ReviewHandbook of experimental pharmacology2017
The Pseudomonas aeruginosa Exoenzyme Y: A Promiscuous Nucleotidyl Cyclase Edema Factor and Virulence Determinant.
Review in Handbook of experimental pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 24 citations in OpenAlex.
- Molecular characterization of virulent genes in Pseudomonas aeruginosa based on componential usage divergence.Scientific reports · 2025Article
- Article
- Lung endothelium, tau, and amyloids in health and disease.Physiological reviews · 2024Review
- Functional and structural insights into the multi-step activation and catalytic mechanism of bacterial ExoY nucleotidyl cyclase toxins bound to actin-profilin.PLoS pathogens · 2023Article
- Airway Epithelial Cell Junctions as Targets for Pathogens and Antimicrobial Therapy.Pharmaceutics · 2022Review
- ExlA: A New Contributor toFrontiers in cellular and infection microbiology · 2022Review
- Perspectives on theToxins · 2021Review
- Roles of Two-Component Systems inInternational journal of molecular sciences · 2021Review
- The Role ofToxins · 2021Review
- Review
- Review
- Prevalence of ExoY Activity inFrontiers in microbiology · 2021Article
- α-Tocopherol Attenuates the Severity ofAmerican journal of respiratory cell and molecular biology · 2020Article
- Virulent Pseudomonas aeruginosa infection converts antimicrobial amyloids into cytotoxic prions.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Observational
- cAMP signaling primes lung endothelial cells to activate caspase-1 duringAmerican journal of physiology. Lung cellular and molecular physiology · 2020Article
- Animal Models of Type III Secretion System-Mediated Pathogenesis.Pathogens (Basel, Switzerland) · 2019Review
- Pseudomonas aeruginosa ExoS Induces Intrinsic Apoptosis in Target Host Cells in a Manner That is Dependent on its GAP Domain Activity.Scientific reports · 2018Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Exoenzyme Y (ExoY) was identified as a component of the Pseudomonas aeruginosa type 3 secretion system secretome in 1998. It is a common contributor to the arsenal of type 3 secretion system effectors, as it is present in approximately 90% of Pseudomonas isolates. ExoY has adenylyl cyclase activity that is dependent upon its association with a host cell cofactor. However, recent evidence indicates that ExoY is not just an adenylyl cyclase; rather, it is a promiscuous cyclase capable of generating purine and pyrimidine cyclic nucleotide monophosphates. ExoY's enzymatic activity causes a characteristic rounding of mammalian cells, due to microtubule breakdown. In endothelium, this cell rounding disrupts cell-to-cell junctions, leading to loss of barrier integrity and an increase in tissue edema. Microtubule breakdown seems to depend upon tau phosphorylation, where the elevation of cyclic nucleotide monophosphates activates protein kinases A and G and causes phosphorylation of endothelial microtubule associated protein tau. Phosphorylation is a stimulus for tau release from microtubules, leading to microtubule instability. Phosphorylated tau accumulates inside endothelium as a high molecular weight, oligomeric form, and is then released from the cell. Extracellular high molecular weight tau causes a transmissible cytotoxicity that significantly hinders cellular repair following infection. Thus, ExoY may contribute to bacterial virulence in at least two ways; first, by microtubule breakdown leading to loss of endothelial cell barrier integrity, and second, by promoting release of a high molecular weight tau cytotoxin that impairs cellular recovery following infection.
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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.