ArticleNature communications2023
Transcription tuned by S-nitrosylation underlies a mechanism for Staphylococcus aureus to circumvent vancomycin killing.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 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
14 citing papers in PubMed, 30 citations in OpenAlex.
- Mechanistic evaluation of pachymic acid in breast cancer via network pharmacology and in vitro validation.BMC complementary medicine and therapies · 2026Article
- Staphylococcal accessory regulator SarA-mediated modulation of autolysis and surface charge enablesmSystems · 2026Article
- Sustained nitric oxide production by engineered E. coli remodels the tumor microenvironment and potentiates immunotherapy.Nature biotechnology · 2026Article
- Expression patterns of core metabolic genes and elevated intracellular ROS confer drug tolerance inMicrobiology spectrum · 2026Article
- Evaluation of Nisin and Cultured Dextrose as Clean Label Preservatives in Braised Chicken Breast: Antibacterial Activity and Quality Preservation.Foods (Basel, Switzerland) · 2026Article
- Lipopeptide Engineering: From Natural Origins to Rational Design Against Antimicrobial Resistance.Antibiotics (Basel, Switzerland) · 2026Review
- The role of nitric oxide synthase in biofilm formation by Staphylococcus aureus.NPJ biofilms and microbiomes · 2025Article
- The toxin-antitoxin system SavRS contributes to vancomycin resistance in vancomycin-intermediate Staphylococcus aureus by mediating cell wall thickening.The Journal of antimicrobial chemotherapy · 2025Article
- Endogenous nitric oxide promotesmBio · 2025Article
- S-Nitrosylation of NOTCH1 Regulates Mesenchymal Stem Cells Differentiation Into Hepatocyte-Like Cells by Inhibiting Notch Signalling Pathway.Journal of cellular and molecular medicine · 2024Article
- Potential Beneficial Role of Nitric Oxide in SARS-CoV-2 Infection: Beyond Spike-Binding Inhibition.Antioxidants (Basel, Switzerland) · 2024Article
- Alkaline shock protein 23 (Asp23)-controlled cell wall imbalance promotes membrane vesicle biogenesis in Staphylococcus aureus.Journal of extracellular vesicles · 2024Article
- Metal natural product complex Ru-procyanidins with quadruple enzymatic activity combat infections from drug-resistant bacteria.Acta pharmaceutica Sinica. B · 2024Article
- Factors impacting the regulation ofMicrobiology spectrum · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Treatment of Staphylococcus aureus infections is a constant challenge due to emerging resistance to vancomycin, a last-resort drug. S-nitrosylation, the covalent attachment of a nitric oxide (NO) group to a cysteine thiol, mediates redox-based signaling for eukaryotic cellular functions. However, its role in bacteria is largely unknown. Here, proteomic analysis revealed that S-nitrosylation is a prominent growth feature of vancomycin-intermediate S. aureus. Deletion of NO synthase (NOS) or removal of S-nitrosylation from the redox-sensitive regulator MgrA or WalR resulted in thinner cell walls and increased vancomycin susceptibility, which was due to attenuated promoter binding and released repression of genes involved in cell wall metabolism. These genes failed to respond to H
Indexed as
Identifiers
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.