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MATRIN3 deficiency leads to cGAS-STING activation

ABSTRACT: MATRIN3 deficiency leads to cGAS-STING activation

PROVIDER: PRJNA895450 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR22085273_1.fastq.gz	Fastqsanger.gz
	SRR22085273_2.fastq.gz	Fastqsanger.gz
	SRR22085274_1.fastq.gz	Fastqsanger.gz
	SRR22085274_2.fastq.gz	Fastqsanger.gz

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MATRIN3 deficiency leads to cGAS-STING activation

Project description:MATRIN3 deficiency leads to cGAS-STING activation

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MATRIN3 deficiency leads to cGAS-STING activation (NanoString)

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

| PRJNA895455 | ENA

MATRIN3 deficiency leads to cGAS-STING activation (PAR-CLIP)

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

| PRJNA895456 | ENA

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

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

| PRJNA895453 | ENA

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

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

| PRJNA895454 | ENA

The gene expression profiling in the brain of cGAS or STING deficiency mice

Project description:Mounting evidence indicates that the cGAS-STING pathway represents the major DNA sensing pathway to invoke immune and inflammatory responses in neuroinflammatory disorders. Here, we examinedgene expression profiling in the brain of cGAS and STING deficiency mice

2025-10-13 | GSE236108 | GEO

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

DNA-Protein Crosslinks Promote cGAS-STING-driven Premature Aging and Embryonic Lethality

Project description:DNA-protein crosslinks (DPCs) are severe DNA lesions that disrupt replication, transcription, and genome stability. However, their role in development and aging remains poorly understood. Here, we show that impaired SPRTN function, a metalloprotease essential for DPC repair during replication and mitosis, leads to DNA damage, mitotic abnormalities, and activation of the immune system. Notably, micronuclei formed upon SPRTN deficiency frequently contain DPCs, exhibit nuclear envelope rupture, and accumulate unrepaired DNA, thereby facilitating activation of the cGAS-STING pathway. Using a Sprtn knock-in mouse model of Ruijs Aalfs progeria syndrome, we demonstrate that chronic cGas-Sting activation drives inflammation, innate immune responses, and embryonic lethality. Surviving mice display a continuum of aging phenotypes from embryogenesis into adulthood. Genetic or pharmacological inhibition of cGas-Sting rescues embryonic viability and ameliorates progeroid features, linking DPC-induced innate immune activation to lifespan defects. Our findings uncover a previously unrecognized role for DPCs in coupling early developmental failure to premature aging.

2025-09-30 | PXD067620 | Pride

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