ReviewFrontiers in cellular and infection microbiology2013
Regulation of the Yersinia type III secretion system: traffic control.
Review in Frontiers in cellular and infection microbiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 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
66 citing papers in PubMed.
- Article
- Fis suppresses late-stage virulence gene expression in Yersinia pseudotuberculosis at environmental temperatures.PLoS pathogens · 2026Article
- Dynamic interaction of the Yersinia pseudotuberculosis type three secretion system proteins LcrV and LcrG.Protein science : a publication of the Protein Society · 2026Article
- Molecular Mechanisms of Priming Innate Immunity by Small Extracellular Vesicles Released during Infection with Gram-negative Bacteria.bioRxiv : the preprint server for biology · 2025Article
- Overexpression ofPlant signaling & behavior · 2025Article
- Yersinia actively downregulates type III secretion and adhesion at higher cell densities.PLoS pathogens · 2025Article
- Article
- The polyadenylase PAPI is required for virulence plasmid maintenance in pathogenic bacteria.PLoS pathogens · 2025Article
- Yersinia pestis Actively Inhibits the Production of Extracellular Vesicles by Human Neutrophils.Journal of extracellular vesicles · 2025Article
- Distinct mechanisms of type 3 secretion system recognition control LTB4 synthesis in neutrophils and macrophages.PLoS pathogens · 2024Article
- Distinct Mechanisms of Type 3 Secretion System Recognition Control LTBbioRxiv : the preprint server for biology · 2024Article
- Type 3 secretion system induced leukotriene B4 synthesis by leukocytes is actively inhibited by Yersinia pestis to evade early immune recognition.PLoS pathogens · 2024Article
- Type III Secretion inMicrobiology and molecular biology reviews : MMBR · 2023Review
- The type III secretion chaperone SctY may shield the hydrophobic export gate-binding C-terminus of its substrate SctX.Acta crystallographica. Section D, Structural biology · 2023Article
- Article
- Direct interaction of a chaperone-bound type III secretion substrate with the export gate.Nature communications · 2022Article
- The Regulatory Circuit Underlying Downregulation of a Type III Secretion System inInternational journal of molecular sciences · 2022Article
- Type III secretion by Yersinia pseudotuberculosis is reliant upon an authentic N-terminal YscX secretor domain.Molecular microbiology · 2022Article
- Role of the Yersinia pseudotuberculosis Virulence Plasmid in Pathogen-Phagocyte Interactions in Mesenteric Lymph Nodes.EcoSal Plus · 2021Review
- Proteogenomic discovery of sORF-encoded peptides associated with bacterial virulence in Yersinia pestis.Communications biology · 2021Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Yersinia species, as well as many other Gram-negative pathogens, use a type III secretion system (T3SS) to translocate effector proteins from the bacterial cytoplasm to the host cytosol. This T3SS resembles a molecular syringe, with a needle-like shaft connected to a basal body structure, which spans the inner and outer bacterial membranes. The basal body of the injectisome shares a high degree of homology with the bacterial flagellum. Extending from the T3SS basal body is the needle, which is a polymer of a single protein, YscF. The distal end of the needle serves as a platform for the assembly of a tip complex composed of LcrV. Though never directly observed, prevailing models assume that LcrV assists in the insertion of the pore-forming proteins YopB and YopD into the host cell membrane. This completes a bridge between the bacterium and host cell to provide a continuous channel through which effectors are delivered. Significant effort has gone into understanding how the T3SS is assembled, how its substrates are recognized and how substrate delivery is controlled. Arguably the latter topic is the least understood; however, recent advances have provided new insight, and therefore, this review will focus primarily on summarizing the current state of knowledge regarding the control of substrate delivery by the T3SS. Specifically, we will discuss the roles of YopK, as well as YopN and YopE, which have long been linked to regulation of translocation. We also propose models whereby the YopK regulator communicates with the basal body of the T3SS to control translocation.
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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.