Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

OLFM4 is a direct target of the cGAS-STING pathway and acts as an extracellular inhibitor for the Hippo signaling in EBV-associated cancer

ABSTRACT: OLFM4 is a direct target of the cGAS-STING pathway and acts as an extracellular inhibitor for the Hippo signaling in EBV-associated cancer

PROVIDER: PRJNA1003081 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

OLFM4 is a direct target of the cGAS-STING pathway and acts as an extracellular inhibitor for the Hippo signaling in EBV-associated cancer

Project description:OLFM4 is a direct target of the cGAS-STING pathway and acts as an extracellular inhibitor for the Hippo signaling in EBV-associated cancer

| PRJNA1003079 | ENA

OLFM4 is a direct target of the cGAS-STING pathway and acts as an extracellular inhibitor for the Hippo signaling in EBV-associated cancer

Project description:OLFM4 is a direct target of the cGAS-STING pathway and acts as an extracellular inhibitor for the Hippo signaling in EBV-associated cancer

| PRJNA1003078 | ENA

OLFM4 is a direct target of the cGAS-STING pathway and acts as an extracellular inhibitor for the Hippo signaling in EBV-associated cancer

Project description:Transcriptome analysis of the function of OLFM4 MV on gastric cancer HGC-27 cells

2024-09-18 | GSE240275 | GEO

OLFM4 is a direct target of the cGAS-STING pathway and acts as an extracellular inhibitor for the Hippo signaling in EBV-associated cancer

Project description:Gene expression profile regulated by EBV infection

2024-09-18 | GSE240274 | GEO

cGAS Senses Translation Stress Through Direct Binding to Ribosomes

Project description:The cGAS-STING pathway, a central component of the innate immune system, senses cytosolic DNA and induces interferon-stimulated genes (ISGs) to mediate inflammation. Here we report the unexpected discovery that cGAS senses dysfunctional protein production. Purified ribosomes interact with and stimulate the catalytic activity of recombinant cGAS in vitro. Disruption of the ribosome-associated protein quality control pathway, which detects and resolves ribosome collisions, results in cGAS- and STING-dependent ISG expression, and causes the re-localization of cGAS from the nucleus to the cytosol. Indeed, cGAS preferentially binds collided ribosomes in vitro, and other orthogonal perturbations that lead to elevated levels of collided ribosomes cause re-localization of cGAS as well. Thus, the cGAS-STING pathway senses and responds to translation stress. These findings have implications for the inflammatory responses to viral infection and tumorigenesis, both of which substantially reprogram cellular protein synthesis.

2021-09-09 | PXD019359 | Pride

Neddylation modification on cGAS of human and mouse

Project description:The cytosolic DNA sensor cyclic GMP-AMP (cGAMP) synthetase (cGAS) has emerged as a fundamental component fueling the anti-pathogen immunity. Because of its pivotal role in initiating innate immune response, the activity of cGAS must be tightly fine-tuned to maintain immune homeostasis in antiviral response. Here, we reported that neddylation modification was indispensable for appropriate cGAS-STING signaling activation. Blocking neddylation pathway using neddylation inhibitor MLN4924 substantially impaired the induction of type I interferon and proinflammatory cytokines, which was selectively dependent on Nedd8 E2 enzyme Ube2m. We further found that deficiency of the Nedd8 E3 ligase Rnf111 greatly attenuated DNA-triggered cGAS activation while not affecting cGAMP induced activation of STING, demonstrating that Rnf111 was the Nedd8 E3 ligase of cGAS. We further identified Lys231 and Lys421 as the key neddylation sites in human cGAS. Mechanistically, Rnf111 interacted with and polyneddylated cGAS, which in turn promoted its dimerization and enhanced the DNA-binding ability, leading to proper cGAS-STING pathway activation. In the same line, the Ube2m or Rnf111 deficiency mice exhibited severe defects in innate immune response and were susceptible to HSV-1 infection. Collectively, our study uncovered a vital role of the Ube2m-Rnf111 neddylation axis in promoting the activity of the cGAS-STING pathway and highlighted the importance of neddylation modification in antiviral defense.

2021-02-22 | PXD024088 | Pride

RNA sequencing for RWPE1 cells, OLFM4-Active RWPE1 cells and OLFM4-KO RWPE1 cells

Project description:OLFM4 gene expressing in RWPE1 stem/progenitor-like cells. To study OLFM4 gene functions and molecular mechanisms, we generated OLFM4-avtive and OLFM4-knock out-GFP reporter RWPE1 cells with CRISP-Cas 9 system. The cell transcriptome was studied with RNA sequencing.

2019-08-05 | GSE126162 | GEO

Transcriptome changes after the transfection of cGAS specific agonist G3-YSD

Project description:The cGAS-STING signalling has been well recognized as the major pathway response to self and non-self DNA molecule in cytoplasm. Here, we measured the temporal transcriptome dynamic changes after cGAS-STING signalling activation based on cGAS specific agonist G3-YSD transfection

2022-12-09 | GSE207458 | GEO

cGAS Senses Translation Stress Through Direct Binding to Ribosomes

Project description:The cGAS-STING pathway, a central component of the innate immune system, senses cytosolic DNA and induces interferon-stimulated genes (ISGs) to mediate inflammation. Here we report the unexpected discovery that cGAS senses dysfunctional translation. Purified ribosomes interact with and stimulate recombinant cGAS catalytic activity in vitro. Disruption of the ribosome-associated protein quality control pathway, which detects and resolves ribosome collisions, results in cGAS- and STING-dependent ISG expression, and cause the re-localization of cGAS from the nucleus to the cytosol. Other orthogonal perturbations that lead to elevated levels of collided ribosomes cause re-localization of cGAS as well. Thus, the cGAS-STING pathway senses and responds to translation stress. These findings have implications for the inflammatory responses to viral infection and tumorigenesis, both of which substantially reprogram cellular protein synthesis.

2020-05-26 | GSE151127 | GEO

cGAS/STING drives ageing-related inflammation and neurodegeneration IV

Project description:Low-grade inflammation is a hallmark of old age and a central driver of ageing-associated impairment and disease. Multiple factors can contribute to ageing-associated inflammation, however the molecular pathways transducing aberrant inflammatory signalling and their impact in natural ageing remain poorly understood. Here we show that the cGAS-STING signalling pathway, mediating immune sensing of DNA, is a critical driver of chronic inflammation and functional decline during ageing. Blockade of STING suppresses the inflammatory phenotypes of senescent human cells and tissues, attenuates ageing-related inflammation in multiple peripheral organs and the brain in mice, and leads to an improvement in tissue function. Focusing on the ageing brain, we reveal that activation of STING triggers reactive microglia transcriptional states, neurodegeneration and cognitive decline. Cytosolic DNA released from perturbed mitochondria elicits cGAS activity in old microglia defining a mechanism by which cGAS-STING signalling is engaged in the ageing brain. Single-nuclei RNA-sequencing (snRNA-seq) of microglia and hippocampi of a newly developed cGAS gain-of-function mouse model demonstrates that engagement of cGAS in microglia is sufficient to direct ageing-associated transcriptional microglia states leading to bystander cell inflammation, neurotoxicity and impaired memory capacity. Our findings establish the cGAS-STING pathway as a critical driver of ageing-related inflammation in peripheral organs and the brain, and reveal blockade of cGAS-STING signalling as a potential strategy to halt (neuro)degenerative processes during old age.

2023-08-20 | GSE234421 | GEO

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