ArticleInfection and immunity2013
Small-molecule inhibitor of the Shigella flexneri master virulence regulator VirF.
Article in Infection and immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 66 citations in OpenAlex.
- Enhanced virulence and stress tolerance are signatures of epidemiologically successful Shigella sonnei.Nature communications · 2025Article
- Dillapiole Dampens the Expression of the Major Virulence Genes ofMolecules (Basel, Switzerland) · 2025Article
- Article
- Targeting bacterial transcription factors for infection control: opportunities and challenges.Transcription · 2025Review
- Novel inhibitors that target bacterial virulence identified via HTS against intra-macrophage survival ofmSphere · 2023Article
- Fatty Acids AbolishMicrobiology spectrum · 2023Article
- Elucidation of the DNA-Binding Activity of VirF from Shigella flexneri for theJournal of bacteriology · 2023Article
- Elucidation of Key Interactions between VirF and theJournal of bacteriology · 2022Article
- Virulence genes expression profiling of different Shigella flexneri serotypes in response to sub-inhibitory concentrations of azithromycin and ciprofloxacin.Gut pathogens · 2022Article
- Identification of Translocation Inhibitors Targeting the Type III Secretion System of Enteropathogenic Escherichia coli.Antimicrobial agents and chemotherapy · 2021Article
- Review
- Secretory System Components as Potential Prophylactic Targets for Bacterial Pathogens.Biomolecules · 2021Review
- On the road to structure-based development of anti-virulence therapeutics targeting the type III secretion system injectisome.MedChemComm · 2019Review
- Zika virus outbreak: a review of neurological complications, diagnosis, and treatment options.Journal of neurovirology · 2018Review
- Review
- Pharmacological Targeting of the Host-Pathogen Interaction: Alternatives to Classical Antibiotics to Combat Drug-Resistant Superbugs.Trends in pharmacological sciences · 2017Review
- Control of Virulence Gene Expression by the Master Regulator, CfaD, in the Prototypical EnterotoxigenicFrontiers in microbiology · 2017Article
- VirF Relieves the Transcriptional Attenuation of the Virulence GeneFrontiers in microbiology · 2017Article
- Ribavirin suppresses bacterial virulence by targeting LysR-type transcriptional regulators.Scientific reports · 2016Article
- Role of Escherichia coli in Biofuel Production.Microbiology insights · 2016Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
VirF is an AraC family transcriptional activator that is required for the expression of virulence genes associated with invasion and cell-to-cell spread by Shigella flexneri, including multiple components of the type three secretion system (T3SS) machinery and effectors. We tested a small-molecule compound, SE-1 (formerly designated OSSL_051168), which we had identified as an effective inhibitor of the AraC family proteins RhaS and RhaR, for its ability to inhibit VirF. Cell-based reporter gene assays with Escherichia coli and Shigella, as well as in vitro DNA binding assays with purified VirF, demonstrated that SE-1 inhibited DNA binding and transcription activation (likely by blocking DNA binding) by VirF. Analysis of mRNA levels using real-time quantitative reverse transcription-PCR (qRT-PCR) further demonstrated that SE-1 reduced the expression of the VirF-dependent virulence genes icsA, virB, icsB, and ipaB in Shigella. We also performed eukaryotic cell invasion assays and found that SE-1 reduced invasion by Shigella. The effect of SE-1 on invasion required preincubation of Shigella with SE-1, in agreement with the hypothesis that SE-1 inhibited the expression of VirF-activated genes required for the formation of the T3SS apparatus and invasion. We found that the same concentrations of SE-1 had no detectable effects on the growth or metabolism of the bacterial cells or the eukaryotic host cells, respectively, indicating that the inhibition of invasion was not due to general toxicity. Overall, SE-1 appears to inhibit transcription activation by VirF, exhibits selectivity toward AraC family proteins, and has the potential to be developed into a novel antibacterial agent.
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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.