Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Tissue-specific inflammation induced by constitutively active STING is mediated by enhanced TNF signaling

ABSTRACT: Tissue-specific inflammation induced by constitutively active STING is mediated by enhanced TNF signaling

PROVIDER: PRJNA1021178 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR26186852_1.fastq.gz	Fastqsanger.gz
	SRR26186852_2.fastq.gz	Fastqsanger.gz
	SRR26186853_1.fastq.gz	Fastqsanger.gz
	SRR26186853_2.fastq.gz	Fastqsanger.gz
	SRR26186854_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 32

Similar Datasets

Tissue-specific inflammation induced by constitutively active STING is mediated by enhanced TNF signaling

Project description:Constitutive activation of STING by gain-of-function mutations triggers manifestation of the systemic autoinflammatory disease STING-associated vasculopathy with onset in infancy (SAVI) in humans and in mice. Murine SAVI is characterized by T cell lymphopenia, severe inflammatory interstitial lung disease, neuroinflammation and neurodegeneration with only limited contribution of type I interferon signaling. Here, we show that pharmacologic inhibition of TNF signaling in SAVI mice improved T cell lymphopenia, but had no effect on interstitial lung disease. However, complete blocking of TNF receptor signaling by knocking out TNFR1 and TNFR2 in SAVI mice rescued both, loss of thymocytes as well as interstitial lung disease. Furthermore, chronic STING signaling in lung endothelial cells of diseased mice enhanced transcription of cytokines, chemokines and adhesions proteins resulting in increased transendothelial migration of neutrophils across the endothelial barrier that could be reverted by genetic inactivation of TNFR1 and 2. Thus, our results demonstrate a pivotal role of TNFR-signaling in the development of SAVI-associated lung disease and suggest this pathway as promising target to ameliorate human SAVI

2024-04-16 | GSE244062 | GEO

Gene expression in STING-/- MEF cells expressing STING R284S variant

Project description:STING R284S variant is constitutively active and induces inflammatory genes even in absence of STING ligand cGAMP.

2019-02-27 | GSE111196 | GEO

Constitutively Active YAP/TAZ Target Genes

Project description:Constitutively Active YAP/TAZ Target Genes

| PRJNA489431 | ENA

Expression analysis of Reh cells after transfection with constitutively active variants of IRF5 (IRF5-4D) and/or constitutively active IKKβ(EE)

Project description:Genome-wide gene expression analysis of Reh cells following transfection with constitutively active IRF5-4D, constitutively active IKKβ(EE), or both in combination.

2014-09-24 | GSE51717 | GEO

Expression analysis of Reh cells after transfection with constitutively active variants of IRF5 (IRF5-4D) and/or constitutively active IKKÎ²(EE)

Project description:Genome-wide gene expression analysis of Reh cells following transfection with constitutively active IRF5-4D, constitutively active IKKÎ²(EE), or both in combination. Affymetrix U133 Plus 2.0 oligonucleotide arrays were hybridized to determine the gene expression profile of acute lymphoblastic leukemia-derived Reh cells following transfection with i) control constructs, ii), a constitutively active variant of IRF5 (IRF5-4D), iii) a constitutively active variant of the IkB kinase Î² (IKKÎ²(EE)), or iv) IRF5-4D in combination with IKKÎ²(EE). All hybridizations were done in biological duplicates.

2014-09-24 | E-GEOD-51717 | biostudies-arrayexpress

Transcription profiling of MCF-7 cell lines stably overexpressing constitutively active Raf-1, constitutively active MEK, constitutively active c-erbB-2, or ligand-activatable EGFR as models of overexpressed growth factor signaling

Project description:Profiling of MCF-7 cell lines stably overexpressing constitutively active Raf-1, constitutively active MEK, constitutively active c-erbB-2, or ligand-activatable EGFR as models of overexpressed growth factor signaling, as well as control vector transfected cells (coMCF-7) and control vector transfected cells long-term adapted for estrogen-independent growth (coMCF-7/lt-E2). Experiment Overall Design: Cell lines were profiled in biological triplicates, 18 arrays in all.

2007-10-02 | E-GEOD-3542 | biostudies-arrayexpress

Constitutively active Stat3 in mouse embryonic fibroblasts (MEFs)

Project description:Signal Transducer and Activator of Transcription 3 (STAT3) is considered as an oncogene being constitutively activated in a wide variety of primary human tumours, which often become addicted to its activity. Using primary fibroblasts derived from a knock-in mouse expressing only the constitutively active form STAT3-C as well as STAT3-dependent tumor cell lines MDA-MB468, DU145 and SKBR3, we provide evidence that STAT3 can act as a central regulator of cell metabolism. STAT3C/C MEFs are resistant to apoptosis and senescence and they show reduced mitochondrial activity but activate aerobic glycolysis, as shown by enhanced expression of master regulators of glycolysis such as PDK-1 and HIF-1α, and by increased lactate production, glucose avidity and sensitivity to glycolysis inhibitors. HIF-1α is up-regulated in the STAT3C/C MEFs and is responsible for the glycolytic phenotype. Moreover, inhibition of STAT3 activity in STAT3-addicted tumour cell lines restores mitochondrial activity and down-regulates glycolytic metabolism, preceding the induction of massive apoptosis. Thus, the essential role observed for STAT3 in so many different cancer cell types may be partly explained by its ability to act as a molecular switch of cellular metabolism triggering abnormal cell survival/proliferation. Three biological replicates of MEFs from mice with constitutively active Stat3 are compared to three biological replicates of wild-type MEFs.

2010-11-17 | E-GEOD-21507 | biostudies-arrayexpress

Genome-wide effect of STING-mediated acivation in endothelial cells in response to TNF

Project description:We report the role of STING in mediating responses to TNF in the mouse endothelial cells

2021-06-16 | GSE178200 | GEO

Activation of STING pathway contributed to cisplatin-induced cardiac dysfunction via promoting the activation of TNF-α-AP-1 signal pathway

Project description:In this study, cisplatin activated cGAS-STING signal pathway and deficiency of STING attenuated cisplatin-induced cardiotoxicity in vivo and in vitro. Mechanistically, STING-TNF-α-AP-1 axis contributed to cisplatin-induced cardiotoxicity by triggering cardiomyocyte apoptosis.

2021-08-12 | GSE181749 | GEO