ArticleStructure (London, England : 1993)2017
Structural Basis for the Subversion of MAP Kinase Signaling by an Intrinsically Disordered Parasite Secreted Agonist.
Article in Structure (London, England : 1993), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 55 citations in OpenAlex.
- Short linear motifs-underexplored players drivingMicrobiology spectrum · 2026Article
- Structural and dynamic insights into the allosteric activation of p38α MAP kinase via specific docking interactions.Communications biology · 2026Article
- Molecular basis of mitogen-activated protein kinase ERK2 activation by its upstream kinase MEK1.bioRxiv : the preprint server for biology · 2026Article
- LiF-MS+, a revised technique for mapping peptide-protein interactions.bioRxiv : the preprint server for biology · 2024Article
- A Combination of Four Nuclear Targeted Effectors ProtectsbioRxiv : the preprint server for biology · 2023Article
- LeishMANIAdb: a comparative resource for Leishmania proteins.Database : the journal of biological databases and curation · 2023Article
- Architecture of the MKK6-p38α complex defines the basis of MAPK specificity and activation.Science (New York, N.Y.) · 2023Article
- Proteome-wide screening for mitogen-activated protein kinase docking motifs and interactors.Science signaling · 2023Article
- Cryptosporidium parvum regulates HCT-8 cell autophagy to facilitate survival via inhibiting miR-26a and promoting miR-30a expression.Parasites & vectors · 2022Article
- The intrinsically disordered protein TgIST from Toxoplasma gondii inhibits STAT1 signaling by blocking cofactor recruitment.Nature communications · 2022Article
- Comparative Phosphoproteomic Analysis of Sporulated Oocysts and Tachyzoites ofMolecules (Basel, Switzerland) · 2022Article
- Genomic insights into host and parasite interactions during intracellular infection by Toxoplasma gondii.PloS one · 2022Article
- The pathogenicity and virulence ofVirulence · 2021Article
- Induction of IL-12p40 and type 1 immunity by Toxoplasma gondii in the absence of the TLR-MyD88 signaling cascade.PLoS pathogens · 2021Article
- Secreted Effectors Modulating Immune Responses toLife (Basel, Switzerland) · 2021Review
- Target acquired: transcriptional regulators as drug targets for protozoan parasites.International journal for parasitology · 2021Review
- Diversity and versatility of p38 kinase signalling in health and disease.Nature reviews. Molecular cell biology · 2021Review
- Transport mechanisms at the malaria parasite-host cell interface.PLoS pathogens · 2021Review
- Seizing control: How dense granule effector proteins enable Toxoplasma to take charge.Molecular microbiology · 2021Review
- Review
Corrections and comments
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Authors and funding
8 authors at 6 institutions in 1 country.
Funding
Abstract
The causative agent of toxoplasmosis, the intracellular parasite Toxoplasma gondii, delivers a protein, GRA24, into the cells it infects that interacts with the mitogen-activated protein (MAP) kinase p38α (MAPK14), leading to activation and nuclear translocation of the host kinase and a subsequent inflammatory response that controls the progress of the parasite. The purification of a recombinant complex of GRA24 and human p38α has allowed the molecular basis of this activation to be determined. GRA24 is shown to be intrinsically disordered, binding two kinases that act independently, and is the only factor required to bypass the canonical mitogen-activated protein kinase activation pathway. An adapted kinase interaction motif (KIM) forms a highly stable complex that competes with cytoplasmic regulatory partners. In addition, the recombinant complex forms a powerful in vitro tool to evaluate the specificity and effectiveness of p38α inhibitors that have advanced to clinical trials, as it provides a hitherto unavailable stable and highly active form of p38α.
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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.