Evidence map›Paper›PMID 32424334›Full record

ReviewNature reviews. Molecular cell biology2020

Molecular mechanisms and cellular functions of cGAS-STING signalling.

Karl-Peter Hopfner, Veit Hornung

Open access · greenAbstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Molecular cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1,162 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1,162citing papers in PubMed, 1 pooled it
66.0field-weighted citation impact, top 1% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

1,162 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,829 citations in OpenAlex.

  1. Mucosal immunity and vaccine development.Signal transduction and targeted therapy · 2026
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  16. Chlorogenic acid attenuates TBI-induced neuroinflammation by suppressing cGAS-STING signaling.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
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1,102 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Karl-Peter HopfnerDepartment of Biochemistry, Ludwig-Maximilians-Universität, Munich, Germany. hopfner@genzentrum.lmu.de.ORCID http://orcid.org/0000-0002-4528-8357
Veit HornungDepartment of Biochemistry, Ludwig-Maximilians-Universität, Munich, Germany. hornung@genzentrum.lmu.de.ORCID http://orcid.org/0000-0002-4150-194X
Ludwig-Maximilians-Universität München · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cGAS-STING signalling axis, comprising the synthase for the second messenger cyclic GMP-AMP (cGAS) and the cyclic GMP-AMP receptor stimulator of interferon genes (STING), detects pathogenic DNA to trigger an innate immune reaction involving a strong type I interferon response against microbial infections. Notably however, besides sensing microbial DNA, the DNA sensor cGAS can also be activated by endogenous DNA, including extranuclear chromatin resulting from genotoxic stress and DNA released from mitochondria, placing cGAS-STING as an important axis in autoimmunity, sterile inflammatory responses and cellular senescence. Initial models assumed that co-localization of cGAS and DNA in the cytosol defines the specificity of the pathway for non-self, but recent work revealed that cGAS is also present in the nucleus and at the plasma membrane, and such subcellular compartmentalization was linked to signalling specificity of cGAS. Further confounding the simple view of cGAS-STING signalling as a response mechanism to infectious agents, both cGAS and STING were shown to have additional functions, independent of interferon response. These involve non-catalytic roles of cGAS in regulating DNA repair and signalling via STING to NF-κB and MAPK as well as STING-mediated induction of autophagy and lysosome-dependent cell death. We have also learnt that cGAS dimers can multimerize and undergo liquid-liquid phase separation to form biomolecular condensates that could importantly regulate cGAS activation. Here, we review the molecular mechanisms and cellular functions underlying cGAS-STING activation and signalling, particularly highlighting the newly emerging diversity of this signalling pathway and discussing how the specificity towards normal, damage-induced and infection-associated DNA could be achieved.

Indexed as

AnimalsAutophagyCyclic AMPCyclic GMPCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseCytosolDNAHumansInterferon Type IMembrane ProteinsNucleotides, CyclicNucleotidyltransferasesSignal TransductionSTING ProteincGAS protein, humanCyclic AMPCyclic GMPcyclic guanosine monophosphate-adenosine monophosphateCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDNAInterferon Type IMembrane ProteinsNucleotides, CyclicNucleotidyltransferasesSTING1 protein, humanSTING Protein

Identifiers

PMID32424334
OpenAlexW3024191006

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.