Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mus musculus

ABSTRACT: mRNA-Seq profiling nephron progenitor and stromal progenitor cells in mouse embryonic kidney

PROVIDER: PRJNA397596 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR5912730_1.fastq.gz	Fastqsanger.gz
	SRR5912730_2.fastq.gz	Fastqsanger.gz
	SRR5912740_1.fastq.gz	Fastqsanger.gz
	SRR5912740_2.fastq.gz	Fastqsanger.gz
	SRR5912731_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 40

Similar Datasets

Protein correlation of Mus musculus tissues

Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from Mus musculus tissues (Heart, Liver, Lung, Kidney, Skeletal Muscle, Thymus)

2021-05-05 | PXD022309 | Pride

Protein correlation of Mus musculus tissues

Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from seven Mus musculus tissues (Heart, Brain, Liver, Lung, Kidney, Skeletal Muscle, Thymus)

2018-04-24 | PXD007288 | Pride

scRNA-seq of Mus musculus subcutaneous Lin- cells derived from the subcutaneous adipose stromal vascular fraction

Project description:We used the resolving power of single-cell transcriptional profiling to molecularly characterize the mouse adipose stem and progenitor cell-enriched, subcutaneous adipose stromal vascular fraction. We molecularly assessed CD45- CD31- SVF cells using the 10x Genomics Chromium (10x) platform.

2019-05-24 | E-MTAB-6677 | biostudies-arrayexpress

Mus musculus

Project description:Transcriptional profile of mouse nephron progenitor cells

| PRJNA354556 | ENA

The Essential Role of ASH2L in Regulating Cell Cycle-Associated Gene Expression to Promote Nephron Progenitor Self-Renewal and Nephron Formation in Mice [CUT&TAG]

Project description:Maintaining adequate nephron number is crucial for normal kidney function, as even slight deficits can predispose individuals to hypertension and other late-onset renal diseases. Congenital anomalies of the kidney and urinary tract arise from abnormal embryonic kidney development, which involves the coordinated reciprocal induction of the ureteric bud and metanephric mesenchyme. Preserving the balance between self-renewal and differentiation of nephron progenitor cells in the metanephric mesenchyme is essential for nephron endowment. Prior work has implicated histone modifications in regulating kidney lineage-specific gene transcription and nephron endowment. Here, we selectively inactivated the H3K4 methyltransferase complex component ASH2L in mouse nephron progenitor cells to elucidate its role in nephron progenitor cell self-renewal and differentiation. The results showed that Ash2l inactivation disrupted H3K4 trimethylation establishment at promoters of genes controlling nephron progenitor cell stemness, differentiation, and cell cycle, leading to premature nephron progenitor cell depletion, cell cycle arrest, and abnormal differentiation of early nephron progenitors, resulting in renal dysplasia at birth. These findings identify ASH2L-mediated H3K4 methylation as a critical epigenetic regulator of kidney development and suggest a novel mechanism contributing to congenital anomalies of the kidney and urinary tract. This knowledge may guide future efforts to unravel the pathogenesis of these conditions and develop targeted therapies.

2025-01-09 | GSE269088 | GEO

The Essential Role of ASH2L in Regulating Cell Cycle-Associated Gene Expression to Promote Nephron Progenitor Self-Renewal and Nephron Formation in Mice [RNA-seq]

2025-01-09 | GSE269089 | GEO

mRNA-Seq profiling nephron progenitor and stromal progenitor cells in mouse embryonic kidney

Project description:To characterize the expression profile of mouse nephron progenitors, we performed intracellular labeling of Six2 by antibody, followed by FACS and RNA-seq. To characterize the expression profile of mouse stromal progenitor cells, we isolated Tdt+ cells from Foxd1Cre;Tdt transgenic mice kidney by FACS followed by RNA-seq.

2018-02-14 | GSE102378 | GEO

miRNA expression in nephron progenitors of the developing kidney

Project description:mIRNA expression profiling of mouse embryonic nephron progenitors at embryonic day 14 isolated by GFP expression driven by Six2-TGC (transgenic mouse line), compared to whole embryonic kidney at day 14

2017-02-01 | GSE86217 | GEO

FACS-sorted Six2-positive nephron progenitor cells at embryonic day 15.5: wildtype (WT) vs. conditional HDAC1&2-null (MUT)

Project description:Transcriptional profiling of FACS-sorted Six2-positive nephron progenitor cells from Six2CreEGFP mice without (WT) or with (MUT) homozygously floxed HDAC1 and HDAC2 alleles at the age of embryonic day 15.5. This experiment aimed to uncover the genome-wide alternation in gene expression resulting from the removal of HDAC1&2 in the nephron progenitor population and successive changes to the series of events in kidney development.

2018-05-08 | GSE84305 | GEO

p53 Enables Self Renewal of Nephron Progenitor Cells

Project description:p53 limits the self-renewing ability of a variety of stem cells. Here, contrary to its classical role in restraining cell proliferation, we demonstrate a divergent function of p53 in maintenance of self-renewal of the nephron progenitor population in the embryonic mouse kidney. p53-null nephron progenitor cells (NPC) exhibit progressive loss of the self-renewing progenitor niche in the cap mesenchyme, identified by Cited1 and Six2 expression, and loss of cap integrity. Nephron endowment is regulated by NPC availability and their differentiation to nephrons. Quantitatively, the Six2p53-/- cap has 30% fewer Six2GFP+ cells. While the apoptotic index is unchanged the proliferation index is significantly lower, in accordance with cell cycle analysis data showing less mutant Six2p53-/-;GFP+ cells in S and G2/M phases in comparison to Six2p53+/+;GFP+ cells. The mutant kidneys also show nephron deficit and decreased Fgf8 expression. To investigate the underlying changes in gene expression in the cap mesenchyme that contribute to the Six2p53-/- phenotype, we utilized RNA-Seq for transcriptome comparison. Top biological processes affected by p53 loss are development and morphogenesis, cell adhesion/migration, cell survival and metabolism. Cells from the mutant CM showed increased cellular ROS levels as well as deregulated expression of energy metabolism and mitochondrial genes suggesting metabolic dysfunction. Adhesion defects are visualized by decreased immunostaining of adhesion marker NCAM, and may possibly contribute to the differentiation defect as well. Altogether our data suggest a novel role for p53 in enabling self-renewal of the NPC and preservation of the progenitor niche, and thus regulating nephron endowment. mRNA profiles of wild-type (WT) and conditional p53 knockout (KO) of Six2+ mouse nephron progenitor cells (NPC) at embryonic day 15.5

2015-02-16 | E-GEOD-56253 | 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