Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Notch activity in tumor cells shapes interferon-gamma response and immune microenvironment in glioma

ABSTRACT: Notch activity in tumor cells shapes interferon-gamma response and immune microenvironment in glioma

PROVIDER: PRJNA674055 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR12967400.fastq.gz	Fastqsanger.gz
	SRR12967401.fastq.gz	Fastqsanger.gz
	SRR12967402.fastq.gz	Fastqsanger.gz
	SRR12967403.fastq.gz	Fastqsanger.gz
	SRR12967404.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 102

Similar Datasets

mRNASeq of glioma cells

Project description:In mouse models of PDGF-driven glioma where Notch is tumor-suppressive, we find that Notch activity shapes interferon-response in tumor cells and the local immune microenvironment early during tumor progression. Notch inhibition disturbs cytokine expression by tumor cells, altering recruitment and activation of immune cell populations and favoring hyper-proliferative "immune niche" independent growth. Genetic inactivation of Notch in glioma cells also attenuates their response to interferon-gamma, establishing a non-cell autonomous inhibitory feedback loop that further promotes immune evasion and aggressiveness. Hence, we propose that Notch signaling levels in tumor cells are key to orchestrate immune escape and microenvironment independency during brain tumor formation.

2022-07-07 | GSE160669 | GEO

Vismodegib and Gamma-Secretase/Notch Signalling Pathway Inhibitor RO4929097 in Treating Patients With Advanced or Metastatic Sarcoma

Project description:This randomized phase I/II clinical trial is studying the side effects and best dose of gamma-secretase/notch signalling pathway inhibitor RO4929097 when given together with vismodegib and to see how well they work in treating patients with advanced or metastatic sarcoma. Vismodegib may slow the growth of tumor cells. Gamma-secretase/notch signalling pathway inhibitor RO4929097 may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth. Giving vismodegib together with gamma-secretase/notch signalling pathway inhibitor RO4929097 may be an effective treatment for sarcoma.

| 2091475 | ecrin-mdr-crc

Single-cell RNA-sequencing of immune cells (CD45+) from the tumor microenvironment

Project description:In mouse models of PDGF-driven glioma where Notch is tumor-suppressive, we find that Notch activity shapes interferon-response in tumor cells and the local immune microenvironment early during tumor progression. Notch inhibition disturbs cytokine expression by tumor cells, altering recruitment and activation of immune cell populations and favoring hyper-proliferative "immune niche" independent growth. Genetic inactivation of Notch in glioma cells also attenuates their response to interferon-gamma establishing a non-cell autonomous inhibitory feedback loop that further promotes immune evasion and aggressiveness. Hence, we propose that Notch signaling levels in tumor cells are key to orchestrate immune escape and microenvironment independency during brain tumor formation.

2022-07-07 | GSE160714 | GEO

Gamma secretase complex and DOCK2 affinity interactome

Project description:γ-Secretase is a transmembrane protease complex responsible for processing multiple type I transmembrane proteins, including the amyloid precursor protein (APP) and NOTCH. Using a proteomics-based screening approach, we found that dedicator of cytokinesis protein 2 (DOCK2) interacts with the γ-secretase complex component Nicastrin (NCSTN), regulating NCSTN N45-mannosylation and the effects of γ-secretase on NOTCH receptors. Both genetically depleting DOCK2 and pharmacologically targeting NCSTN mannosylation via Kifunensine ameliorate Notch-dependent leukemia progression in vivo. Together, these results reveal a mechanism by which γ-secretase specifically recognizes its substrate and provide a direction for treating Notch-related diseases.

2025-06-26 | PXD065491 |

Analysis of Notch-regulated lncRNA in human glioma stem cell

Project description:Glioblastomas show heterogeneous histological features. These distinct phenotypic states are thought to be associated with the presence of glioma stem cells (GSCs), which are highly tumorigenic and self-renewing sub-population of tumor cells that have different functional characteristics. To investigate Glioblastomas (GBMs) show heterogeneous histological features. These distinct phenotypic states are thought to be originated by the glioma stem cells (GSCs), which are highly tumorigenic and self-renewing sub-population of tumor cells. Notch signaling has been shown to be important for maintenance of GSC population both in vitro and in vivo. A recent study showed that NOTCH -triggered oncogenic activity can be due to not only its ability to regulate coding genes but also long non-coding RNAs (lncRNAs). Here, we investigated the molecular effects of lncRNA in GSC, whose expression is induced by Notch signaling. We searched for downregulated lncRNAs in GSCs by treatment of small interfering RNA (siRNA) targeting Notch1 and JAG1 (si-Notch1 and si-JAG1) and γ-secretase inhibitors (N-S-phenyl-glycine-t-butyl ester (DAPT) and RO4929097) using SurePrint G3 Human GE 8×60K array slides (G4851B, Agilent Technologies).gene expression profiling in GSC, we have performed microarray experiment using Agilent Whole Human Genome Oligo Microarrays (G4112F).

2016-11-23 | GSE79897 | GEO

RNA-seq of co-culture experiment between human endothelial cells (HUVECs) and mouse glioma (Gl261) with or without Notch Inhibitor Gamma Secretase Inhibitor (GSI)

Project description:Increased awareness for the role for angiocrine factors in stem cell biology, in general, has suggested a role for angiocrine factors in the maintenance of GSC stemness and also there are reciprocal bi-directional signals from endothelial cells (ECs) to glioma (Gl261) and vice versa. To extend, refine and elucidate perfusion-independent modes of GBM-EC communication (i.e., distinguishing contact dependent or contact independent routes), we carried-out the following experiments: ECs from umbilical veins tagged with RFP (HUVEC-RFP) were cultured with mouse glioma line Gl261 fluorescently labelled with GFP (Gl261-GFP) until reaching confluency by 72 h post culturing. Cells were than harvested, RNA extracted, and the combined co-culture transcriptomes were sequenced from a generated cDNA library without prior separation of the respective cell types (sample named as Co). The Co transcriptome was compared to that of an artificial mixtures of the two cell types (Gl261-GFP and HUVEC-RFP) in the exact cells ratio attained by the end of the co-cluttering aided by FACS-based determination of the GFP/RFP ratio (sample named as Sep). In this procedure advantage was taken on the different species from which GBM and ECs are derived and specialized bioinformatics tools allowing to unambiguously assign the transcripts to their respective GBM (mouse) or EC (human) origins, thereby circumventing confounding factors associated with cell purification. Considering that contact-dependent EC signaling is primarily regulated by canonical Notch pathway and that the Notch pathway was reported to play a role in self-renewal of GSCs, we also treated GBM-EC co-cultures with the Notch pathway inhibitor Gamma secretase inhibitor (GSI) (or with the DMSO vehicle alone) for 24 h before harvesting.

2022-01-01 | E-MTAB-9604 | biostudies-arrayexpress

RNA-seq of monocyte derived macrophages exposed to arachidonic acid, interferon beta, or interferon gamma

Project description:Monocyte derived macrophages were exposed to arachidonic acid, interferon beta, or interferon gamma

2021-12-31 | E-MTAB-10867 | biostudies-arrayexpress

Manx Shearwater Interferon gamma gene

Project description:sequencing of the Manx Shearwater Interferon gamma gene

| PRJEB20061 | ENA

Notch activity in tumor cells shapes interferon-gamma response and immune microenvironment in glioma

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

2022-07-07 | GSE160715 | GEO

Transcription profiling of Toxoplasma-infected human fibroblasts treated with human recombinant interferon gamma

Project description:Human fibroblasts were infected or not with Toxoplasma gondii (Pru strain) for 18 h at a nominal MOI of 3. Cells were subsequently treated with human recombinant interferon gamma (0.5 ng/ml = 30 pM) for 0, 2, 4 and 8 h before RNA was harvested for cDNA microarray experiments. Uninfected samples were named N0, N2, N4 and N8 (i.e., N2 indicated uninfected cells treated with interferon gamma for 2 h); infected samples were named P0, P2, P4 and P8. Duplicate cultures were analyzed for each condition (indicated as "a" and "b"). The reference channel (ch1, green) contained Universal Human Reference RNA. Using a genome-wide microarray analysis we show here a complete dysregulation of interferon-gamma-inducible gene expression in human fibroblasts infected with Toxoplasma. Notably, 46 of the 127 interferon-gamma-responsive genes were induced and 19 were suppressed in infected cells before they were exposed to interferon gamma, indicating that other stimuli produced during infection may also regulate these genes. Following interferon-gamma treatment, none of the 127 interferon-gamma-responsive genes could be significantly induced in infected cells.

2007-06-06 | E-SMDB-3827 | 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