Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptomic analysis of embryonic hearts with conditional deletion of Wt1

ABSTRACT: Transcriptomic analysis of embryonic hearts with conditional deletion of Wt1

PROVIDER: PRJNA737788 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR14816467_1.fastq.gz	Fastqsanger.gz
	SRR14816467_2.fastq.gz	Fastqsanger.gz
	SRR14816468_1.fastq.gz	Fastqsanger.gz
	SRR14816468_2.fastq.gz	Fastqsanger.gz
	SRR14816469_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Transcriptomic analysis of embryonic hearts with conditional deletion of Wt1

Project description:We performed a conditional ablation of Wt1 in the myocardium of mice embryos. RNASeq analysis identified differential expression of 137 genes in the E13.5 mutant heart as compared to controls. GO functional enrichment analysis suggested that both calcium ion regulation and modulation of potassium channels are deeply altered in the mutant myocardium

2021-07-10 | GSE178220 | GEO

Digital Gene Expression Tag Profiling after Wt1 deletion in Sertoli cell

Project description:The Wilms tumor gene, Wt1, is specifically expressed in Sertoli cells (SCs) which support spermatogenesis. Germ cell loss was found in Wt1 knockout mice. In vitro studies demonstrated that Wt1 was essential for cell polarity maintenance in SCs. We used Digital Gene Expression Tag Profiling to detail the global programme of gene expression after Wt1 deletion in sertoli cell and identified 710 gene expression level change more than 2 times.

2014-05-06 | GSE46664 | GEO

Genomic landscape of the developing kidney upon conditional and time-dependent knockout of Wt1

Project description:We are characterizing global expression in the whole kidney at developmental stage E18.5, where we have used three Cre strains that result in knock out Wt1 in different cell types during renal development. Here the purpose is to identify the developmental stage at which the loss of Wt1 impacts kidney development, specifically in the context of a degree of disruption capable of ending in pediatric kidney cancers. Total RNA was isolated from whole kidneys of E18.5 mouse embryos following a variety of conditional knockouts of Wt1, plus appropriate control animals.

2015-07-27 | E-GEOD-70892 | biostudies-arrayexpress

Expression changes following conditional deletion of SMARCA4 (Brg) in mouse embryonic stem cells [RNA-seq]

Project description:We performed RNA-seq 72 h after acute deletion of Smarca4 in a line of conditional knockout mouse embryonic stem cells to examine altered gene expression.

2016-10-21 | GSE88967 | GEO

Digital Gene Expression Tag Profiling after Wt1 deletion in Sertoli cell

2014-05-06 | E-GEOD-46664 | biostudies-arrayexpress

Single cell RNA Sequencing Analysis of Gene Expression Profile in Dgcr8 Conditional KO Embryonic Hearts

Project description:Single cell RNA Sequencing Analysis of Gene Expression Profile in Dgcr8 Conditional KO Embryonic Hearts

| PRJNA433327 | ENA

MEF-mKras-WT1

2010-03-01 | GSE15325 | GEO

RNA-sequence analysis of WT mice hearts and cardiomyocyte-specific deletion of STAT3 mice hearts

Project description:The RNA-sequence analysis of cardiomyocyte-specific deletion of STAT3 mice hearts showed that comparing with WT mice hearts, the STAT3cKO mice hearts showed reduced cardiac function by affecting some key pathways.

2023-10-12 | GSE160248 | GEO

MEF-mKras-WT1

Project description:K-ras is one of the most frequently mutated human oncogenes. Activation of K-ras can lead to either senescence or proliferation in primary cells. The precise mechanism governing these distinct outcomes remains unclear. Here we utilized a loss-of-function screen to assess the role of specific genes identified as potential key regulators of K-ras driven oncogenesis. Using this approach, we identify the transcription factor Wt1 as an inhibitor of senescence in primary cells expressing oncogenic K-ras. Deletion or suppression of Wt1 expression leads to senescence of primary cells expressing oncogenic K-ras under the control of the native promotor at physiological levels, but has no effect on cells expressing wild-type K-ras. Wt1 contributes to K-ras driven lung tumorigenesis in vivo and loss of Wt1 is specifically deleterious to human lung cancer cell lines that are dependent on oncogenic K-ras. Taken together, these observations reveal a novel role for Wt1 as a key regulator of the complex genetic network required for the oncogenic effect of the small GTPase K-ras. We compare the expression profiles of Wild type, K-ras mutant, Wt1-null, and double K-ras mutant/Wt1-null mouse embryonic fibroblasts (MEFs). The study provides insights into the transcriptional role of Wt1 in the context of oncogenic K-ras. MEFs were infected with adenoviral Cre to activate K-ras (6 samples), knockout Wt1 (5 samples), both activate K-ras and knockout Wt1 (7 samples). As a control, MEFs were infected with adenoviral GFP (5 samples). RNA was isolated using Trizol 7 days after infection. RNA was further prepared by passage over an RNeasy column. cDNA synthesis, biotinylation of cRNA and hybridization to mouse Genechip 430A v2 containing 39,000 probes was performed according to the manufacturer's instructions (Affymetrix, Santa Clara). Microarray data was normalized with Expression Console software (Affymetrix, Santa Clara) using RMA algorithms.

2010-03-06 | E-GEOD-15325 | biostudies-arrayexpress

Discrete WT1-positive hepatic fibrogenic cell lineages of distinct developmental mesothelial origin are paradoxically inhibited by WT1

Project description:Activated hepatic stellate cells orchestrate scar formation during fibrotic liver injury. Recent evidence has shown limited quiescent precursor derivation from the mesoderm during development. Here, we use lineage-tracing from development, through adult homeostasis, to adult fibrotic injury, to show that discreet subpopulations of activated hepatic stellate cells are defined by expression of WT1, a transcription factor controlling morphological transitions in organogenesis and adult homeostasis. Morphologically and transcriptionally distinct subpopulations are evident in fibrotic human disease and animal models. Populations defined by WT1 expression after injury derive from a discreet population of quiescent adult precursors originating from the embryonic mesothelium. WT1-deletion permits morphological transition to an enhanced fibrotic myofibroblast phenotype. Our findings demonstrate functional heterogeneity of adult scar-forming cells that can be whole-life traced back through specific quiescent precursors in adult homeostasis to differential origin in development, and defines WT1 as a paradoxical anti-fibrotic regulator during adult injury.

2019-08-21 | GSE103103 | 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