ArticleNature microbiology2020
An exported kinase family mediates species-specific erythrocyte remodelling and virulence in human malaria.
Article in Nature microbiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
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Who cites it
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.
- Phosphorylation in theJournal of proteome research · 2024Pooled it
- FIKK1, a member of the FIKK kinase family, phosphorylates VAR2CSA and regulates adhesion of Plasmodium falciparum-infected erythrocytes to the placental receptor CSA.PLoS pathogens · 2026Article
- Associations between the Plasmodium falciparum genome and sickle haemoglobin identified in mild malaria cases from Ghana.Malaria journal · 2026Article
- Febrile Temperature Augments Ring-stage Plasmodium falciparum Adhesion to Brain Endothelial Cells.The Journal of infectious diseases · 2026Article
- Physiological febrile heat stress increases cytoadhesion through increased protein trafficking ofeLife · 2026Article
- Molecular Investigation of FIKK Kinase Family to Develop PCR-Based Diagnosis of Plasmodium falciparum.Molecular biotechnology · 2025Article
- Plasmodium falciparum gene expression signatures and antibody profiling implicate the fikk, phist, and surf multigene families in severe malaria syndromes.The Journal of infection · 2025Article
- The fast-evolving FIKK kinase family of Plasmodium falciparum can be inhibited by a single compound.Nature microbiology · 2025Article
- Towards next-generation treatment options to combat Plasmodium falciparum malaria.Nature reviews. Microbiology · 2025Review
- A scaleable inducible knockout system for studying essential gene function in the malaria parasite.Nucleic acids research · 2025Article
- Systematic in vitro evolution inScience (New York, N.Y.) · 2024Article
- Article
- Heterochromatin dynamics during the initial stages of sexual development in Plasmodium falciparum.Scientific reports · 2024Article
- Proteomic approaches for protein kinase substrate identification in Apicomplexa.Molecular and biochemical parasitology · 2024Review
- Experimental vaccination by single dose sporozoite injection of blood-stage attenuated malaria parasites.EMBO molecular medicine · 2024Article
- Temporal and spatial dynamics of Plasmodium falciparum clonal lineages in Guyana.PLoS pathogens · 2024Article
- A screen for Plasmodium falciparum sporozoite surface protein binding to human hepatocyte surface receptors identifies novel host-pathogen interactions.Malaria journal · 2024Article
- Gene expression analyses reveal differences in children's response to malaria according to their age.Nature communications · 2024Article
- Article
- Gene expression analyses reveal differences in children's response to malaria according to their age.bioRxiv : the preprint server for biology · 2023Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
Abstract
The most severe form of human malaria is caused by Plasmodium falciparum. Its virulence is closely linked to the increase in rigidity of infected erythrocytes and their adhesion to endothelial receptors, obstructing blood flow to vital organs. Unlike other human-infecting Plasmodium species, P. falciparum exports a family of 18 FIKK serine/threonine kinases into the host cell, suggesting that phosphorylation may modulate erythrocyte modifications. We reveal substantial species-specific phosphorylation of erythrocyte proteins by P. falciparum but not by Plasmodium knowlesi, which does not export FIKK kinases. By conditionally deleting all FIKK kinases combined with large-scale quantitative phosphoproteomics we identified unique phosphorylation fingerprints for each kinase, including phosphosites on parasite virulence factors and host erythrocyte proteins. Despite their non-overlapping target sites, a network analysis revealed that some FIKKs may act in the same pathways. Only the deletion of the non-exported kinase FIKK8 resulted in reduced parasite growth, suggesting the exported FIKKs may instead support functions important for survival in the host. We show that one kinase, FIKK4.1, mediates both rigidification of the erythrocyte cytoskeleton and trafficking of the adhesin and key virulence factor PfEMP1 to the host cell surface. This establishes the FIKK family as important drivers of parasite evolution and malaria pathology.
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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.