ArticleInfection and immunity2007
Pseudolipasin A is a specific inhibitor for phospholipase A2 activity of Pseudomonas aeruginosa cytotoxin ExoU.
Article in Infection and immunity, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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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
45 citing papers in PubMed, 74 citations in OpenAlex.
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- Molecular Mechanisms Underlying the Pathogenicity ofMedicina (Kaunas, Lithuania) · 2026Review
- Infection-driven proliferative phase impairment in chronic wounds: a mechanistic framework for precision regenerative therapy.Frontiers in immunology · 2026Review
- Beyond pathogenicity: applications of the type III secretion system (T3SS) ofFrontiers in microbiology · 2025Review
- Unravelling bacterial virulence factors in yeast: From identification to the elucidation of their mechanisms of action.Archives of microbiology · 2024Review
- Review
- Research Progress on Small Molecular Inhibitors of the Type 3 Secretion System.Molecules (Basel, Switzerland) · 2022Review
- The Pseudomonas aeruginosa Type III Secretion System Exoenzyme Effector ExoU Induces Mitochondrial Damage in a Murine Bone Marrow-Derived Macrophage Infection Model.Infection and immunity · 2022Article
- ExoU Induces Lung Endothelial Cell Damage and Activates Pro-Inflammatory Caspase-1 duringToxins · 2022Article
- Epidemiology, Molecular Characteristics, and Virulence Factors of Carbapenem-ResistantInfection and drug resistance · 2022Article
- Using Structure-guided Fragment-Based Drug Discovery to TargetFrontiers in molecular biosciences · 2022Review
- Perspectives on theToxins · 2021Review
- Review
- Baicalin Represses Type Three Secretion System ofMolecules (Basel, Switzerland) · 2021Article
- Molecular Targets and Strategies for Inhibition of the Bacterial Type III Secretion System (T3SS); Inhibitors Directly Binding to T3SS Components.Biomolecules · 2021Review
- A pipeline to evaluate inhibitors of the Pseudomonas aeruginosa exotoxin U.The Biochemical journal · 2021Article
- Alternative Therapeutic Interventions: Antimicrobial Peptides and Small Molecules to Treat Microbial Keratitis.Frontiers in chemistry · 2021Review
- Prevalence of ExoY Activity inFrontiers in microbiology · 2021Article
- Virulence-Inhibiting Herbal Compound Falcarindiol Significantly Reduced Mortality in Mice Infected withAntibiotics (Basel, Switzerland) · 2020Article
- Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
A number of bacterial pathogens utilize the type III secretion pathway to deliver effector proteins directly into the host cell cytoplasm. Certain strains of Pseudomonas aeruginosa associated with acute infections express a potent cytotoxin, exoenzyme U (ExoU), that is delivered via the type III secretion pathway directly into contacting host cells. Once inside the mammalian cell, ExoU rapidly lyses the intoxicated cells via its phospholipase A(2) (PLA(2)) activity. A high-throughput cell-based assay was developed to screen libraries of compounds for those capable of protecting cells against the cytotoxic effects of ExoU. A number of compounds were identified in this screen, including one group that blocks the intracellular activity of ExoU. In addition, these compounds specifically inhibited the PLA(2) activity of ExoU in vitro, whereas eukaryotic secreted PLA(2) and cytosolic PLA(2) were not inhibited. This novel inhibitor of ExoU-specific PLA(2) activity, named pseudolipasin A, may provide a new lead for virulence factor-based therapeutic design.
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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.