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Effect of STING-TRIM29 interaction inhibitor SB24011 on gene expression upon solo or co-treatment with STING agonist in Raw264.7 murine macrophage-like cells.

ABSTRACT: SB24011 upregulates cellular STING levels through inhibition of STING-TRIM29 E3 ligase interaction. We performed gene expression profiling using RNA-seq in Raw264.7 cells, to investigate the effect of SB24011 on 1) STING downstream pathways upon combination with cGAMP, or 2) the novel gene expressions upon STING upregulation by SB24011.

ORGANISM(S): Mus musculus

PROVIDER: GSE207257 | GEO | 2025/06/28

REPOSITORIES: GEO

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Effect of STING-TRIM29 interaction inhibitor SB24011 on gene expression upon solo or co-treatment with STING agonist in Raw264.7 murine macrophage-like cells.

Project description:Effect of STING-TRIM29 interaction inhibitor SB24011 on gene expression upon solo or co-treatment with STING agonist in Raw264.7 murine macrophage-like cells.

| PRJNA854386 | ENA

A Phosphotriester-Masked Dideoxy-cGAMP Derivative as a Cell-Permeable STING Agonist

Project description:2’3’-cyclic GMP-AMP (cGAMP) is a cyclic dinucleotide second messenger in which guanosine and adenosine are connected by one 3’-5’ and one 2’-5’ phosphodiester linkage. It is formed in the cytosol upon detection of pathogenic DNA by the enzyme guanosine-monophosphate-adenosine monophosphate synthase (cGAS). cGAMP subsequently binds to the adaptor protein stimulator of interferon genes (STING) to elicit an innate immune response leading to the production of type I interferons and cytokines. STING agonists are a highly promising avenue for an immuno-oncological anticancer therapy. A particular challenge with cyclic dinucleotide STING agonists are the two negative charges of the phosphodiester linkages, which strongly reduce the ability of such compounds to penetrate cell membranes. The development of cell-permeable STING agonists that can stimulate the immune system to enhance their anticancer potency is currently of utmost importance in the field. Here, we report the development of a dideoxy derivative of cGAMP as a phosphotriester prodrug, where the negative charge of the phosphate backbone has been masked with a thioester. We found that this thioester-protected compound features a dramatic increase in its cellular potency that rises from EC50 = 5 µM to 25 nM. The new compound is envisioned to enable an efficient STING-agonist-based anticancer therapy.

2025-05-07 | PXD057395 | Pride

BJ cyto-nuclear translocation upon STING activation

Project description:The goal of this project is to identify changes of cyto-nuclear import upon STING activation by cGAMP. BJ cells stably expressing TurboID-NES were treated with biotin to label cytoplasmic proteins, after which cells were further treated with or without cGAMP to activate STING signaling. Cells were then fractionated to collect the nuclei. The biotinylated proteins in the nuclear pellets were purified by streptavidin beads for mass spectrometry analysis.

2024-09-19 | PXD049018 | Pride

Transcriptome-wide identification of STING agonist programed B cells

Project description:We employed RNA-seq to study the transcriptomic change in B lymphocytes in response to STING agonist. Transcriptomic analysis of wild type and TMEM173–/– B cells stimulated with STING agonist revealed that the inflammatory response pathway enriched in 3'3'-cGAMP treated WT B cells but lacking in Tmem173-/-B cells comprised of a cluster containing inhibitory regulators, provoking STING signal to evade immune surveillance by inducing an immunosuppressive B cell population.

2022-08-10 | GSE199343 | GEO

Human Breast Cells: Control vs. TRIM29 cDNA- or TRIM29 shRNA-transfected

Project description:Transcriptional profiling of human normal-like breast cells MCF10A comparing control MCF10A cells transfected with a pLenti6/BLOCK-iT™-DEST vector with MCF10A cells transfected with a pLenti6/BLOCK-iT™-DEST vector containing TRIM29 shRNA targeting nucleotides 1265–1285 of the TRIM29 open reading frame (ORF, NM_012101). Transcriptional profiling of human breast cancer cells MCF7 comparing control MCF7 cells transfected with a pLenti6.2/N-LumioTM/V5-DEST vector with MCF7 cells transfected with a pLenti6.2/N-LumioTM/V5-DEST vector containing TRIM29 full-length cDNA (ORF, NM_012101). Two-condition experiment, MCF10A-vector control vs. MCF10A-TRIM29 shRNA cells; MCF7-vector control vs. MCF7-TRIM29 cells.

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Gene expression in STING-/- MEF cells expressing STING R284S variant

Project description:STING R284S variant is constitutively active and induces inflammatory genes even in absence of STING ligand cGAMP.

2019-02-27 | GSE111196 | GEO

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

ENPP1 is an innate immune checkpoint of the anticancer cGAMP-STING pathway

Project description:ENPP1 expression correlates with poor prognosis in many cancers, and we previously discovered that ENPP1 is the dominant hydrolase of extracellular cGAMP: a cancer-cell-produced immunotransmitter that activates the anticancer STING pathway. However, ENPP1 has other catalytic activities and the molecular and cellular mechanisms contributing to its tumorigenic effects remain unclear. Here, using single cell RNA-seq (scRNA-seq), we show that ENPP1 overexpression drives primary tumor growth and metastasis by synergistically dampening extracellular cGAMP-STING mediated antitumoral immunity and activating immunosuppressive extracellular adenosine (eADO) signaling. In addition to cancer cells, stromal and immune cells in the tumor microenvironment (TME) also express ENPP1 which functions as a gate keeper to block cGAMP sensing in these cells. Enpp1 knockout in both cancer cells and normal tissues slowed primary tumor growth and prevented metastasis in an extracellular cGAMP- and STING-dependent manner. Lastly, an ENPP1 knock-in mutation that selectively abolishes ENPP1’s cGAMP hydrolysis activity phenocopied total ENPP1 knockout, demonstrating that restoration of paracrine cGAMP-STING signaling is the dominant anti-cancer mechanism of ENPP1 inhibition. In summary, selectively blocking ENPP1’s cGAMP hydrolysis activity is a promising therapeutic approach for treating cancer.

2023-08-07 | GSE233659 | GEO

Human Breast Cells: Control vs. TRIM29 cDNA- or TRIM29 shRNA-transfected

2010-12-23 | GSE26238 | GEO

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

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