ArticleProceedings of the National Academy of Sciences of the United States of America2023
STAT2 hinders STING intracellular trafficking and reshapes its activation in response to DNA damage.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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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.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Article
- Mpox virus poxin-schlafen fusion protein suppresses innate antiviral response by sequestering STAT2.Emerging microbes & infections · 2025Article
- STING: a multifaced player in cellular homeostasis.Human molecular genetics · 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
- Article
- Suppressors of cGAS-STING are downregulated during fin-limb regeneration and aging in aquatic vertebrates.Journal of experimental zoology. Part B, Molecular and developmental evolution · 2024Article
- Carbon Ion Irradiation Activates Anti-Cancer Immunity.International journal of molecular sciences · 2024Review
- Interferon induction by STING requires its translocation to the late endosomes.Traffic (Copenhagen, Denmark) · 2023Article
- Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
In cancer cells, endogenous or therapy-induced DNA damage leads to the abnormal presence of DNA in the cytoplasm, which triggers the activation of cGAS (cyclic GMP-AMP synthase) and STING (stimulator of interferon genes). STAT2 suppresses the cGAMP-induced expression of IRF3-dependent genes by binding to STING, blocking its intracellular trafficking, which is essential for the full response to STING activation. STAT2 reshapes STING signaling by inhibiting the induction of IRF3-dependent, but not NF-κB-dependent genes. This noncanonical activity of STAT2 is regulated independently of its tyrosine phosphorylation but does depend on the phosphorylation of threonine 404, which promotes the formation of a STAT2:STING complex that keeps STING bound to the endoplasmic reticulum (ER) and increases resistance to DNA damage. We conclude that STAT2 is a key negative intracellular regulator of STING, a function that is quite distinct from its function as a transcription factor.
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Registered trials
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