Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mouse atrial tissue quantitative proteomics

ABSTRACT: Project description: Proteomics study of the role of nucleotide oligomerization domain type 1 (NOD1) in a mouse model of heart failure. A high-throughput quantitative proteomic analysis was performed in atrial myocardium obtained from Wt- and Nod1-/--Tac mice and their respective Sham groups.

ORGANISM(S): Mus Musculus (mouse)

SUBMITTER: Jesús María Vázquez Cobos

PROVIDER: PXD053998 | JPOST Repository | Thu Jul 17 00:00:00 BST 2025

REPOSITORIES: jPOST

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	IJ_TMT1.raw	Raw
	IJ_TMT1_f1.raw	Raw
	IJ_TMT1_f2.raw	Raw
	IJ_TMT1_f3.raw	Raw
	IJ_TMT1_f4.raw	Raw

Items per page:

1 - 5 of 20

Similar Datasets

Changes of Muramyl Dipeptide in Intestinal and Extra-intestinal Diseases

Project description:Nucleotide-binding oligomerization domain 2 (Nod2) signaling is critical for human health.To figure out the clinical relevance of NOD2 ligands, the investigators plan to evaluate the change of NOD2 ligands in inflammatory bowel diseases (IBD), CRC, atherosclerotic cardiovascular disease (ACVD), and type 2 diabetes mellitus (DM2 ).

| 2380440 | ecrin-mdr-crc

Mouse heart tissue: wild-type vs. aMHC-Calcineurin transgenic (CnTg)

Project description:Cardiac profiling of miR expression levels in a transgenic mouse model of heart failure (MHC-CnA) to identify miRs that are co-regulated with the development of calcineurin-induced heart failure. Two-condition experiment: WT vs CnTg. Biological replicates: one array was performed on 3 pooled samples of each genotype (2 arrays in total).

2011-11-02 | E-GEOD-25006 | biostudies-arrayexpress

Mouse heart tissue: wild-type vs. aMHC-Calcineurin transgenic (CnTg)

2011-11-02 | GSE25006 | GEO

MS-based quantitative proteomic analysis of MAM from WT and obese mice.

Project description:Diabetic cardiomyopathy (DCM) strongly leads to heart failure, notably with preserved ejection fraction (HFpEF). The involvement of mitochondria-associated reticular membranes (MAM) in T2D-related metabolic disorders starts to be demonstrated. In order to characterize the cardiac phenotype of an obesogenic type II diabetic mouse model (leptin-deficient ob/ob), we compared the proteome of its MAMs with those from WT mice.

2025-06-16 | PXD054672 | Pride

Impact of NOD2 Genotype on the Innate Monocyte Transcriptome in Crohn’s Disease

Project description:Short title: Innate Gene/miRNA MDP-response in CD RNA-seq and small RNA-seq were used to identify the expression of gene and microRNA (miRNA) in monocytes from healthy controls and patients with Crohn's Disease (CD), with and without NOD2 (nucleotide-binding oligomerization domain-containing protein 2) single nucleotide polymorphisms (SNPs) after stimulation with muramyl dipeptide (MDP).

2017-02-15 | GSE69446 | GEO

Heart Failure with Preserved Ejection Fraction - Mouse Heart and Lung Tissue & Comorbidities

Project description:FASILOX analysis of heart and lung tissue form mice with heart failure with preserved ejection fraction and several comorbidities.

2024-10-02 | PXD056447 | JPOST Repository

Set7 deletion attenuates isoproterenol-induced cardiac fibrosis and prevents heart failure

Project description:The Set7 methyltransferase regulates the expression of several genes through the methylation of histones and modulates the activity of non-histone proteins. However, the role of Set7 in cardiac remodeling and heart failure remains unknown. To address this question, wild type (WT) and Set7 knockout (KO) male mice were injected with isoproterenol (60 mg/kg) or saline subcutaneously for 14 days. WT mice injected with isoproterenol displayed a decrease in Set7 activity in the heart, although Set7 protein levels were unchanged. WT and Set7 KO mice injected with isoproterenol exhibited an increase in the heart weight and cardiomyocyte area compared to their respective controls. However, Set7 KO mice displayed an exacerbated cardiac hypertrophy in response to isoproterenol compared to WT mice. In addition, Set7 deletion attenuated isoproterenol-induced cardiac fibrosis. Echocardiograms revealed that WT mice injected with isoproterenol had lowered ejection fractions and fractional shortening, and increased E/A ratios compared to their controls. Conversely, Set7 KO mice did not show alteration in these parameters in response to isoproterenol. Both isoproterenol and Set7 deletion changed the transcriptional profile of the heart. Moreover, Set7 deletion increased the expression of mitochondrial biogenesis and antioxidant factors in the heart and reduced the expression of cellular senescence and inflammation markers. Taken together, our data suggest that Set7 deletion reduces isoproterenol-induced myocardial fibrosis and prevents heart failure, suggesting that Set7 plays an important role in cardiac remodeling and function.

2024-04-18 | GSE207581 | GEO

Analysis of cardiac gene expression in response to isoproterenol-induced heart failure (part 1)

Project description:Myoglobin knockout mice (myo-/-) adapt to the loss of myoglobin by the activation of a variety of compensatory mechanisms on the structural and functional level. In order to analyze to what extent myo-/- mice would tolerate cardiac stress we used the model of chronic isoproterenol application to induce cardiac hypertrophy in myo-/- mice and wild type (WT) controls. After 14 d of isoproterenol infusion cardiac hypertrophy in WT and myo-/- mice reached a similar level. WT mice developed lung oedema and left ventricular dilatation indicating the development of heart failure. In contrast, myo-/- mice displayed conserved cardiac function and no signs of heart failure. Analysis of the cardiac gene expression profile using 40 k mouse oligonucleotide arrays showed that isoproterenol affected the expression of 180 genes in WT but only 92 genes of myo-/- hearts. Only 40 of these genes were regulated in WT and myo-/- hearts. Whereas in WT hearts a prononced induction of genes of the extracellular matrix occurred suggesting a higher level of remodelling, in myo-/- hearts genes of carbon metabolism and genes linked to inhibition of apoptosis and muscular repair were altered. Interestingly, a subset of genes which was altered in myo-/- mice already under basal conditions was differentially expressed in WT hearts under isoproterenol treatment. In summary, our data show, that the genetic background (WT, myo-/-) has a major impact on cardiac gene expression even in the context of an aggressive hypertrophy model such as chronic isoproterenol stimulation. Keywords: gene expression profiling of isoproterenol induced heart failure in WT and myo-/- mice We analysed the cardiac gene expression profiles in a total of 32 hearts subdivided into 4 groups (8 WT vehicle, 8 WT ISO, 8 myo-/- vehicle, 8 myo-/- ISO).

2010-05-31 | E-GEOD-16243 | biostudies-arrayexpress

Analysis of cardiac gene expression in response to isoproterenol-induced heart failure (part 2)

2010-05-31 | E-GEOD-16246 | biostudies-arrayexpress

Cardiac microRNA profiling in mice treated with lipopolysacharide

Project description:To identify the microRNA (miR) profile in the hearts of mice that were treated with lipopolysaccharide (LPS) and compare this profile with respective profiles that have been published in studies with mice that underwent pressure overload heart failure, 8 mouse samples were hybridized to Sanger 14 Multi-Species miR microarrays. As a result, we observed that particular cardiac miRs that are modulated during pressure overload heart failure are not affected significantly by treatment with LPS

2011-06-14 | GSE29914 | 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