ArticleNature communications2020
Plasmodium translocon component EXP2 facilitates hepatocyte invasion.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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.
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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
11 citing papers in PubMed, 17 citations in OpenAlex.
- CSP ubiquitylation favours Plasmodium berghei survival during early liver stage infection.Scientific reports · 2025Article
- Parasite and vector circadian clocks mediate efficient malaria transmission.Nature microbiology · 2025Article
- Flp/Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Subversion from Within and Without: Effector Molecule Transfer from Obligate Intracellular Apicomplexan Parasites to Human Host Cells.Results and problems in cell differentiation · 2024Review
- Membrane Proteins and Membrane Curvature: Mutual Interactions and a Perspective on Disease Treatments.Biomolecules · 2023Review
- Article
- Mid-Liver Stage Arrest ofFrontiers in cellular and infection microbiology · 2022Article
- Maria M. Mota: BringingFrontiers in cellular and infection microbiology · 2022Article
- Structured to conquer: transport across the Plasmodium parasitophorous vacuole.Current opinion in microbiology · 2021Review
- A single-cell atlas of Plasmodium falciparum transmission through the mosquito.Nature communications · 2021Article
- Transport mechanisms at the malaria parasite-host cell interface.PLoS pathogens · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Plasmodium parasites possess a translocon that exports parasite proteins into the infected erythrocyte. Although the translocon components are also expressed during the mosquito and liver stage of infection, their function remains unexplored. Here, using a combination of genetic and chemical assays, we show that the translocon component Exported Protein 2 (EXP2) is critical for invasion of hepatocytes. EXP2 is a pore-forming protein that is secreted from the sporozoite upon contact with the host cell milieu. EXP2-deficient sporozoites are impaired in invasion, which can be rescued by the exogenous administration of recombinant EXP2 and alpha-hemolysin (an S. aureus pore-forming protein), as well as by acid sphingomyelinase. The latter, together with the negative impact of chemical and genetic inhibition of acid sphingomyelinase on invasion, reveals that EXP2 pore-forming activity induces hepatocyte membrane repair, which plays a key role in parasite invasion. Overall, our findings establish a novel and critical function for EXP2 that leads to an active participation of the host cell in Plasmodium sporozoite invasion, challenging the current view of the establishment of liver stage infection.
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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 Socratic graph.