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SESN1 alleviates autoimmunity by potentiating STING autophagic degradation

ABSTRACT: SESN1 alleviates autoimmunity by potentiating STING autophagic degradation

PROVIDER: PRJNA1107113 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28870521_1.fastq.gz	Fastqsanger.gz
	SRR28870521_2.fastq.gz	Fastqsanger.gz
	SRR28870522_1.fastq.gz	Fastqsanger.gz
	SRR28870522_2.fastq.gz	Fastqsanger.gz
	SRR28870523_1.fastq.gz	Fastqsanger.gz

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SESN1 alleviates autoimmunity by potentiating STING autophagic degradation

Project description:STING, the pivotal adaptor protein of CGAS-STING signaling, is critical for type I IFN production of innate immunity. However, excessive or prolonged activation of STING is associated with autoinflammatory and autoimmune diseases. Thus, preventing STING from over-activation is important to maintain immune homeostasis. Here, we reported that SESN1 was essential to prevent the excessive activation of STING-mediated type I IFN signaling through autophagic degradation of STING.

2025-05-29 | GSE266409 | GEO

CK1α suppresses autoimmunity by restraining the cGAS-STING signaling

Project description:Stimulator of interferon genes (STING), the central hub protein of the cGAS-STING signaling, is essential for type I IFN production of innate immunity. However, prolonged or excessive activation of STING is highly related to autoimmune diseases, most of which exhibit the hallmark of elevated expression of type I interferons and IFN-stimulated genes (ISGs). Thus, the activity of STING must be stringently controlled to maintain immune homeostasis. Here, we reported that CK1α, a protein serine/threonine kinase, was essential to prevent the over-activation of STING-mediated type I IFN signaling through autophagic degradation of STING. Mechanistically, CK1α interacted with STING upon the cGAS-STING pathway activation and promoted STING autophagic degradation by enhancing the phosphorylation of p62 at serine 349, which was critical for p62 mediated STING autophagic degradation. Consistently, SSTC3, a selective CK1α agonist, significantly attenuated the response of the cGAS-STING signaling by promoting STING autophagic degradation. Importantly, pharmaceutical activation of CK1α using SSTC3 markedly repressed the systemic autoinflammatory responses in the Trex1-/- mouse autoimmune disease model and effectively suppressed the production of IFNs and ISGs in the PBMCs of SLE patients. Taken together, our study reveals a novel regulatory role of CK1α in the autophagic degradation of STING to maintain immune homeostasis. Manipulating CK1α through SSTC3 might be a potential therapeutic strategy for alleviating STING-mediated aberrant type I IFNs in autoimmune diseases.

2024-01-31 | GSE226593 | GEO

CK1α suppresses autoimmunity by restraining the cGAS-STING signaling

Project description:CK1α suppresses autoimmunity by restraining the cGAS-STING signaling

| PRJNA940749 | ENA

STING aggravates ferroptosis-dependent myocardial ischemia-reperfusion injury by targeting GPX4 for autophagic degradation

Project description:STING aggravates ferroptosis-dependent myocardial ischemia-reperfusion injury by targeting GPX4 for autophagic degradation

| PRJNA1233788 | ENA

ESCRT-dependent STING degradation curtails steady-state and cGAMP-induced signaling

Project description:STING is an intracellular sensor of cyclic di-nucleotides involved in response to pathogen- or self-derived DNA that induces protective immunity, or if dysregulated, autoimmunity. STING trafficking is tightly linked to its activity. We aimed to systematically characterize genes regulating STING trafficking and to define their impact on STING responses. Based on proximity-ligation proteomics and genetic screens, an ESCRT complex containing HGS, VPS37A and UBAP1 was found to be required for STING degradation and signaling shutdown. Oligomerization-driven STING ubiquitination by UBE2N formed a platform for ESCRT recruitment at the endosome, responsible for STING signaling shutdown. A UBAP1 mutant that underlies human spastic paraplegia and disrupts ESCRT function led to STING-dependent type I IFN responses at the steady-state, defining ESCRT as a homeostatic regulator of STING signaling.

2022-12-14 | MSV000090900 | MassIVE

STING aggravates ferroptosis-dependent myocardial ischemia-reperfusion injury by targeting GPX4 for autophagic degradation

Project description:To investigate the potential signal pathways affected by the deletion of the Sting gene in mice during ischemia-reperfusion (IR), we extracted the myocardial tissues of mice 24 hours after ischemia-reperfusion. Subsequently, we conducted gene expression profiling analysis using the data obtained from RNA-seq of STING-CKO mice and their control counterparts.

2025-04-10 | GSE291453 | GEO

Characterization of a Novel Compound that Stimulates STING-Mediated Innate Immune Activity in an Allele-Specific Manner

Project description:A small molecule termed M04 behaves as a novel agonist of human STING. Importantly, we find that the molecule exhibits a differential ability to activate STING based on the allelic variant examined. Furthermore, while M04 is inactive in mice, expression of human STING in mouse cells rescues reactivity to the compound. Using primary human cells in ex vivo assays we were also able to show that M04 is capable of simulating innate responses important for adaptive immune activation such as cytokine secretion, dendritic cell maturation, and T cell cross-priming. Collectively, this work demonstrates the conceivable utility of a novel agonist of human STING both as a research tool for exploring STING biology and as an immune potentiating molecule.

2020-06-11 | GSE152179 | GEO

The cGAS/STING pathway suppresses TLR-dependent systemic autoimmunity in TMPD-mediated SLE

Project description:The cGAS/STING pathway suppresses TLR-dependent systemic autoimmunity in TMPD-mediated SLE

| PRJNA717269 | ENA

STING mediates immune responses in a unicellular choanoflagellate

Project description:To reconstruct the ancestry of animal innate immunity, we have developed the choanoflagellate Monosiga brevicollis, one of the closest living relatives of animals, as a model for studying mechanisms underlying pathogen recognition and immune response. We found that M. brevicollis is killed by exposure to Pseudomonas aeruginosa bacteria and selectively avoids ingesting them. Moreover, M. brevicollis expresses STING, which, in animals, activates innate immune pathways in response to cyclic dinucleotides during pathogen sensing. M. brevicollis STING increases the susceptibility of M. brevicollis to P. aeruginosa-induced cell death and is required for responding to the cyclic dinucleotide 2’3’ cGAMP. Furthermore, similar to animals, autophagic signaling in M. brevicollis is induced by 2’3’ cGAMP in a STING-dependent manner.

2021-05-13 | GSE174340 | GEO

Inflammation-Driven Carcinogenesis is Mediated through STING [MEFs]

Project description:Chronic stimulation of innate immune pathways by microbial agents or damaged tissue is known to promote inflammation-driven tumorigenesis by unclarified mechanisms1-3. Here we demonstrate that mutagenic 7,12-dimethylbenz(a)anthracene (DMBA), etoposide or cisplatin induces nuclear DNA leakage into the cytosol to intrinsically activate STING (Stimulator of Interferon Genes) dependent cytokine production. Inflammatory cytokine levels were subsequently augmented in a STING-dependent extrinsic manner by infiltrating phagocytes purging dying cells. Consequently, STING-/- mice, or wild type mice adoptively transferred with STING-/- bone marrow, were almost completely resistant to DMBA-induced skin carcinogenesis compared to their wild type counterparts. Our data emphasizes, for the first time, a role for STING in the induction of cancer, sheds significant insight into the causes of inflammation-driven carcinogenesis, and may provide therapeutic strategies to help prevent malignant disease Total RNA obtained from wild type murine embryonic fibroblasts (WT MEFs), STING deficient MEFs (SKO), Trex1 deficient MEFs (TKO), and both STING and Trex1 deficient MEFs (STKO) treated with DMBA and examined cytokine production by these cells.

2014-05-31 | E-GEOD-57603 | biostudies-arrayexpress

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