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

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

ORGANISM(S): Mus musculus

PROVIDER: GSE216897 | GEO | 2023/03/17

REPOSITORIES: GEO

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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

RNA-seq of parental MC38 and anti-PD-1 resistant MC38 subcutaneous tumors

Project description:MC38 tumors resistant to anti-PD-1 treatment (MC38-resistant) were generated through serial in vivo passaging, and global gene expression analysis was used to compare resistant and parental tumors. MC38 and MC38-resistant tumors exhibited widespread changes in global gene expression.

2021-07-22 | GSE180309 | GEO

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

Project description: Not available

| S-EPMC4366210 | biostudies-literature

RNA-seq of parental MC38 and anti-PD-1 resistant MC38 subcutaneous tumors

Project description:RNA-seq of parental MC38 and anti-PD-1 resistant MC38 subcutaneous tumors

| PRJNA747799 | ENA

Cyclic-Di-Nucleotides Trigger ULK1 (ATG1) Phosphorylation of STING to Prevent Sustained Innate Immune Signaling

Project description:Activation of the STING (Stimulator of Interferon Genes) pathway by microbial or self-DNA, as well as cyclic di nucleotides (CDN), results in the induction of numerous genes that suppress pathogen replication and facilitate adaptive immunity. However, sustained gene transcription is rigidly prevented to avoid lethal STING-dependent pro-inflammatory disease by mechanisms that remain unknown. We demonstrate here that after autophagy-dependent STING delivery of TBK1 (TANK-binding kinase 1) to endosomal/lysosomal compartments and activation of transcription factors IRF3 (interferon regulatory factors 3) and NF-κB (nuclear factor kappa beta), that STING is subsequently phosphorylated by serine/threonine UNC-51-like kinase (ULK1/ATG1) and IRF3 function is suppressed. ULK1 activation occurred following disassociation from its repressor adenine monophosphate activated protein kinase (AMPK), and was elicited by CDN’S generated by the cGAMP synthase, cGAS. Thus, while CDN’s may initially facilitate STING function, they subsequently trigger negative-feedback control of STING activity, thus preventing the persistent transcription of innate immune genes. Total RNA obtained from primary STING deficient mouse embryonic fibroblast reconstituted with mSTING (W), S365A variant (A), or S365D variant (D). These cells were transfected with dsDNA (ISD) for 3 hours.

2013-10-10 | E-GEOD-51199 | biostudies-arrayexpress

RNA-seq of untreated- or STING inhibitor treated control and ZNFKD iN.

Project description:hiPSC were treated or not with STING inhibitor, transduced with KD or control lentivectors and differentiated in induced neurons.

2020-02-18 | GSE145405 | GEO

Immunopeptidome on MC38 Cell line

Project description:PTM – driven antigenicity – immunopeptidome of MC38 cell line

2022-10-12 | PXD017448 | Pride

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

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

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