ArticleNature cell biology2023
STING signalling is terminated through ESCRT-dependent microautophagy of vesicles originating from recycling endosomes.
Article in Nature cell biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers.
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Who cites it
139 citing papers in PubMed, 177 citations in OpenAlex.
- Neoliensinine promotes lysosomal cell death in T cell malignancies via a novel STING-TUBA1B pathway.Genes & diseases · 2026Article
- The cGAS-STING pathway in inflammaging and neuroinflammation.Science China. Life sciences · 2026Review
- Bone Marrow Macrophage STING Signaling is a Direct Nexus Linking Marrow Adipose Expansion to NADAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeting Macrophage STING O-GlcNAcylation via Small-Molecule Allosteric Modulation for Psoriasis Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Programmed cell death in inflammation: interactions and holistic perspective.Cellular & molecular immunology · 2026Review
- Emerging mechanisms of ATG8-independent non-canonical autophagy.Journal of physiology and biochemistry · 2026Review
- Proteostasis and ageing dissidence.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026Review
- The cGAS-STING/MITA pathway in innate antiviral immunity and beyond.Cell insight · 2026Review
- Mitochondrial Fis1 tunes Rab7A activity via TBC1D15 modulating STING degradation.Cell reports · 2026Article
- Review
- The cGAS-STING Pathway: A Double-Edged Regulator of Neuroinflammation and Myelin Regeneration.Molecular neurobiology · 2026Review
- A versatile cGAMP reporter reveals principles of cGAS activation by DNA damage and chromosome instability.Nature cell biology · 2026Article
- A molecular glue induces aberrant STING oligomerization and inhibits autoinflammatory diseases.Signal transduction and targeted therapy · 2026Article
- Macrophage USP7 aggravates acute myocardial infarction by inhibiting STING degradation through the ESCRT pathway.Cell death and differentiation · 2026Article
- The cGAS/STING pathway in cancer: translating innate DNA sensing into therapeutic potential.The Journal of clinical investigation · 2026Review
- VPS37A loss creates CASP8-dependent vulnerability via the MAP3K7-NF-κB-CFLAR axis.Cancer gene therapy · 2026Article
- Bio-orthogonal Chemistry-Facilitated Zn-Mn Double-Layered Nanobombs Abrogate cGAS-STING Evasion of Tumor Cells.Advanced healthcare materials · 2026Article
- Molecular mechanisms regulating cGAS/STING activation in health and disease.The Journal of clinical investigation · 2026Review
- Cell surface liposome binding (CLiB) allows lipid-binding probe engineering via high-throughput screening.Nature cell biology · 2026Article
- cGAS/STING sensing in dendritic cells discriminates between daptomycin sensitive and resistantiScience · 2026Article
79 more citing papers are in PubMed but not listed here.
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Authors and funding
24 authors at 9 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stimulator of interferon genes (STING) is essential for the type I interferon response against a variety of DNA pathogens. Upon emergence of cytosolic DNA, STING translocates from the endoplasmic reticulum to the Golgi where STING activates the downstream kinase TBK1, then to lysosome through recycling endosomes (REs) for its degradation. Although the molecular machinery of STING activation is extensively studied and defined, the one underlying STING degradation and inactivation has not yet been fully elucidated. Here we show that STING is degraded by the endosomal sorting complexes required for transport (ESCRT)-driven microautophagy. Airyscan super-resolution microscopy and correlative light/electron microscopy suggest that STING-positive vesicles of an RE origin are directly encapsulated into Lamp1-positive compartments. Screening of mammalian Vps genes, the yeast homologues of which regulate Golgi-to-vacuole transport, shows that ESCRT proteins are essential for the STING encapsulation into Lamp1-positive compartments. Knockdown of Tsg101 and Vps4, components of ESCRT, results in the accumulation of STING vesicles in the cytosol, leading to the sustained type I interferon response. Knockdown of Tsg101 in human primary T cells leads to an increase the expression of interferon-stimulated genes. STING undergoes K63-linked ubiquitination at lysine 288 during its transit through the Golgi/REs, and this ubiquitination is required for STING degradation. Our results reveal a molecular mechanism that prevents hyperactivation of innate immune signalling, which operates at REs.
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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.