biostudies-arrayexpress

Cardiac gene expression profiling of apoE-deficient mice receiving heart failure treatment with the anti-ischemic drug ranolazine

Project description:Heart failure is a leading cause of cardiovascular mortality with limited options for treatment. We used 18 month-old apolipoprotein E (apoE)- deficient mice as a model of atherosclerosis-induced heart failure to analyze whether the anti-ischemic drug ranolazine could retard the progression of heart failure. The study showed that 2 months of ranolazine treatment improved cardiac function of 18 month-old apoE-deficient mice with symptoms of heart failure as assessed by echocardiography. To identify changes in cardiac gene expression induced by treatment with ranolazine a microarray study was performed with heart tissue from failing hearts relative to ranolazine-treated and healthy control hearts. The microarray approach identified heart failure-specific genes that were normalized during treatment with the anti-ischemic drug ranolazine. Microarray gene expression profiling was performed with heart tissue isolated from (i) untreated 18 month-old apoE-deficient mice with heart failure relative to (ii) 18 month-old apoE-deficient mice treated for two months with the anti-ischemic drug ranolazine (200 mg/kg), and (iii) age-matched non-transgenic C57BL/6J (B6) control mice.

2010-12-03 | E-GEOD-25767 | biostudies-arrayexpress

SRF Overexpression Leads to Altered Expression of MicroRNAs and Contributes to Cardiac Hypertrophy

Project description:The role of SRF in the regulation of microRNA expression and microRNA biogenesis in cardiac hypertrophy has not been well established. In this report, we employed a distinct transgenic mouse model to study the impact of SRF on cardiac microRNA expression and microRNA biogenesis. Cardiac-specific overexpression of SRF (SRF-Tg) led to altered expression of a number of microRNAs. To study the effect of SRF level on cardiac gene expression and function in the mouse heart, we employed the cardiac-specific transgenic approach to increase the SRF protein level in one mouse model. The ventricular tissue samples used for the microRNA array analysis were obtained from 6-month-old wild-type mice and age-matched SRF-Tg mice. The RNA sample isolation and microRNA array were performed in triplets for both wild-type and transgenic mice.

2011-02-16 | E-GEOD-23044 | biostudies-arrayexpress

Transcription profiling of mice hearts comparing microRNA-22 overexpression to wildtype

Project description:To explore the role of miR-22 in the heart, we generated miR-22 null and transgenic mice. Cardiac transgenic overexpression of miR-22 in vivo led to cardiac hypertrophy that evolved into progressive dilated cardiomyopathy (DCM) in unstressed hearts. We found that miR-22 directly regulates two transcriptional antagonists, purine rich element binding protein B (PURB), a repressor, and serum response factor (SRF), an activator, in the heart. Through these gain- and loss-of-function experiments in mice, we suggest that a primary function of miR-22 is to fine tune the relative expression and activity of these two transcriptional antagonists to influence contractile gene expression, function, growth and adaptation of the heart to stress.

2012-12-01 | E-MTAB-501 | biostudies-arrayexpress

RNA-seq of splenic and LN B cells from WT and Gm40600 Tg mice with or without LPS stimulation

Project description:We found that Gm40600 significantly affects plasmablast(PB)-like SP 2/0 cells. To explore the role of Gm40600 in B-cell especially plasma cell (PC) differentiation, we developed Gm40600 Transgenic (Gm40600 Tg) mice. B cells from spleen and lymph nodes (LNs) of WT and Gm40600 Tg mice were sorted by using B220 microbeads. B cells were also stimulated for 3 days by 10 ug/ml LPS. To explore the effect of Gm40600 overexpression on gene expression, we determined mRNA profiles in B cells from WT and Gm40600 Tg mice and LPS-stimulated B cells by RNA-seq. RNA-seq was done with an Illumina HiSeq 2500 instrument at GENEWIZ, Suzhou, China.

2020-07-31 | E-MTAB-8320 | 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