ArticlePloS one2018
Knockdown of the translocon protein EXP2 in Plasmodium falciparum reduces growth and protein export.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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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
25 citing papers in PubMed, 38 citations in OpenAlex.
- The parasitophorous vacuole membrane of Toxoplasma gondii: A custom structural framing with smart interior plumbing for resource allocation.PLoS pathogens · 2026Review
- Targeting protein-protein interactions in Plasmodium: from asexual replication to sexual development.Parasites & vectors · 2026Review
- Article
- Detection of Developmental Asexual Stage-Specific RNA Editing Events inMicroorganisms · 2024Article
- Time-resolved proximity biotinylation implicates a porin protein in export of transmembrane malaria parasite effectors.Journal of cell science · 2023Article
- 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
- Timing of dense granule biogenesis in asexual malaria parasites.Microbiology (Reading, England) · 2023Article
- PTEX helps efficiently traffic haemoglobinases to the food vacuole in Plasmodium falciparum.PLoS pathogens · 2023Article
- Chemogenomic Profiling of a Plasmodium falciparum Transposon Mutant Library Reveals Shared Effects of Dihydroartemisinin and Bortezomib on Lipid Metabolism and Exported Proteins.Microbiology spectrum · 2023Article
- An Sfi1-like centrin-interacting centriolar plaque protein affects nuclear microtubule homeostasis.PLoS pathogens · 2023Article
- Dissecting EXP2 sequence requirements for protein export in malaria parasites.Frontiers in cellular and infection microbiology · 2023Article
- Article
- Dual role of an essential HtrA2/Omi protease in the human malaria parasite: Maintenance of mitochondrial homeostasis and induction of apoptosis-like cell death under cellular stress.PLoS pathogens · 2022Article
- The Plasmodium falciparum parasitophorous vacuole protein P113 interacts with the parasite protein export machinery and maintains normal vacuole architecture.Molecular microbiology · 2022Article
- 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
- Some conditions apply: Systems for studying Plasmodium falciparum protein function.PLoS pathogens · 2021Review
- The Role of Malaria Parasite Heat Shock Proteins in Protein Trafficking and Remodelling of Red Blood Cells.Advances in experimental medicine and biology · 2021Review
- Plasmodium falciparum parasites exit the infected erythrocyte after haemolysis with saponin and streptolysin O.Parasitology research · 2020Article
- The parasitophorous vacuole of the blood-stage malaria parasite.Nature reviews. Microbiology · 2020Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Malaria parasites remodel their host erythrocytes to gain nutrients and avoid the immune system. Host erythrocytes are modified by hundreds of effector proteins exported from the parasite into the host cell. Protein export is mediated by the PTEX translocon comprising five core components of which EXP2 is considered to form the putative pore that spans the vacuole membrane enveloping the parasite within its erythrocyte. To explore the function and importance of EXP2 for parasite survival in the asexual blood stage of Plasmodium falciparum we inducibly knocked down the expression of EXP2. Reduction in EXP2 expression strongly reduced parasite growth proportional to the degree of protein knockdown and tended to stall development about half way through the asexual cell cycle. Once the knockdown inducer was removed and EXP2 expression restored, parasite growth recovered dependent upon the length and degree of knockdown. To establish EXP2 function and hence the basis for growth reduction, the trafficking of an exported protein was monitored following EXP2 knockdown. This resulted in severe attenuation of protein export and is consistent with EXP2, and PTEX in general, being the conduit for export of proteins into the host compartment.
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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.