ArticleScientific reports2021
A cell-free assay implicates a role of sphingomyelin and cholesterol in STING phosphorylation.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 26 citations in OpenAlex.
- Review
- Lactylation: a novel post-translational modification for cGAS-STING pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Article
- STING Innate Immunity Signalling from the Golgi.Sub-cellular biochemistry · 2026Review
- Lipid metabolism: a potential checkpoint for cGAS-STING regulation in colorectal cancer.Frontiers in immunology · 2026Review
- Regulation of STING activation by phosphoinositide and cholesterol.bioRxiv : the preprint server for biology · 2025Article
- Defining STING-sterol interactions with chemoproteomics.RSC chemical biology · 2025Article
- Cell biological insights into human STING variants.Cell structure and function · 2025Review
- A quantitative method to monitor STING degradation with dual-luciferase reporters.Cell structure and function · 2025Article
- Regulation and Function of the cGAS-STING Pathway: Mechanisms, Post-Translational Modifications, and Therapeutic Potential in Immunotherapy.Drug design, development and therapy · 2025Review
- Cholesterol-binding motifs in STING that control endoplasmic reticulum retention mediate anti-tumoral activity of cholesterol-lowering compounds.Nature communications · 2024Article
- Activation of human STING by a molecular glue-like compound.Nature chemical biology · 2024Article
- Applications of cryo-EM in drug development for STING.Current opinion in structural biology · 2024Review
- Single-molecule localization microscopy reveals STING clustering at the trans-Golgi network through palmitoylation-dependent accumulation of cholesterol.Nature communications · 2024Article
- Effector memory T cells induce innate inflammation by triggering DNA damage and a non-canonical STING pathway in dendritic cells.Cell reports · 2023Article
- A non-nucleotide agonist that binds covalently to cysteine residues of STING.Cell structure and function · 2023Article
- 25-hydroxycholesterol: an integrator of antiviral ability and signaling.Frontiers in immunology · 2023Review
- Compartmentalization of casein kinase 1 γ CSNK1G controls the intracellular trafficking of ceramide.iScience · 2022Article
- Specific association of TBK1 with the trans-Golgi network following STING stimulation.Cell structure and function · 2022Article
- Post-Translational Modifications of STING: A Potential Therapeutic Target.Frontiers in immunology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stimulator of interferon genes (STING) is essential for the type I interferon response induced by microbial DNA from virus or self-DNA from mitochondria/nuclei. In response to emergence of such DNAs in the cytosol, STING translocates from the endoplasmic reticulum to the Golgi, and activates TANK-binding kinase 1 (TBK1) at the trans-Golgi network (TGN). Activated TBK1 then phosphorylates STING at Ser365, generating an interferon regulatory factor 3-docking site on STING. How this reaction proceeds specifically at the TGN remains poorly understood. Here we report a cell-free reaction in which endogenous STING is phosphorylated by TBK1. The reaction utilizes microsomal membrane fraction prepared from TBK1-knockout cells and recombinant TBK1. We observed agonist-, TBK1-, "ER-to-Golgi" traffic-, and palmitoylation-dependent phosphorylation of STING at Ser365, mirroring the nature of STING phosphorylation in vivo. Treating the microsomal membrane fraction with sphingomyelinase or methyl-β-cyclodextrin, an agent to extract cholesterol from membranes, suppressed the phosphorylation of STING by TBK1. Given the enrichment of sphingomyelin and cholesterol in the TGN, these results may provide the molecular basis underlying the specific phosphorylation reaction of STING at the TGN.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.