ArticlePloS one2016
Contrasting Inducible Knockdown of the Auxiliary PTEX Component PTEX88 in P. falciparum and P. berghei Unmasks a Role in Parasite Virulence.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 40 citations in OpenAlex.
- G6PD deficiency and the exportome of plasmodium falciparum FCB-2: A comparative analysis utilizing one-dimensional blue-native electrophoresis and timstof mass spectrometry.Parasitology research · 2026Article
- Erythrocyte Membrane Protein 3 (EMAP3) Is Exposed on the Surface of the Plasmodium berghei Infected Red Blood Cell.Molecular microbiology · 2026Article
- Novel Ion Channel Genes in Malaria Parasites.Genes · 2024Review
- Transcriptome analysis reveals molecular targets of erythrocyte invasion phenotype diversity in naturalFrontiers in parasitology · 2024Article
- Knock-sideways by inducible ER retrieval enables a unique approach for studyingProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Dissecting EXP2 sequence requirements for protein export in malaria parasites.Frontiers in cellular and infection microbiology · 2023Article
- Genetic and chemical validation ofeLife · 2022Article
- The Plasmodium falciparum parasitophorous vacuole protein P113 interacts with the parasite protein export machinery and maintains normal vacuole architecture.Molecular microbiology · 2022Article
- A toolbox for conditional control of gene expression in apicomplexan parasites.Molecular microbiology · 2022Review
- A revised mechanism for how Plasmodium falciparum recruits and exports proteins into its erythrocytic host cell.PLoS pathogens · 2022Article
- Transport mechanisms at the malaria parasite-host cell interface.PLoS pathogens · 2021Review
- Absence of PEXEL-Dependent Protein Export inFrontiers in genetics · 2021Article
- The parasitophorous vacuole of the blood-stage malaria parasite.Nature reviews. Microbiology · 2020Review
- Crossing the Vacuolar Rubicon: Structural Insights into Effector Protein Trafficking in Apicomplexan Parasites.Microorganisms · 2020Review
- Article
- Knockdown of the translocon protein EXP2 in Plasmodium falciparum reduces growth and protein export.PloS one · 2018Article
- Article
- Host cell remodeling by pathogens: the exomembrane system in Plasmodium-infected erythrocytes.FEMS microbiology reviews · 2016Review
- Plasmodium species: master renovators of their host cells.Nature reviews. Microbiology · 2016Review
- Substrate and Inhibitor Specificity of the Plasmodium berghei Equilibrative Nucleoside Transporter Type 1.Molecular pharmacology · 2016Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pathogenesis of malaria infections is linked to remodeling of erythrocytes, a process dependent on the trafficking of hundreds of parasite-derived proteins into the host erythrocyte. Recent studies have demonstrated that the Plasmodium translocon of exported proteins (PTEX) serves as the central gateway for trafficking of these proteins, as inducible knockdown of the core PTEX constituents blocked the trafficking of all classes of cargo into the erythrocyte. However, the role of the auxiliary component PTEX88 in protein export remains less clear. Here we have used inducible knockdown technologies in P. falciparum and P. berghei to assess the role of PTEX88 in parasite development and protein export, which reveal that the in vivo growth of PTEX88-deficient parasites is hindered. Interestingly, we were unable to link this observation to a general defect in export of a variety of known parasite proteins, suggesting that PTEX88 functions in a different fashion to the core PTEX components. Strikingly, PTEX88-deficient P. berghei were incapable of causing cerebral malaria despite a robust pro-inflammatory response from the host. These parasites also exhibited a reduced ability to sequester in peripheral tissues and were removed more readily from the circulation by the spleen. In keeping with these findings, PTEX88-deficient P. falciparum-infected erythrocytes displayed reduced binding to the endothelial cell receptor, CD36. This suggests that PTEX88 likely plays a specific direct or indirect role in mediating parasite sequestration rather than making a universal contribution to the trafficking of all exported proteins.
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