Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Activation of Notch2 signaling drives cyst growth in kidney [RNA-seq: R26NICD2 Pax-rtTA]

ABSTRACT: Activation of Notch2 signaling drives cyst growth in kidney [RNA-seq: R26NICD2 Pax-rtTA]

PROVIDER: PRJNA953775 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Activation of Notch2 signaling drives cyst growth in kidney [RNA-seq: R26NICD2 Pax-rtTA]

Project description:In order to investigate how NICD2 promotes cyst growth, we carried out bulk RNA-Seq analysis of kidneys from PKD mouse model R26NICD2/+ Pax8-rtTA mice.

2025-01-17 | GSE229268 | GEO

Activation of Notch2 signaling drives cyst growth in kidney

Project description:Activation of Notch2 signaling drives cyst growth in kidney

| PRJNA953772 | ENA

Activation of Notch2 signaling drives cyst growth in kidney [RNA-seq: R26NICD2 KspCre]

Project description:Activation of Notch2 signaling drives cyst growth in kidney [RNA-seq: R26NICD2 KspCre]

| PRJNA953776 | ENA

Activation of Notch2 signaling drives cyst growth in kidney [RNA-seq: R26NICD2 KspCre]

Project description:In order to investigate how NICD2 promotes cyst growth, we carried out bulk RNA-Seq analysis of kidneys from PKD mouse models R26NICD2/+KspCre.

2025-01-17 | GSE229267 | GEO

Activation of Notch2 signaling drives cyst growth in kidney

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-01-17 | GSE229269 | GEO

NOTCH2 mutants

Project description:NOTCH2 mutants

| PRJNA967022 | ENA

Jagged1/Notch2 controls kidney fibrosis via Tfam-mediated metabolic reprogramming

Project description:While Notch signaling has been proposed to play a key role in fibrosis, the direct molecular pathways targeted by Notch signaling and the precise ligand and receptor pair that are responsible for kidney disease remain poorly defined. In this study, we found that JAG1 and NOTCH2 showed the strongest correlation with the degree of interstitial fibrosis in a genome wide expression analysis of a large cohort of human kidney samples. Transcript analysis of mouse kidney disease models, including folic-acid-induced nephropathy, unilateral ureteral obstruction, or APOL1-associated kidney disease, indicated that Jag1 and Notch2 levels were higher in all analyzed kidney fibrosis models. Mice with tubule-specific deletion of Jag1 or Notch2 (Kspcre/Jag1flox/flox and Kspcre/Notch2flox/flox) had no kidney-specific alterations at baseline, but showed protection from folic acid induced kidney fibrosis. Tubule-specific genetic deletion of Notch1 and global knock-out of Notch3 had no effect on fibrosis. In vitro chromatin immunoprecipitation experiments and genome-wide expression studies identified the mitochondrial transcription factor A (Tfam) as a direct Notch target. Re-expression of Tfam in tubule cells prevented Notch-induced metabolic and profibrotic reprogramming. Kidney tubule specific deletion of Tfam resulted in fibrosis. In summary, Jag1/Notch2 plays a key role in kidney fibrosis development by regulating Tfam expression and metabolic reprogramming.

2018-12-31 | GSE118600 | GEO

Effect of Notch2 in chondrocytes

Project description:To investigate the role of Notch2 in the inflammatory response in chondrocytes, we cultured primary chondrocytes derived from wild type and Notch2 mutant mice and treated TNFalpha or vehicle. We then performed gene expression profiling analysis using data obtained from RNA-seq of wild type and Notch2 mutant chondrocytes.

2023-10-16 | GSE224255 | GEO

Transcriptomic Profiling of Polycystic Kidney Disease Identifies Paracrine Factors in the Early Cyst Microenvironment

Project description:Initial cysts that are formed upon Pkd1 loss in mice impose persistent stress on surrounding tissue and trigger a cystic snowball effect, in which local aberrant PKD-related signaling increases the likelihood of new cyst formation, ultimately leading to accelerated disease progression. Although many pathways have been associated with PKD progression, the knowledge of early changes near initial cysts is limited. To perform an unbiased analysis of transcriptomic alterations in the cyst microenvironment, microdomains were collected from kidney sections of iKsp-Pkd1del mice with scattered Pkd1-deletion using Laser Capture Microdissection. These microdomains were defined as F4/80-low cystic, representing early alterations in the cyst microenvironment, F4/80-high cystic, with more advanced alterations, or non-cystic. RNA sequencing and differential gene expression analysis revealed 953 and 8088 dysregulated genes in the F4/80-low and F4/80-high cyst microenvironment, respectively, when compared to non-cystic microdomains. In the early cyst microenvironment, several injury-repair, growth, and tissue remodeling-related pathways were activated, accompanied by mild metabolic changes. In the more advanced F4/80-high microdomains, these pathways were potentiated and the metabolism was highly dysregulated. Upstream regulator analysis revealed a series of paracrine factors with increased activity in the early cyst microenvironment, including TNFSF12 and OSM. In line with the upstream regulator analysis, TWEAK and Oncostatin-M promoted cell proliferation and inflammatory gene expression in renal epithelial cells and fibroblasts in vitro. Collectively, our data provide an overview of molecular alterations that specifically occur in the cyst microenvironment and identify paracrine factors that may mediate early and advanced alterations in the cyst microenvironment.

2023-12-27 | GSE231304 | GEO

Notch2 controls non-autonomous Wnt-signalling in chronic lymphocytic leukaemia

Project description:The Wnt-signalling pathway is one of the core de-regulated pathways in chronic lymphocytic leukemia (CLL), activated in a subset of patients by somatic coding mutations. Here we describe an alternative mechanism of Wnt-activation in malignant B cells, mediated by Notch2 activity in mesenchymal stromal cells (MSC) in the tumor microenvironment. We identified that tumor cells specifically induce and activate Notch2 in MSCs. Notch2 orchestrates the expression of target genes essential for the activation of canonical Wnt-signaling in CLL cells. Mechanistically, stromal Notch2 mediates the stabilization of â-catenin by inhibiting the activation of Gsk3-â in malignant B cells. Pharmacological inhibition of the Wnt-pathway mitigates microenvironment-mediated survival of malignant B cells in vitro. Similarly, inhibition of Notch-signaling impaired survival of CLL cells and disease engraftment in a PDX mouse model. Notch2 activation in the tumour microenvironment is a pre-requisite for the GSK3-â dependent activation of the canonical Wnt-signaling in tumor cells.

2018-09-19 | PXD010401 | Pride

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