Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Constitutive active STING signaling in MC38 tumor cells [RNA-Seq]

ABSTRACT: Constitutive active STING signaling in MC38 tumor cells [RNA-Seq]

PROVIDER: PRJNA896153 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR22105821_1.fastq.gz	Fastqsanger.gz
	SRR22105821_2.fastq.gz	Fastqsanger.gz
	SRR22105822_1.fastq.gz	Fastqsanger.gz
	SRR22105822_2.fastq.gz	Fastqsanger.gz
	SRR22105823_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Constitutive active STING signaling in MC38 tumor cells

Project description:Constitutive active STING signaling in MC38 tumor cells

| PRJNA896150 | ENA

Constitutive active STING signaling in MC38 tumor cells [CITE-seq]

Project description:Constitutive active STING signaling in MC38 tumor cells [CITE-seq]

| PRJNA896152 | ENA

Constitutive active STING signaling in MC38 tumor cells [CITE-seq]

Project description:Parental MC38 tumor cells were transduced with the STING-N153S mutant

2023-03-17 | GSE216897 | GEO

Constitutive active STING signaling in MC38 tumor cells [RNA-Seq]

Project description:Parental MC38 tumor cells were transduced with the STING-N153S mutant and RNA-seq for differential gene expression analysis was performed

2023-03-17 | GSE216896 | GEO

Constitutive active STING signaling in MC38 tumor cells

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

2023-03-17 | GSE216898 | GEO

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

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

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

| PRJNA1021178 | ENA

Single amino acid change in STING leads to constitutive active signaling.

Project description:The production of cytokines by the immune system in response to cytosolic DNA plays an important role in host defense, autoimmune disease, and cancer immunogenicity. Recently a cytosolic DNA signaling pathway that is dependent on the endoplasmic reticulum adaptor and cyclic dinucleotide sensor protein STING has been identified. Association of cytosolic DNA with cyclic-GMP-AMP synthase (cGAS) activates its enzymatic activity to synthesize the cyclic dinucleotide second messenger cGAMP from GTP and ATP. Direct detection of cGAMP by STING triggers the activation of IRF3 and NF-kB, and the production of type I interferons and proinflammatory cytokines. The mechanism of how STING is able to mediate downstream signaling remains incompletely understood although it has been shown that dimerization is a prerequisite. Here, we identify a single amino acid change in STING that confers constitutive active signaling. This mutation appears to both enhance ability of STING to both dimerize and associate with its downstream target TBK1.

| S-EPMC4366210 | biostudies-literature

Genome-wide effect of constitutive IFN-signaling

Project description:Genome-wide effect of constitutive IFN-signaling

| PRJNA434236 | ENA

STING-mediated proton channel activity, signaling, and autoimmune disease require ArfGAP2

Project description:STING transmits signals downstream of the cytosolic DNA sensor cGAS, leading to transcriptional up-regulation of cytokines. However, components of the STING signaling pathway, such as IRF3 and IFNAR1, are not essential for autoinflammatory disease in STING gain-of-function (SAVI) mice. Recent findings indicate that STING can also function as a proton channel that deacidifies the Golgi. Since pH impacts Golgi enzyme activity, protein maturation, and trafficking, we hypothesized that STING proton channel activity influences multiple Golgi functions. Here, we show that STING-mediated proton efflux non-transcriptionally regulates Golgi trafficking of protein cargos. This process requires the Golgi-associated protein ArfGAP2, a cell type-specific dual regulator of STING-mediated proton efflux and signaling. Deletion of ArfGAP2 in hematopoietic and endothelial cells markedly reduces STING-mediated cytokine and chemokine secretion, immune cell activation, and autoinflammatory pathology in SAVI mice. Thus, ArfGAP2 facilitates STING-mediated signaling and cytokine release in hematopoietic cells, significantly contributing to autoinflammatory disease pathogenesis.

2024-11-30 | PXD058416 | 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