ArticleeLife2016
Bile salt receptor complex activates a pathogenic type III secretion system.
Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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
52 citing papers in PubMed, 87 citations in OpenAlex.
- TsrA modulates type III secretion system 2 expression as a co-regulator of H-NS inJournal of bacteriology · 2026Article
- Bile-mediated ToxS homodimerization provides a model for ToxRS periplasmic interactions.bioRxiv : the preprint server for biology · 2026Article
- Effects of Bile on PathogenicBiomolecules · 2025Article
- A critical role forProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Article
- Role of the TPR family protein VPA1365 in regulating type III secretion system 2 and virulence inApplied and environmental microbiology · 2025Article
- Bile acids activate the antibacterial T6SS1 in the gut pathogenMicrobiology spectrum · 2024Article
- Article
- Identification of virulence-associated factors in Vibrio parahaemolyticus with special reference to moonlighting protein: a secretomics study.International microbiology : the official journal of the Spanish Society for Microbiology · 2024Article
- The antagonistic transcription factors, EspM and EspN, regulate the ESX-1 secretion system inmBio · 2024Article
- The read-through transcription-mediated autoactivation circuit for virulence regulator expression drives robust type III secretion system 2 expression in Vibrio parahaemolyticus.PLoS pathogens · 2024Article
- Microbially catalyzed conjugation of GABA and tyramine to bile acids.Journal of bacteriology · 2024Article
- Insights into virulence: structure classification of themSystems · 2023Article
- Microbially-catalyzed conjugation of GABA and tyramine to bile acids.bioRxiv : the preprint server for biology · 2023Article
- Potent Bile Acid Microbial Metabolites ModulatePathogens (Basel, Switzerland) · 2023Article
- Article
- Attenuation of a DNA cruciform by a conserved regulator directs T3SS1 mediated virulence in Vibrio parahaemolyticus.Nucleic acids research · 2023Article
- Transmembrane Transcription Regulators Are Widespread in Bacteria and Archaea.Microbiology spectrum · 2023Article
- Article
- Molecular determinants for differential activation of the bile acid receptor from the pathogen Vibrio parahaemolyticus.The Journal of biological chemistry · 2023Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Bile is an important component of the human gastrointestinal tract with an essential role in food absorption and antimicrobial activities. Enteric bacterial pathogens have developed strategies to sense bile as an environmental cue to regulate virulence genes during infection. We discovered that Vibrio parahaemolyticus VtrC, along with VtrA and VtrB, are required for activating the virulence type III secretion system 2 in response to bile salts. The VtrA/VtrC complex activates VtrB in the presence of bile salts. The crystal structure of the periplasmic domains of the VtrA/VtrC heterodimer reveals a β-barrel with a hydrophobic inner chamber. A co-crystal structure of VtrA/VtrC with bile salt, along with biophysical and mutational analysis, demonstrates that the hydrophobic chamber binds bile salts and activates the virulence network. As part of a family of conserved signaling receptors, VtrA/VtrC provides structural and functional insights into the evolutionarily conserved mechanism used by bacteria to sense their environment.
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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.