ReviewTrends in cell biology2020
Regulation and Consequences of cGAS Activation by Self-DNA.
Review in Trends in cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 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
58 citing papers in PubMed, 87 citations in OpenAlex.
- NRF2 activation attenuates obesity-induced adipose inflammation by suppressing STING signaling, with depot-specific regulation.Journal of translational medicine · 2026Article
- A versatile cGAMP reporter reveals principles of cGAS activation by DNA damage and chromosome instability.Nature cell biology · 2026Article
- Biosensor reveals unexpected variability in the cGAS response to DNA damage.Nature cell biology · 2026Article
- Histone H4 lysine 20 tri-methylation safeguards breast cancer lineage fidelity and unfolded protein response.Nature communications · 2026Article
- Mitochondrial stress-induced cuproptosis: a metabolic bridge to reprogramming the GBM immune microenvironment.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- Crosstalk between autophagy-dependent ferroptosis and PANoptosis in myocardial and cerebral ischemia-reperfusion injury: mechanisms and therapeutic implications.Frontiers in pharmacology · 2026Review
- Mitotic errors as triggers of cell death and inflammation.Nature cell biology · 2026Review
- Advances in Clinical Trials of Boron Neutron Capture Therapy.Research (Washington, D.C.) · 2026Review
- Review
- Divergent Immunomodulatory Roles of Fungal DNA in Shaping Treg and Inflammatory Responses.Journal of fungi (Basel, Switzerland) · 2025Article
- PRRs-Dependent and Independent Mechanisms of STING Signaling in Inflammatory and Autoimmune Diseases.Biomedicines · 2025Review
- A Dual-Targeting T6SS DNase Drives Bacterial Antagonism and Eukaryotic Apoptosis via the cGAS-STING-TNF Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The cGAS-STING axis: a comprehensive review from immune defense to disease pathogenesis.Immunologic research · 2025Review
- Sulfasalazine improves neuronal function in mice with ischemic stroke by inhibiting the STING/NF-κB pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- A20 attenuates oxidized self-DNA-mediated inflammation in acute kidney injury.Signal transduction and targeted therapy · 2025Article
- PCBP2 promotes immune evasion via cGAS-STING pathway in biochemical recurrence of prostate cancer.APL bioengineering · 2025Article
- RNA sensing induced by chromosome missegregation augments anti-tumor immunity.Molecular cell · 2025Article
- Boron neutron capture therapy in the context of tumor heterogeneity: progress, challenges, and future perspectives.Frontiers in oncology · 2025Review
- Mechanisms of fungal pathogenic DNA-activated STING pathway in biofilms and its implication in dental caries onset.Frontiers in cellular and infection microbiology · 2025Review
- Quantitative Live-Cell Imaging to Study Chromatin Segregation and Nuclear Reformation.Methods in molecular biology (Clifton, N.J.) · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cyclic GMP-AMP (cGAMP) synthase (cGAS) is a major responder to the pathogenic DNA of viruses and bacteria. Upon DNA binding, cGAS becomes enzymatically active to generate the second messenger cGAMP, leading to activation of inflammatory genes, type I interferon production, autophagy, and cell death. Following genotoxic stress, cGAS can also respond to endogenous DNA, deriving from mitochondria, endogenous retroelements, and chromosomes to affect cellular signaling, secretion, and cell fate decisions. However, under unperturbed conditions, signaling from self-DNA is largely, but not completely, inhibited. Here we review how endogenous DNA is exposed to cGAS, how signaling is attenuated but activated under pathological conditions, and how low-level signaling under unperturbed conditions might prime antipathogenic responses.
Indexed as
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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.