ArticleCell structure and function2022
Specific association of TBK1 with the trans-Golgi network following STING stimulation.
Article in Cell structure and function, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Mitochondrial Fis1 tunes Rab7A activity via TBC1D15 modulating STING degradation.Cell reports · 2026Article
- Review
- Mechanistic insights and therapeutic potential of targeting the cGAS-STING pathway in neurodegenerative diseases.Journal of neuroinflammation · 2026Review
- Dual roles of TRPV2 in the innate immune response to cytosolic DNA: Arresting dormant and boosting activated STING.Cell reports · 2026Article
- STING Innate Immunity Signalling from the Golgi.Sub-cellular biochemistry · 2026Review
- Molecular Mechanisms of cGAS-STING Axis and Mitochondrial Dysfunction-Related Diseases in Humans: A Comprehensive Review.Current neuropharmacology · 2026Review
- Microautophagy: current understanding of its molecular mechanisms and functions.Autophagy reports · 2026Review
- 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
- The activation of the adaptor protein STING depends on its interactions with the phospholipid PI4P.Science signaling · 2024Article
- Single-molecule localization microscopy reveals STING clustering at the trans-Golgi network through palmitoylation-dependent accumulation of cholesterol.Nature communications · 2024Article
- STING signalling is terminated through ESCRT-dependent microautophagy of vesicles originating from recycling endosomes.Nature cell biology · 2023Article
- A non-nucleotide agonist that binds covalently to cysteine residues of STING.Cell structure and function · 2023Article
- The activity of disease-causative STING variants can be suppressed by wild-type STING through heterocomplex formation.Frontiers in cell and developmental biology · 2022Article
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Authors and funding
4 authors at 1 institution 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 or self-DNA leaked from mitochondria/nuclei. In response to the emergence of such DNAs in the cytosol, STING relocates from the endoplasmic reticulum (ER) to the Golgi, and activates TANK-binding kinase 1 (TBK1), a cytosolic kinase essential for the activation of STING-dependent downstream signalling. To understand at which subcellular compartments TBK1 becomes associated with STING, we generated cells stably expressing fluorescent protein-tagged STING (mNeonGreen-STING) and TBK1 (TBK1-mScarletI). We found that after STING stimulation, TBK1 became associated with the trans-Golgi network (TGN), not the other parts of the Golgi. STING variants that constitutively induce the type I interferon response have been identified in patients with autoinflammatory diseases named "STING-associated vasculopathy with onset in infancy (SAVI)". Even in cells expressing these constitutively active STING variants, TBK1 was found to be associated with TGN, not the other parts of the Golgi. These results suggest that TGN acts as a specific platform where STING associates with and activates TBK1.Key words: the Golgi, membrane traffic, innate immunity, STING.
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