ArticleNucleic acids research2018
A novel transcript isoform of STING that sequesters cGAMP and dominantly inhibits innate nucleic acid sensing.
Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 71 citations in OpenAlex.
- Polyelectrolyte nanoparticles enable intracellular delivery of STING protein fragments for ovarian cancer immunotherapy.Materials today. Bio · 2026Article
- Carriers Multimerize STING Protein Fragments to Activate Type I Interferon Signaling in STING-Deficient Cancer Cells.Molecular pharmaceutics · 2025Article
- RNA processing in innate immunity: regulation by RNA-binding proteins.Trends in biochemical sciences · 2025Review
- STING-ΔN, a novel splice isoform of STING, modulates innate immunity and autophagy in response to DNA virus infection.Cell communication and signaling : CCS · 2025Article
- Centrosome protein TAX1BP2 mediates STING-dependent immune response and potentiates anti-PD-1 efficacy in hepatocellular carcinoma.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- IFI204 in microglia mediates traumatic brain injury-induced mitochondrial dysfunction and pyroptosis via SENP7 interaction.Cell biology and toxicology · 2025Article
- Inflammatory responses revealed through HIV infection of microglia-containing cerebral organoids.Journal of neuroinflammation · 2025Article
- C1orf115 interacts with clathrin adaptors to undergo endocytosis and induces ABCA1 to promote enteric cholesterol efflux.Cellular and molecular life sciences : CMLS · 2025Article
- The role of cGAS-STING signaling in HPV infection and HPV-related cancers.Frontiers in immunology · 2025Review
- Identification of Nonfunctional Alternatively Spliced Isoforms of STING in Human Acute Myeloid Leukemia.Cancer research communications · 2024Article
- The cGAS-STING pathway: a therapeutic target in diabetes and its complications.Burns & trauma · 2024Review
- Immunomodulatory Gene-Splicing Dysregulation in Tumorigenesis: Unmasking the Complexity.Molecules (Basel, Switzerland) · 2023Review
- Virus usurps alternative splicing to clear the decks for infection.Virology journal · 2023Review
- FACI is a novel clathrin adaptor protein 2-binding protein that facilitates low-density lipoprotein endocytosis.Cell & bioscience · 2023Article
- Current understanding of the cGAS-STING signaling pathway: Structure, regulatory mechanisms, and related diseases.Zoological research · 2023Review
- SARS-CoV-2, HIV, and HPV: Convergent evolution of selective regulation of cGAS-STING signaling.Journal of medical virology · 2023Review
- SARS-CoV-2 ORF10 antagonizes STING-dependent interferon activation and autophagy.Journal of medical virology · 2022Article
- African Swine Fever Virus EP364R and C129R Target Cyclic GMP-AMP To Inhibit the cGAS-STING Signaling Pathway.Journal of virology · 2022Article
- SARS-CoV-2 NSP5 and N protein counteract the RIG-I signaling pathway by suppressing the formation of stress granules.Signal transduction and targeted therapy · 2022Article
- An antibody-based proximity labeling map reveals mechanisms of SARS-CoV-2 inhibition of antiviral immunity.Cell chemical biology · 2022Article
Corrections and comments
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Authors and funding
14 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
STING is a core adaptor in innate nucleic acid sensing in mammalian cells, on which different sensing pathways converge to induce type I interferon (IFN) production. Particularly, STING is activated by 2'3'-cGAMP, a cyclic dinucleotide containing mixed phosphodiester linkages and produced by cytoplasmic DNA sensor cGAS. Here, we reported on a novel transcript isoform of STING designated STING-β that dominantly inhibits innate nucleic acid sensing. STING-β without transmembrane domains was widely expressed at low levels in various human tissues and viral induction of STING-β correlated inversely with IFN-β production. The expression of STING-β declined in patients with lupus, in which type I IFNs are commonly overproduced. STING-β suppressed the induction of IFNs, IFN-stimulated genes and other cytokines by various immunostimulatory agents including cyclic dinucleotides, DNA, RNA and viruses, whereas depletion of STING-β showed the opposite effect. STING-β interacted with STING-α and antagonized its antiviral function. STING-β also interacted with TBK1 and prevented it from binding with STING-α, TRIF or other transducers. In addition, STING-β bound to 2'3'-cGAMP and impeded its binding with and activation of STING-α, leading to suppression of IFN-β production. Taken together, STING-β sequesters 2'3'-cGAMP second messenger and other transducer molecules to inhibit innate nucleic acid sensing dominantly.
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