ArticlePloS one2011
The RACK1 signaling scaffold protein selectively interacts with Yersinia pseudotuberculosis virulence function.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 53 citations in OpenAlex.
- RACK1 in host immune response to infections: molecular mechanisms and therapeutic potentials.Frontiers in immunology · 2026Review
- Unraveling the Pathogenetic Potential and Immune Crosstalk of Yersinia spp. in Inflammatory Bowel Disease.Journal of immunology research · 2026Review
- Pathogenicity and virulence ofVirulence · 2024Review
- RACK1 mediates NLRP3 inflammasome activation during Pasteurella multocida infection.Veterinary research · 2023Article
- Article
- 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
- Proteome Profiling of PMJ2-R and Primary Peritoneal Macrophages.International journal of molecular sciences · 2021Article
- RACK1 Mediates NLRP3 Inflammasome Activation by Promoting NLRP3 Active Conformation and Inflammasome Assembly.Cell reports · 2020Article
- Mycobacterial EST12 activates a RACK1-NLRP3-gasdermin D pyroptosis-IL-1β immune pathway.Science advances · 2020Article
- Effector-triggered immunity and pathogen sensing in metazoans.Nature microbiology · 2020Review
- Extracellular Vesicles From Liver Progenitor Cells Downregulates Fibroblast Metabolic Activity and Increase the Expression of Immune-Response Related Molecules.Frontiers in cell and developmental biology · 2020Article
- The type III secretion system needle, tip, and translocon.Protein science : a publication of the Protein Society · 2019Review
- Immunomodulatory Yersinia outer proteins (Yops)-useful tools for bacteria and humans alike.Virulence · 2017Review
- Guanylate Binding Proteins Regulate Inflammasome Activation in Response to Hyperinjected Yersinia Translocon Components.Infection and immunity · 2017Article
- Yersinia pestis YopK Inhibits Bacterial Adhesion to Host Cells by Binding to the Extracellular Matrix Adaptor Protein Matrilin-2.Infection and immunity · 2017Article
- Galectin-3 directs antimicrobial guanylate binding proteins to vacuoles furnished with bacterial secretion systems.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Yersinia pseudotuberculosis Blocks Neutrophil Degranulation.Infection and immunity · 2016Article
- The Amino-Terminal Part of the Needle-Tip Translocator LcrV ofFrontiers in cellular and infection microbiology · 2016Article
- Modulation of the host innate immune and inflammatory response by translocated bacterial proteins.Cellular microbiology · 2015Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Many gram-negative bacteria use type III secretion systems to translocate effector proteins into host cells. These effectors interfere with cellular functions in a highly regulated manner resulting in effects that are beneficial for the bacteria. The pathogen Yersinia can resist phagocytosis by eukaryotic cells by translocating Yop effectors into the target cell cytoplasm. This is called antiphagocytosis, and constitutes an important virulence feature of this pathogen since it allows survival in immune cell rich lymphoid organs. We show here that the virulence protein YopK has a role in orchestrating effector translocation necessary for productive antiphagocytosis. We present data showing that YopK influences Yop effector translocation by modulating the ratio of the pore-forming proteins YopB and YopD in the target cell membrane. Further, we show that YopK that can interact with the translocators, is exposed inside target cells and binds to the eukaryotic signaling protein RACK1. This protein is engaged upon Y. pseudotuberculosis-mediated β1-integrin activation and localizes to phagocytic cups. Cells with downregulated RACK1 levels are protected from antiphagocytosis. This resistance is not due to altered levels of translocated antiphagocytic effectors, and cells with reduced levels of RACK1 are still sensitive to the later occurring cytotoxic effect caused by the Yop effectors. Further, a yopK mutant unable to bind RACK1 shows an avirulent phenotype during mouse infection, suggesting that RACK1 targeting by YopK is a requirement for virulence. Together, our data imply that the local event of Yersinia-mediated antiphagocytosis involves a step where YopK, by binding RACK1, ensures an immediate specific spatial delivery of antiphagocytic effectors leading to productive inhibition of phagocytosis.
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