ArticleProceedings of the National Academy of Sciences of the United States of America2020
The
Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled 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.
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
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.
- The cGAS-STING signaling pathway in the regulation of pulmonary infections: a systematic review.Frontiers in cellular and infection microbiology · 2025Pooled it
- Mycobacterial surface-mediated mechanical priming initiates spacious to compact phagosome switching for egress.iScience · 2026Article
- Mycobacterium tuberculosis IDH-PPARγ interaction suppresses GPX4 to drive macrophage ferroptosis and sustain persistent infection.Nature communications · 2026Article
- Article
- Targeting cGAS-STING signaling to overcome antibiotic-resistant bacterial infections: Challenges and opportunities.Science advances · 2026Review
- Host mitochondrial DNA in bacterial pathogenesis: Friend, Foe, or Both?Archives of microbiology · 2026Review
- Macrophage adaptation to hypoxia in the tuberculous granuloma potentiates mycobacterium-induced mitochondrial damage and granuloma necrosis.bioRxiv : the preprint server for biology · 2026Article
- Molecular Mechanisms of cGAS-STING Axis and Mitochondrial Dysfunction-Related Diseases in Humans: A Comprehensive Review.Current neuropharmacology · 2026Review
- Functional analysis of type VII secretion system links to host immune evasion mechanism inFrontiers in cellular and infection microbiology · 2026Review
- Hepatic mitochondrial signaling as a systemic hub: inter-organ communication networks in aging and aging-related diseases.Frontiers in cell and developmental biology · 2026Review
- Review
- Nucleotide-Binding Oligomerization Domain 2 in Signaling, Immunity, and Mycobacterial Infection.Immunity, inflammation and disease · 2025Review
- Review
- Mitochondrial DNA signals driving immune responses: Why, How, Where?Cell communication and signaling : CCS · 2025Review
- Article
- Real-time visualization reveals Mycobacterium tuberculosis ESAT-6 disrupts phagosome-like compartment via fibril-mediated vesiculation.Cell reports · 2025Article
- In vivo regulation of the monocyte phenotype by Mycobacterium marinum and the ESX-1 type VII secretion system.Scientific reports · 2025Article
- Type VII secretion system gene mutations driving global mycobacterium tuberculosis transmission revealed by whole genomic sequence.Frontiers in cellular and infection microbiology · 2025Article
- Cytosolic serpins act in a cytoprotective feedback loop that limits ESX-1-dependent death ofmBio · 2024Article
- PE/PPE Proteome and ESX-5 Substrate Spectrum inInternational journal of molecular sciences · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Following mycobacterial entry into macrophages the ESX-1 type VII secretion system promotes phagosomal permeabilization and type I IFN production, key features of tuberculosis pathogenesis. The current model states that the secreted substrate ESAT-6 is required for membrane permeabilization and that a subsequent passive leakage of extracellular bacterial DNA into the host cell cytosol is sensed by the cyclic GMP-AMP synthase (cGAS) and stimulator of IFN genes (STING) pathway to induce type I IFN production. We employed a collection of
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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.