ArticleNature communications2024
S-nitrosothiol homeostasis maintained by ADH5 facilitates STING-dependent host defense against pathogens.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- The Multi-Omics Landscape of Enzymatic Alterations in Systemic Lupus Erythematosus.Proteomics. Clinical applications · 2026Article
- Characterization, expression and evolution analysis of NLRC3, NLRC5 and NLRX1 in Mastacembelus armatus under Aeromonas veronii infection.Journal of fish biology · 2026Article
- An Engineered Solidified Peptide Hemocyte Sponge as Nanomotor Storage to Combat Bacterial Colitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- STING: a multifaced player in cellular homeostasis.Human molecular genetics · 2025Review
- STING inhibits the progression of esophageal squamous cell carcinoma by suppressing CPT1A-mediated fatty acid β-oxidation.Acta pharmacologica Sinica · 2025Article
- Bionic Microneedle Patch Inspired by Drosophila Tarsal Paws Boosts Healing in Bacterial Infectious Stomatitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- An updated review of HSV-1 infection-associated diseases and treatment, vaccine development, and vector therapy application.Virulence · 2024Review
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative (or respiratory) burst confers host defense against pathogens by generating reactive species, including reactive nitrogen species (RNS). The microbial infection-induced excessive RNS damages many biological molecules via S-nitrosothiol (SNO) accumulation. However, the mechanism by which the host enables innate immunity activation during oxidative burst remains largely unknown. Here, we demonstrate that S-nitrosoglutathione (GSNO), the main endogenous SNO, attenuates innate immune responses against herpes simplex virus-1 (HSV-1) and Listeria monocytogenes infections. Mechanistically, GSNO induces the S-nitrosylation of stimulator of interferon genes (STING) at Cys257, inhibiting its binding to the second messenger cyclic guanosine monophosphate-adenosine monophosphate (cGAMP). Alcohol dehydrogenase 5 (ADH5), the key enzyme that metabolizes GSNO to decrease cellular SNOs, facilitates STING activation by inhibiting S-nitrosylation. Concordantly, Adh5 deficiency show defective STING-dependent immune responses upon microbial challenge and facilitates viral replication. Thus, cellular oxidative burst-induced RNS attenuates the STING-mediated innate immune responses to microbial infection, while ADH5 licenses STING activation by maintaining cellular SNO homeostasis.
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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 Socratic graph.