Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq profiling of transcriptomes of control and Hif1a mutant E12.5 hearts

ABSTRACT: Purpose: to identify genes aberrantly expressed upon myocardial ablation of Hif1a Methods: a floxed Hif1a allele was deleted in mouse embryonic hearts using a NXK2.5Cre line. Total RNA was extracted from E12.5 hearts (n=3 for controls and mutants) usinz Trizol and processed for RNA-seq. Reads were mapped to Mm10 reference genome using TopHat2 and Bowtie2. Transcript expression values were determined after transcript normalization with AltAnalyze Results: this analysis revealed a total of 1451 genes significantely (|Fold| > 20% and P<0.05) modulated in Hif1a cKO hearts

ORGANISM(S): Mus musculus

PROVIDER: GSE61209 | GEO | 2015/04/29

SECONDARY ACCESSION(S): PRJNA260617

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNA-seq profiling of transcriptomes of control and Hif1a mutant E12.5 hearts

Project description:Purpose: to identify genes aberrantly expressed upon myocardial ablation of Hif1a Methods: a floxed Hif1a allele was deleted in mouse embryonic hearts using a NXK2.5Cre line. Total RNA was extracted from E12.5 hearts (n=3 for controls and mutants) usinz Trizol and processed for RNA-seq. Reads were mapped to Mm10 reference genome using TopHat2 and Bowtie2. Transcript expression values were determined after transcript normalization with AltAnalyze Results: this analysis revealed a total of 1451 genes significantely (|Fold| > 20% and P<0.05) modulated in Hif1a cKO hearts 6 total RNAseq runs with 3 experimental samples and 3 controls samples

2015-04-29 | E-GEOD-61209 | biostudies-arrayexpress

ChIP-seq profiling of loci bound by HIF1a in wild-type E12.5 hearts

Project description:Purpose: to identify genes directly bound by HIF1a in cardiomycoytes Methods: crosslinked chromatin isolated from E12.5 mouse hearts was precipitated using an anti-HIF1a antibody and processed for sequencing. A list of genes containing a HIF1a peak (Minimum score 3.5) was compared with RNA-seq results to identify genes that are bound by HIF1a and expressed in E12.5 hearts Results: this analysis identified 1016 genes expressed and bound by HIF1a in embryonic hearts

2015-04-29 | GSE61247 | GEO

The Gene Expression Analysis in E12.5 Mouse Hearts with GATA4-FOG2 Interaction Loss

Project description:In order to identify the targets of GATA4-FOG2 action in mammalian heart development we performed Affymetrix microarray comparisons of gene expression in normal and mutant at embryonic (E) day E12.5 hearts. We compared RNA samples from both Fog2-null and Gata4ki/ki mutant E12.5 hearts to the wild-type control E12.5 hearts. We reasoned that as the phenotypes of the Fog2 knockout and Gata4ki/ki mutation (a V217G mutation that specifically cripples the interaction between GATA4 and FOG proteins) are similar, we should expect to identify a similar set of differentially expressed genes in both experiments. As an additional control, we expected to find the Fog2 gene expression absent in the mutant (null) Fog2 cardiac sample, but not Gata4ki/ki sample. We have analyzed 6 RNA samples total (3 from control hearts, 2 from FOG2 null hearts and 1 from GATA4ki hearts)

2010-02-21 | E-GEOD-14906 | biostudies-arrayexpress

The Gene Expression Analysis in E12.5 Mouse Hearts with GATA4-FOG2 Interaction Loss

2010-02-18 | GSE14906 | GEO

Gene expression profiling of E12.5 wildtype- and Sp3 null hearts

Project description:Mice lacking the zinc finger transcription factor Specificity protein 3 (Sp3) die prenatally in the C57Bl/6 background. To elucidate the cause of mortality we analyzed the potential role of Sp3 in embryonic heart development. Sp3 null hearts display defective looping at E10.5, and at E14.5 the Sp3 null mutants have developed a range of severe cardiac malformations. In an attempt to position Sp3 in the cardiac developmental hierarchy, we analysed the expression patterns of >15 marker genes in Sp3 null hearts. Expression of Cardiac ankyrin repeat protein (Carp) was downregulated prematurely after E12.5, while expression of the other marker genes was not affected. ChIP analysis revealed that Sp3 is bound to the Carp promoter region in vivo. Microarray analysis indicates that small molecule metabolism and cell-cell interactions are the most significantly affected biological processes in E12.5 Sp3 null myocardium. Since the epicardium showed distension from the myocardium, we studied expression of Wt1, a marker for epicardial cells. Wt1 expression was diminished in epicardium-derived cells in the myocardium of Sp3 null hearts. We conclude that Sp3 is required for normal cardiac development, and suggest that it has a crucial role in myocardial differentiation. ( Keywords: Transcription factors, Sp3, knockout mice, cardiac malformations, E12.5

2007-11-01 | GSE9124 | GEO

Gene expression analysis of control and Tbx20 mutant Tie2Cre lineage from E12.5 hearts

Project description:To investigate roles for Tbx20 in endocardium, we ablated Tbx20 utilizing Tie2Cre. Tie2Cre;Tbx20 mutants died at E14, exhibiting defects in multiple aspects of cardiac septation. Although endocardial cells lacking Tbx20 were able to undergo endothelial-to-mesenchymal transition, cushion mesenchymal cells lacking Tbx20 did not disperse normally. Non-cell autonomous roles of endocardial Tbx20 were also revealed, as evidenced by decreased myocardialization of outflow tract and failure of dorsal mesenchymal protrusion formation in mutants. To examine how ablation of Tbx20 in endocardial lineages affected gene expression, we performed global gene expression analysis on purified endocardial lineages. E12.5 hearts were dissociated, and Tie2Cre;RosatdTom lineage traced cells of controls and mutants were isolated by fluorescence activated cell sorting (FACS), after exclusion of blood cells (Ter119+, CD41+ and/or CD45+). Mutant endocardial lineages exhibited decreased expression of genes associated with extracellular matrix and cell migration. E12.5 hearts were dissociated, and Tie2Cre;RosatdTom lineage traced cells of controls and mutants were isolated by fluorescence activated cell sorting (FACS), after exclusion of blood cells (Ter119+, CD41+ and/or CD45+). FACS sorted Tie2Cre lineage from E12.5 hearts: Tie2Cre;Tbx20 +/loxP Control hearts versus Tie2Cre;Tbx20 loxP/- mutant hearts

2016-07-01 | E-GEOD-73858 | biostudies-arrayexpress

Gene expression profiling of Hif1α defective hearts in E12.5 mice

Project description:Gene expression profiling of Hif1α defective hearts in E12.5 mice

| PRJNA690777 | ENA

Gene expression analysis of control and Tbx20 mutant Tie2Cre lineage from E12.5 hearts

2016-07-01 | GSE73858 | GEO

Expression data from E12.5 mouse embryonic heart

Project description:We prepared RNA from mouse embryonic hearts and performed mRNA micro-array analysis to compare gene expression profiles between control and Rhau-deletion mice (E12.5), in order to understand how RHAU regulates heart development.

2015-10-10 | GSE73544 | GEO

Transcription profiling of mouse heart from E12.5 wildtype- and Sp3 animals

Project description:Mice lacking the zinc finger transcription factor Specificity protein 3 (Sp3) die prenatally in the C57Bl/6 background. To elucidate the cause of mortality we analyzed the potential role of Sp3 in embryonic heart development. Sp3 null hearts display defective looping at E10.5, and at E14.5 the Sp3 null mutants have developed a range of severe cardiac malformations. In an attempt to position Sp3 in the cardiac developmental hierarchy, we analysed the expression patterns of >15 marker genes in Sp3 null hearts. Expression of Cardiac ankyrin repeat protein (Carp) was downregulated prematurely after E12.5, while expression of the other marker genes was not affected. ChIP analysis revealed that Sp3 is bound to the Carp promoter region in vivo. Microarray analysis indicates that small molecule metabolism and cell-cell interactions are the most significantly affected biological processes in E12.5 Sp3 null myocardium. Since the epicardium showed distension from the myocardium, we studied expression of Wt1, a marker for epicardial cells. Wt1 expression was diminished in epicardium-derived cells in the myocardium of Sp3 null hearts. We conclude that Sp3 is required for normal cardiac development, and suggest that it has a crucial role in myocardial differentiation. ( Experiment Overall Design: Hearts were dissected from E12.5 wildtype (n=3) and Sp3 knockout (n=3) fetuses. Total RNA was isolated from individual hearts; 5Î¼g was used for labelling and hybridization to 430 2.0 Gene Chips (a total of 6).

2008-06-17 | E-GEOD-9124 | 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