ArticleInfection and immunity1999
YopJ of Yersinia spp. is sufficient to cause downregulation of multiple mitogen-activated protein kinases in eukaryotic cells.
Article in Infection and immunity, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 109 citations in OpenAlex.
- Guards and decoys: RIPoptosome and inflammasome pathway regulators of bacterial effector-triggered immunity.PLoS pathogens · 2025Review
- Non-canonical autophosphorylation of RIPK1 drives timely pyroptosis to control Yersinia infection.Cell reports · 2024Article
- Translocation of YopJ family effector proteins through the VirB/VirD4 T4SS ofProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Macrophage innate immune responses delineate between defective translocon assemblies produced byVirulence · 2023Article
- Roles of RIPK1 as a stress sentinel coordinating cell survival and immunogenic cell death.Nature reviews. Molecular cell biology · 2023Review
- Molecular mechanisms of gasdermin D pore-forming activity.Nature immunology · 2023Review
- Article
- RIPK1 Distinctly RegulatesImmunoHorizons · 2020Article
- Caspase-8 induces cleavage of gasdermin D to elicit pyroptosis duringProceedings of the National Academy of Sciences of the United States of America · 2018Article
- RIPK1-dependent apoptosis bypasses pathogen blockade of innate signaling to promote immune defense.The Journal of experimental medicine · 2017Article
- YopJ Family Effectors Promote Bacterial Infection through a Unique Acetyltransferase Activity.Microbiology and molecular biology reviews : MMBR · 2016Review
- Cell-Extrinsic TNF Collaborates with TRIF Signaling To Promote Yersinia-Induced Apoptosis.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- A Single Bacterial Immune Evasion Strategy Dismantles Both MyD88 and TRIF Signaling Pathways Downstream of TLR4.Cell host & microbe · 2015Article
- Article
- Structural insight into effector proteins of Gram-negative bacterial pathogens that modulate the phosphoproteome of their host.Protein science : a publication of the Protein Society · 2015Review
- Random mutagenesis identifies a C-terminal region of YopD important for Yersinia type III secretion function.PloS one · 2015Article
- The GAP activity of type III effector YopE triggers killing of Yersinia in macrophages.PLoS pathogens · 2014Article
- Effector CD8+ T cells are generated in response to an immunodominant epitope in type III effector YopE during primary Yersinia pseudotuberculosis infection.Infection and immunity · 2014Article
- Direct neutralization of type III effector translocation by the variable region of a monoclonal antibody to Yersinia pestis LcrV.Clinical and vaccine immunology : CVI · 2014Article
- A type III secretion system inhibitor targets YopD while revealing differential regulation of secretion in calcium-blind mutants of Yersinia pestis.Antimicrobial agents and chemotherapy · 2014Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Pathogenic Yersinia spp. utilize a plasmid-encoded type III secretion system to deliver a set of Yop effector proteins into eukaryotic cells. Previous studies have shown that the effector YopJ is required for Yersinia to cause downregulation of the mitogen-activated protein (MAP) kinases c-Jun N-terminal kinase (JNK), p38, and extracellular signal-regulated kinase (ERK) 1 and 2 in infected macrophages. Here we demonstrate that YopJ is sufficient to cause downregulation of multiple MAP kinases in eukaryotic cells. Cellular fractionation experiments confirmed that YopJ is delivered into the cytoplasmic fraction of macrophages by the type III system. Production of YopJ in COS-1 cells by transfection significantly reduced (5- to 10-fold) activation of JNK, p38, and ERK in response to several different stimuli, including serum and tumor necrosis factor alpha. JNK activation mediated by RacV12, an activated mutant of Rac1, was also blocked by YopJ in COS-1 cells, indicating that YopJ acts downstream of this small GTPase to downregulate MAP kinase signaling. Analysis of transfected COS-1 cells by immunofluorescence microscopy revealed that YopJ is recruited from the cytoplasmic compartment to the cell periphery in response to stimuli (e.g., serum) that induce membrane ruffling. These data indicate that YopJ functions as a "MAP kinase toxin" to selectively block nuclear responses that are triggered by Yersinia-host cell interaction.
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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.