ArticleParasitology research2016
Deletion of mitogen-activated protein kinase 1 inhibits development and growth of Toxoplasma gondii.
Article in Parasitology research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Bumped Kinase Inhibitors Inhibit bothACS infectious diseases · 2025Article
- Versatile Imidazole Scaffold with Potent Activity against Multiple Apicomplexan Parasites.ACS infectious diseases · 2025Article
- Article
- Review
- Genome-Wide Identification and Evolutionary Analysis of Sarcocystis neurona Protein Kinases.Pathogens (Basel, Switzerland) · 2017Article
- Immunization withFrontiers in immunology · 2017Article
- The heat shock protein 90 of Toxoplasma gondii is essential for invasion of host cells and tachyzoite growth.Parasite (Paris, France) · 2017Article
- Observations on bradyzoite biology.Microbes and infectionReview
- Immune Responses Induced by pVAX/Iranian journal of parasitologyArticle
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitogen-activated protein kinases (MAPKs) regulate key signaling events in a variety of eukaryotic cells. Toxoplasma gondii, the causative agents of toxoplasmosis, possesses a p38α MAPK homologue, MAPK1, which is an important manipulator of host immunity and virulence in mice. In this work, we showed an increased transcript level of MAPK1 in T. gondii during bradyzoite differentiation induced by alkaline treatment and heat shock in vitro, suggesting that MAPK1 may be associated with bradyzoite differentiation. The biological roles of MAPK1 of T. gondii were investigated by construction of a MAPK1 deletion mutant (Δmapk1) and a complementation mutant with restored MAPK1 expression using a type I strain. Knockout of MAPK1 resulted in markedly defective bradyzoite differentiation, host-cell attachment and parasite replication in vitro, and the inability to cause lethal infection in a murine model of acute toxoplasmosis, with lower parasite burden in infected tissues, showing that MAPK1 is associated with the acute virulence of parasite in mice. Complementation of MAPK1-deficient parasites restored bradyzoite development, attachment, replication, and virulence. Our findings demonstrate that MAPK1 is involved in asexual development and growth of T. gondii.
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