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MATRIN3 deficiency leads to cGAS-STING activation

ABSTRACT: MATRIN3 deficiency leads to cGAS-STING activation

PROVIDER: PRJNA1092701 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28479449.fastq.gz	Fastqsanger.gz
	SRR28479450.fastq.gz	Fastqsanger.gz
	SRR28479451.fastq.gz	Fastqsanger.gz

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MATRIN3 deficiency leads to cGAS-STING activation

Project description:MATRIN3 deficiency leads to cGAS-STING activation

| PRJNA895450 | ENA

MATRIN3 deficiency leads to cGAS-STING activation (NanoString)

Project description:MATRIN3 deficiency leads to cGAS-STING activation (NanoString)

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MATRIN3 deficiency leads to cGAS-STING activation (MinION RNA-Seq)

Project description:MATRIN3 deficiency leads to cGAS-STING activation (MinION RNA-Seq)

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MATRIN3 deficiency leads to cGAS-STING activation (Illumina RNA-Seq)

Project description:MATRIN3 deficiency leads to cGAS-STING activation (Illumina RNA-Seq)

| PRJNA895454 | ENA

MATRIN3 deficiency leads to cGAS-STING activation

Project description:To determine the direct targets of MATR3 in human HAP1 cells, we performed PAR-CLIP.

2024-05-15 | GSE262647 | GEO

MATRIN3 deficiency leads to cGAS-STING activation

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

2024-05-15 | GSE216830 | GEO

cGAS Suppresses β-cell Proliferation by a STING-independent but CEBPβ-dependent Mechanism

Project description:Aims/hypothesis cGAS (cyclic GMP-AMP synthase) has been implicated in various cellular processes, but its role in β-cell proliferation and diabetes is not fully understood. This study investigates the impact of cGAS on β-cell proliferation, particularly in the context of diabetes. Methods Utilizing mouse models, including cGAS and STING (stimulator of interferon genes) knockout mice, we explored the role of cGAS in β-cell function. This involved β-cell-specific cGAS knockout (cGASβKO) mice, created by breeding cGAS floxed mice with transgenic mice expressing Cre recombinase under the insulin II promoter. We analyzed cGAS expression in diabetic mouse models, evaluated the effects of cGAS deficiency on glucose tolerance, and investigated the molecular mechanisms underlying these effects through RNA sequencing. Results Our study found that cGAS expression is upregulated in the islets of diabetic mice and in response to high glucose conditions in MIN6 cells. Global cGAS deficiency enhanced glucose tolerance, while β-cell-specific cGAS knockout improved glucose intolerance under high-fat diet conditions. Interestingly, STING knockout did not affect pancreatic β-cell mass, suggesting a STING-independent mechanism for cGAS's role in β-cells. Further analyses revealed that cGAS deficiency leads to increased β-cell proliferation and reduced expression of CEBPβ, a known suppressor of β-cell proliferation. This effect appears to be mediated by a STING-independent pathway and is specific to pancreatic tissue. Conclusions/interpretation Our findings indicate that cGAS plays a pivotal role in modulating β-cell proliferation and glucose homeostasis, potentially through regulating CEBPβ expression in a STING-independent manner. This study highlights the importance of cGAS in diabetes pathology and suggests it as a potential therapeutic target for enhancing β-cell proliferation in diabetes treatment.

2025-04-18 | GSE264386 | GEO

MATRIN3 deficiency leads to cGAS-STING activation (NanoString)

Project description:To investigate the role of Matrin 3 (MATR3) in innate immune response, we analyzed and compared MATR3 KO clones versus wildtype HAP1 cells.

2024-05-15 | GSE216829 | GEO

Deposition of onco-histone H3.3-G34W leads to DNA repair deficiency and activates cGAS/STING-mediated immune responses

Project description:Mutations in histone H3.3-encoding genes causing mutant histone tails are associated with specific cancers such as pediatric glioblastomas (H3.3-G34R/V) and giant cell tumor of the bone (H3.3-G34W). The mechanisms by which these mutations promote malignancy are not completely understood. Here we show that cells expressing H3.3-G34W exhibit DNA double-strand breaks (DSBs) repair defects and increased cellular sensitivity to ionizing radiation. Mechanistically, H3.3-G34W can be deposited to damaged chromatin, but in contrast to wild-type H3.3, does not interact with non-homologous end-joining (NHEJ) key effectors KU70/80 and XRCC4 leading to NHEJ deficiency. As a consequence H3.3-G34W cells displayed an accumulation of micronuclei and cytosolic DNA, which led to activation of the cyclic GMP–AMP synthase/stimulator of interferon genes (cGAS/STING) pathway, thereby inducing release of immunestimulatory cytokines. These findings suggest a potential for radiotherapy for tumors expressing H3.3- G34W, which can be further improved by combination with STING agonists to induce immune-mediated therapeutic efficacy.

2025-04-08 | PXD047223 | Pride

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

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