ArticleNeuroscience letters2015
Phenazine derivatives cause proteotoxicity and stress in C. elegans.
Article in Neuroscience letters, 2015. 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
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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.
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, 33 citations in OpenAlex.
- Patterns of pathogenesis in innate immunity: insights from C. elegans.Nature reviews. Immunology · 2025Review
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- Role of UDP-Glycosyltransferase (Chemical research in toxicology · 2024Article
- Reactive oxygen species drive foraging decisions in Caenorhabditis elegans.Redox biology · 2023Article
- Mitochondria in the Spotlight:Cells · 2023Review
- PcaR, a GntR/FadR Family Transcriptional Repressor Controls the Transcription of Phenazine-1-Carboxylic Acid 1,2-Dioxygenase Gene Cluster in Sphingomonas histidinilytica DS-9.Applied and environmental microbiology · 2023Article
- Evaluation of Blood-Brain-Barrier Permeability, Neurotoxicity, and Potential Cognitive Impairment byOxidative medicine and cellular longevity · 2022Article
- Identification of the Genes of the Plant PathogenFrontiers in microbiology · 2022Article
- Proteomic analysis of Caenorhabditis elegans against Salmonella Typhi toxic proteins.Genes and immunity · 2021Article
- Combating Parasitic Nematode Infections, Newly Discovered Antinematode Compounds from Marine Epiphytic Bacteria.Microorganisms · 2020Review
- Membrane-Interactive Compounds FromFrontiers in microbiology · 2020Article
- Recent Progress in Lab-On-a-Chip Systems for the Monitoring of Metabolites for Mammalian and Microbial Cell Research.Sensors (Basel, Switzerland) · 2019Review
- Mitochondrial UPR repression duringProceedings of the National Academy of Sciences of the United States of America · 2019Article
- Application ofPreventive nutrition and food science · 2018Review
- Novel Three-Component Phenazine-1-Carboxylic Acid 1,2-Dioxygenase in Sphingomonas wittichii DP58.Applied and environmental microbiology · 2017Article
- Transient Proteotoxicity of Bacterial Virulence Factor Pyocyanin in Renal Tubular Epithelial Cells Induces ER-Related Vacuolation and Can Be Efficiently Modulated by Iron Chelators.Toxicological sciences : an official journal of the Society of Toxicology · 2016Article
- A widespread bacterial phenazine forms S-conjugates with biogenic thiols and crosslinks proteins.Chemical science · 2016Article
- A bacterial metabolite induces glutathione-tractable proteostatic damage, proteasomal disturbances, and PINK1-dependent autophagy in C. elegans.Cell death & disease · 2015Article
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 1 institution in 1 country.
Funding
Abstract
It is widely recognized that bacterial metabolites have toxic effects in animal systems. Phenazines are a common bacterial metabolite within the redox-active exotoxin class. These compounds have been shown to be toxic to the soil invertebrate Caenorhabditis elegans with the capability of causing oxidative stress and lethality. Here we report that chronic, low-level exposure to three separate phenazine molecules (phenazine-1-carboxylic acid, pyocyanin and 1-hydroxyphenazine) upregulated ER stress response and enhanced expression of a superoxide dismutase reporter in vivo. Exposure to these molecules also increased protein misfolding of polyglutamine and α-synuclein in the bodywall muscle cells of C. elegans. Exposure of worms to these phenazines caused additional sensitivity in dopamine neurons expressing wild-type α-synuclein, indicating a possible defect in protein homeostasis. The addition of an anti-oxidant failed to rescue the neurotoxic and protein aggregation phenotypes caused by these compounds. Thus, increased production of superoxide radicals that occurs in whole animals in response to these phenazines appears independent from the toxicity phenotype observed. Collectively, these data provide cause for further consideration of the neurodegenerative impact of phenazines.
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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.