Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Ribosomal profiling of WT and mORF4/NBDY KO hearts

ABSTRACT: Left ventricles from the hearts of adult WT and mORR4/NBDY KO mice were obtained. Per heart, RNA-sequencing and ribosomal profiling was performed on the same heart

ORGANISM(S): Mus musculus

PROVIDER: GSE154940 | GEO | 2020/07/23

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Ribosomal profiling of WT and mORF4/NBDY KO hearts [WT_vs_mORF4-NBDYKO_RNAseq]

Project description:Left ventricles from the hearts of adult WT and mORR4/NBDY KO mice were obtained.

2020-07-27 | GSE155133 | GEO

Ribosomal profiling of WT and mORF4/NBDY KO hearts

Project description:Ribosomal profiling of WT and mORF4/NBDY KO hearts

| PRJNA647908 | ENA

Ribosomal profiling of WT and mORF4/NBDY KO hearts [WT_vs_mORF4-NBDYKO_RNAseq]

Project description:Ribosomal profiling of WT and mORF4/NBDY KO hearts [WT_vs_mORF4-NBDYKO_RNAseq]

| PRJNA648762 | ENA

ERRalpha wt vs. ko hearts, baseline

Project description:We hypothesized that the estrogen-related receptor a (ERRa), which recruits PGC-1a to metabolic target genes in heart, exerts protective effects in the context of stressors known to cause heart failure. ERRa-/- mice subjected to left ventricular (LV) pressure overload developed signatures of heart failure including chamber dilatation and reduced LV fractional shortening. 31P-NMR studies revealed abnormal phosphocreatine depletion in ERRa-/- hearts subjected to hemodynamic stress, indicative of a defect in ATP reserve. Mitochondrial respiration studies demonstrated reduced maximal ATP synthesis rates in ERRa-/- hearts. Cardiac ERRa target genes involved in energy substrate oxidation, ATP synthesis, and phosphate transfer were downregulated in ERRa-/- mice at baseline or with pressure overload. These results demonstrate that ERRa, a potential therapeutic target, is indispensable for the adaptive bioenergetic response to hemodynamic stressors known to cause heart failure. Keywords: Genetic modification, stress response

2007-10-16 | GSE8106 | GEO

RNA-seq of CCBE1 KO and WT murine hearts

Project description:CCBE1 is a secreted extracellular matrix protein expressed by epicardial cells but its role during epicardial development was still unknown.Using a Ccbe1 knockout (KO) mouse model, we observed that loss of CCBE1 leads to congenital heart defects including thinner and hyper-trabeculated ventricular myocardium. In addition, Ccbe1 mutant hearts displayed reduced proliferation of cardiomyocyte and epicardial cells. RNA-seq data of CCBE1 KO and WT murine hearts indicated deregulation of genes associated with development and morphogenesis including the epithelial-to-mesenchymal transition.

2022-10-23 | E-MTAB-12217 | biostudies-arrayexpress

Chamber-Enriched gene expression profiles in failing human hearts with reduced ejection fraction [snRNA-Seq]

Project description:To generate the reference for cell composition deconvolution and characterize the cellular expression landscape, we performed single nucleus RNA-Seq (snRNA-Seq) on left ventricles from four non-failing hearts and one failing heart.

2021-06-04 | GSE161470 | GEO

Gene expression of murine STAT3-KO hearts vs WT

Project description:Gene expression analysis of heart tissue probes from a mouse model with a cardiomyocyte-restricted STAT3 deficiency in comparison to corresponding WT mice. (Hilfiker-Kleiner, D. et al. 2004) Comparison of heart left ventricle tissue probes from STAT3-KO and WT mice. Each sample is a pool of 5 tissue probes from each genotype.

2011-06-30 | E-GEOD-30306 | biostudies-arrayexpress

Transcriptome of E9.5 WT and Smyd1-KO mouse hearts

Project description:Purpose: The goal of this study is to identify the differential cardiac transcriptome profiling between WT and Smyd1 null (Smyd1-KO) hearts at E9.5 using RNA-seq. Methods: mRNA profiles of E9.5 WT and Smyd1-KO mouse hearts were generated by deep sequencing, n=3 for each genotype, using Illumina HiSeq2500. The sequence reads were aligned to the mm10 reference genome using STAR via the bcbio-nextgen RNA-sequencing pipeline. Differential gene expression was determined by DEseq2. Results: 1756 genes were differentially expressed between WT and Smyd1-KO hearts [adjusted P value <0.05, |log2(Fold Change)| > 0.5], with 1130 upregulated and 626 downregulated in E9.5 Smyd1-KO hearts.

2024-04-18 | GSE260692 | GEO

ATAC-seq of E9.5 WT and Smyd1-KO mouse hearts

Project description:Purpose: The goal of this study is to identify the differential cardiac chromatin accessibility between WT and Smyd1 null (Smyd1-KO) hearts at E9.5 using ATAC-seq. Methods: Four hearts at E9.5 were pooled per genotype per replicate, and were then dissociated into single cells. 40,000 viable cells were taken for were lysed to isolate nuclei, which were treated with Tn5 transposase (Nextera DNA Sample Prep Kit, Illumina) to isolate DNA. Fragmented DNA was then amplified using bar-coded PCR primers and libraries were seuqenced. Results: 25851 differential peaks (2-fold change) were identified between E9.5 WT and Smyd1-KO hearts.

2024-04-18 | GSE260690 | GEO

RNA-sequencing analysis of transcriptoms in Wild Type (WT) and Trdn-as knockout (KO) hearts.

Project description:The goal of this study is to examine differential gene expression between WT and Trdn-as KO heart using RNA-sequencing (RNA-seq). Total RNA was extracted from mouse hearts and subjected for RNA-seq. The conclusion of the study is that deletion of Trdn-as affects expression levels of a group of genes.

2022-11-01 | GSE185522 | 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