Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profiling of Wt1 mutant renal anlagen

ABSTRACT: Wt1 is required for renal development and homozyogus knockout mice show renal agenesis caused by apoptosis of the metanepric mesnchyme. To identify genes regulated by WT1, we performed comparative gene expression profiling on kidney rudmients of Wt1 heterozygous and homozygous mutant E10.25 embryos.

ORGANISM(S): Mus musculus

PROVIDER: GSE58073 | GEO | 2014/06/01

SECONDARY ACCESSION(S): PRJNA249083

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expression profiling of Wt1 mutant renal anlagen

Project description:Wt1 is required for renal development and homozyogus knockout mice show renal agenesis caused by apoptosis of the metanepric mesnchyme. To identify genes regulated by WT1, we performed comparative gene expression profiling on kidney rudmients of Wt1 heterozygous and homozygous mutant E10.25 embryos. To identify deregulated genes, timed matings were performed and embryos isolated at E10.25, a time point before the onset of apoptosis in Wt1 mutants. The region containing the metanephric mesenchyme was microdissected, RNA isolated and after labeling, hybridized to Mouse Genome Survey Microarrays. Deregulated genes were identified using GeneSpring (GSX) software.

2014-06-01 | E-GEOD-58073 | biostudies-arrayexpress

N-degradomic analysis of proteolytic processing in WT1 heterozygous mice

Project description:N-degradomic analysis of proteolytic processing in WT1 heterozygous mice, suffering from genetically induced chronic kidney injury, compared to wild type

2021-02-15 | PXD023292 | Pride

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

WT1+ parietal epithelial progenitor cells are essential for renal proximal tubule repair and regeneration

Project description:Purpose: We have found that WT1+ parietal epithelial progenitor cells contribute to renal proximal tubule repair and regeneration by cell lineage tracing and direct differentiation analysis, but the transcription profile of these WT1+ PECs is largely unkown. Here, we aimed to unveil the transcriptional features of WT1+ PECs through single-cell RNA sequencing (scRNA-seq). Methods: Single cell suspension was prepared from kidney cortex of WT1CreERT2; Rosa26-tdTfl/+ mice that underwent sham or ischemic reperfusion injury (IRI) 24h .TdT+ cells were enriched by fluorescence activated cell sorter (FACS) and further analyzed with BD Rhapsody platform. Results: After quality control and cell filtering, 26,759 cells were informative (Dataset S1) and divided into 10 clusters using Harmony algorithm to reduce batch effects. GO analysis and QuSAGE heatmap suggested that WT1+ PECs might promote kidney regeneration after AKI through TGF-β and Notch signaling pathway. Marker gene expression analysis showed that WT1+ PECs shared the characteristics of STCs. Pseudotemporal analysis indicated that that WT1+ PECs developed to PTECs through STCs intermediate stage. Conclusions: scRNA-seq indicated that the rare, quiescent PECs supplied PTECs through STCs intermediate stage after severe ischemic injury, and this process most likely was regulated through TGF-β and Notch signaling pathway.

2023-03-22 | GSE184601 | GEO

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

2015-07-27 | GSE70892 | GEO

Oviductal expression data from wild type and Wt1 heterozygous mice

Project description:Comparison of gene expression in wild type and Wt1 (Wilms tumor suppressor gene 1) heterozygous knockout mice. Background: in Wt1+/- mice (MF1 strain) litter sizes are significantly smaller than in wild type animals. In addition, we observe retarded embryonic development of pre-implantation embryos that are still within the oviduct. By gene expression analysis we want to elucidate the molecular basis for these phenomena. 3 wild type and 3 heterozygous RNA samples

2015-12-12 | E-GEOD-75924 | biostudies-arrayexpress

Oviductal expression data from wild type and Wt1 heterozygous mice

2015-12-12 | GSE75924 | GEO

Genetic and epigenetic evolution as a contributor to WT1-mutant leukemogenesis

Project description:Genetic studies have identified recurrent somatic mutations in Acute Myeloid Leukemia (AML) patients, including in WT1 (Wilms’ tumor gene 1). The molecular mechanisms by which WT1 mutations contribute to leukemogenesis have not yet been fully elucidated. We investigated the role of Wt1 gene dosage in steady state and pathologic hematopoiesis. Wt1 heterozygous loss enhanced stem cell self-renewal in an age-dependent manner, with increased stem cell function over time and age-dependent leukemic transformation. Wt1-haploinsufficient leukemias were characterized by progressive genetic and epigenetic alterations, including in known leukemia disease alleles, demonstrating a requirement for additional events to promote hematopoietic transformation. Consistent with this observation, we found that Wt1 haploinsufficiency cooperates with Flt3-ITD mutation to induce fully penetrant AML. Our studies provide insight into mechanisms of Wt1-loss in leukemogenesis and into the evolutionary events required to induce transformation of Wt1-haploinsufficient stem/progenitor cells.

2018-09-01 | GSE109922 | GEO

Gestational high salt stressed new born BdkrB2 knockout collecting duct cells vs BdkrB2 wild type collecting duct cells

Project description:Transcriptional profiling of new born mouse kidney collecting duct (CD) cells comparing the infuence of gestational high salt stress on gene expression remolding of BdkrB2 receptor knockout CD cells with that of BdkrB2 receptor wild type CD cells. The BdkrB2 receptor has been shown to be playing a role in renal vascular tone, kidney secretion and reabsorption function, normal kidney development, while impaired BdkrB2 receptor in kidney shown being associated with renal agenesis and renal dysplasia. Goal was to determine the effects of BdkrB2 receptor knockout together with gestational high salt stress on collecting duct gene expression pattern. Single color microarray experiment, BdkrB2 knockout new born mouse CD cells vs. BdkrB2 WT mosue CD cells with both on gestational high salt stress. Biological replicates: 3 BdkrB2 null replicates, 3 BdkrB2 WT replicates. Expression level of each sample was normalized to WT1 replicate.

2013-08-08 | E-GEOD-49616 | biostudies-arrayexpress

Gene Expression of Kidney from HSRA-S (congenital solitary kidney) and HSRA-C (two-kidney) using Rat Gene 1.1 ST Array [RaGene-1_1-st]

Project description:We recently developed a new model of renal agenesis [i.e., the heterogeneous stock derived model of unilateral renal agenesis, (HSRA)]. The HSRA model consistently exhibits unilateral renal agenesis ranging from 50-75% in each generation and is characterized by low nephron number, early kidney hypertrophy, and an inherent susceptibility to develop significant kidney injury and decline in renal function with age. Whole transcriptome analysis was evaluated at month 1 to identify early changes in genes/networks that may be involved in increased susceptibility of HSRA-S to develop kidney injury in the long-term. An n=4 per group (independent samples) were evaluated for HSRA-S (congenital solitary kidney) and HSRA-C (two-kidney). HSRA-C (two-kidney) samples were set as the control.

2014-10-07 | E-GEOD-62092 | 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