ArticleCellular microbiology2015
Discovery of a novel and conserved Plasmodium falciparum exported protein that is important for adhesion of PfEMP1 at the surface of infected erythrocytes.
Article in Cellular microbiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- RNA polymerase III is involved in regulatingeLife · 2024Article
- A newly characterized malaria antigen on erythrocyte and merozoite surfaces induces parasite inhibitory antibodies.The Journal of experimental medicine · 2021Article
- Some conditions apply: Systems for studying Plasmodium falciparum protein function.PLoS pathogens · 2021Review
- Cutting back malaria: CRISPR/Cas9 genome editing of Plasmodium.Briefings in functional genomics · 2019Review
- Plasmodium falciparum In Vitro Drug Resistance Selections and Gene Editing.Methods in molecular biology (Clifton, N.J.) · 2019Article
- New and emerging uses of CRISPR/Cas9 to genetically manipulate apicomplexan parasites.Parasitology · 2018Review
- In-depth comparative analysis of malaria parasite genomes reveals protein-coding genes linked to human disease in Plasmodium falciparum genome.BMC genomics · 2018Article
- A Specific PfEMP1 Is Expressed in P. falciparum Sporozoites and Plays a Role in Hepatocyte Infection.Cell reports · 2018Article
- TheeLife · 2017Article
- Endothelial-Leukocyte Interaction in Severe Malaria: Beyond the Brain.Mediators of inflammation · 2015Review
- Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Plasmodium falciparum virulence is linked to its ability to sequester in post-capillary venules in the human host. Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1) is the main variant surface antigen implicated in this process. Complete loss of parasite adhesion is linked to a large subtelomeric deletion on chromosome 9 in a number of laboratory strains such as D10 and T9-96. Similar to the cytoadherent reference line FCR3, D10 strain expresses PfEMP1 on the surface of parasitized erythrocytes, however without any detectable cytoadhesion. To investigate which of the deleted subtelomeric genes may be implicated in parasite adhesion, we selected 12 genes for D10 complementation studies that are predicted to code for proteins exported to the red blood cell. We identified a novel single copy gene (PF3D7_0936500) restricted to P. falciparum that restores adhesion to CD36, termed here virulence-associated protein 1 (Pfvap1). Protein knockdown and gene knockout experiments confirmed a role of PfVAP1 in the adhesion process in FCR3 parasites. PfVAP1 is co-exported with PfEMP1 into the host cell via vesicle-like structures called Maurer's clefts. This study identifies a novel highly conserved parasite molecule that contributes to parasite virulence possibly by assisting PfEMP1 to establish functional adhesion at the host cell surface.
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