ArticleThe Journal of biological chemistry2014
WITHDRAWN: Toxoplasma gondii virulence factor ROP18 inhibits the host NF-κB pathway by promoting p65 degradation.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. 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.
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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, 69 citations in OpenAlex.
- Therapeutic Antitoxoplasmosis Potential ofJournal of tropical medicine · 2026Article
- Review
- A novel mRNA vaccine, TGGT1_278620 mRNA-LNP, prolongs the survival time in BALB/c mice with acute toxoplasmosis.Microbiology spectrum · 2024Article
- Toxoplasma-host endoplasmic reticulum interaction: HowCurrent research in microbial sciences · 2024Review
- Genetic diversity of Toxoplasma gondii in South America: occurrence, immunity, and fate of infection.Parasites & vectors · 2023Review
- Inhibition of Cell Apoptosis by Apicomplexan Protozoa-Host Interaction in the Early Stage of Infection.Animals : an open access journal from MDPI · 2023Review
- Exploiting the Macrophage Production of IL-12 in Improvement of Vaccine Development againstVaccines · 2022Review
- Activation of NF-κB signaling by the dense granule protein GRA15 of a newly isolated type 1 Toxoplasma gondii strain.Parasites & vectors · 2022Article
- Host cell proteins modulated upon Toxoplasma infection identified using proteomic approaches: a molecular rationale.Parasitology research · 2022Review
- The Role of Nuclear Factor Kappa B (NF-κB) in the Immune Response against Parasites.Pathogens (Basel, Switzerland) · 2022Review
- Parasitomimetics: Can We Utilize Parasite-Derived Immunomodulatory Molecules for Interventions to Immunological Disorders?Frontiers in immunology · 2022Review
- Article
- High resistance toiScience · 2021Article
- Lessons from Toxoplasma: Host responses that mediate parasite control and the microbial effectors that subvert them.The Journal of experimental medicine · 2021Review
- Article
- NF-κB and Its Regulators During Pregnancy.Frontiers in immunology · 2021Review
- The NF-κB Pathway: Modulation byFrontiers in cellular and infection microbiology · 2021Review
- Article
- Strain-specific disruption of interferon-stimulated N-myc and STAT interactor (NMI) function byParasitology · 2020Article
- TgROP18 targets IL20RB for host-defense-related-STAT3 activation during Toxoplasma gondii infection.Parasites & vectors · 2020Article
Corrections and comments
- Retracted
Authors and funding
17 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The obligate intracellular parasite Toxoplasma gondii secretes effector molecules into the host cell to modulate host immunity. Previous studies have shown that T. gondii could interfere with host NF-κB signaling to promote their survival, but the effectors of type I strains remain unclear. The polymorphic rhoptry protein ROP18 is a key serine/threonine kinase that phosphorylates host proteins to modulate acute virulence. Our data demonstrated that the N-terminal portion of ROP18 is associated with the dimerization domain of p65. ROP18 phosphorylates p65 at Ser-468 and targets this protein to the ubiquitin-dependent degradation pathway. The kinase activity of ROP18 is required for p65 degradation and suppresses NF-κB activation. Consistently, compared with wild-type ROP18 strain, ROP18 kinase-deficient type I parasites displayed a severe inability to inhibit NF-κB, culminating in the enhanced production of IL-6, IL-12, and TNF-α in infected macrophages. In addition, studies have shown that transgenic parasites carrying kinase-deficient ROP18 induce M1-biased activation. These results demonstrate for the first time that the virulence factor ROP18 in T. gondii type I strains is responsible for inhibiting the host NF-κB pathway and for suppressing proinflammatory cytokine expression, thus providing a survival advantage to the infectious agent.
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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.