ArticleNature chemical biology2017
Inhibition of innate immune cytosolic surveillance by an M. tuberculosis phosphodiesterase.
Article in Nature chemical biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 2 of them syntheses that pooled it.
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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.
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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
65 citing papers in PubMed, 2 syntheses or guidelines pooled it, 111 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
- Meta-Analysis of Peripheral Blood Transcriptome Datasets Reveals a Biomarker Panel for Tuberculosis in Patients Infected With HIV.Frontiers in cellular and infection microbiology · 2021Pooled it
- Structural and biochemical insights into the inhibition ofRSC chemical biology · 2026Article
- Targeting cGAS-STING signaling to overcome antibiotic-resistant bacterial infections: Challenges and opportunities.Science advances · 2026Review
- Characterization of a novel cell wall-associated nucleotidase of Enterococcus faecalis that degrades extracellular c-di-AMP.PLoS pathogens · 2026Article
- The c-di-AMP binding protein NadD from Mesomycoplasma ovipneumoniae functions as a phosphodiesterase that inhibits host inflammatory responses.Veterinary research · 2026Article
- Exploring the evolutionary divergence of cyclic di-nucleotide signaling in diverse mycobacterial species.Archives of microbiology · 2026Article
- Functional analyses of bacterial NanoRNase B proteins reveals defining features of this enzyme family.Nucleic acids research · 2025Article
- Cyclic Di-AMP Affects Cell Membrane Integrity of Streptococcus pneumoniae.Molecular microbiology · 2025Article
- Discovery of natural CdnP inhibitors through structure-based virtual screening and molecular dynamics simulations.Microbiology spectrum · 2025Article
- Phagosomal RNA sensing through TLR8 controls susceptibility to tuberculosis.Cell reports · 2025Article
- Review
- A bovine pulmosphere model and multiomics reveal early host response signature in tuberculosis.Communications biology · 2025Article
- Structural dynamics-guided engineering of a riboswitch RNA for evolving c-di-AMP synthases.Science advances · 2025Article
- TowardMicroorganisms · 2024Review
- ER-transiting bacterial toxins amplify STING innate immune responses and elicit ER stress.Infection and immunity · 2024Article
- Comparison of the transcriptome, lipidome, and c-di-GMP production between BCGΔBCG1419c and BCG, with Mincle- and Myd88-dependent induction of proinflammatory cytokines in murine macrophages.Scientific reports · 2024Article
- The substrate-binding domains of the osmoregulatory ABC importer OpuA transiently interact.eLife · 2024Article
- The activation of the adaptor protein STING depends on its interactions with the phospholipid PI4P.Science signaling · 2024Article
- Structure-based virtual screening andMicrobiology spectrum · 2024Article
5 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
Mycobacterium tuberculosis infection leads to cytosolic release of the bacterial cyclic dinucleotide (CDN) c-di-AMP and a host-generated CDN, cGAMP, both of which trigger type I interferon (IFN) expression in a STING-dependent manner. Here we report that M. tuberculosis has developed a mechanism to inhibit STING activation and the type I IFN response via the bacterial phosphodiesterase (PDE) CdnP, which mediates hydrolysis of both bacterial-derived c-di-AMP and host-derived cGAMP. Mutation of cdnP attenuates M. tuberculosis virulence, as does loss of a host CDN PDE known as ENPP1. CdnP is inhibited by both US Food and Drug Administration (FDA)-approved PDE inhibitors and nonhydrolyzable dinucleotide mimetics specifically designed to target the enzyme. These findings reveal a crucial role of CDN homeostasis in governing the outcome of M. tuberculosis infection as well as a unique mechanism of subversion of the host's cytosolic surveillance pathway (CSP) by a bacterial PDE that may serve as an attractive antimicrobial target.
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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.