ArticleMolecular microbiology2020
A Plasmodium homolog of ER tubule-forming proteins is required for parasite virulence.
Article in Molecular microbiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 7 citations in OpenAlex.
- The long and winding road: On the endoplasmic reticulum of Plasmodium and implications for pathogenesis.PLoS pathogens · 2026Review
- Deciphering Membrane Protein Complexes in Plasmodium falciparum Gametocytes via Integrative Structural Systems Biology.Molecular & cellular proteomics : MCP · 2026Article
- Long-term survival ofMicrobiology spectrum · 2025Article
- Oligomeric scaffolding for curvature generation by ER tubule-forming proteins.Nature communications · 2023Article
- Mannose inhibitsFrontiers in immunology · 2022Article
- Attenuated T Cell Responses Are Associated With the Blockade of Cerebral Malaria Development by YOP1-DeficientFrontiers in immunology · 2021Article
- A Plasmodium homolog of ER tubule-forming proteins is required for parasite virulence.Molecular microbiology · 2020Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Reticulon and REEP family of proteins stabilize the high curvature of endoplasmic reticulum (ER) tubules. Plasmodium berghei Yop1 (PbYop1) is a REEP5 homolog in Plasmodium. Here, we characterize its function using a gene-knockout (Pbyop1∆). Pbyop1∆ asexual stage parasites display abnormal ER architecture and an enlarged digestive vacuole. The erythrocytic cycle of Pbyop1∆ parasites is severely attenuated and the incidence of experimental cerebral malaria is significantly decreased in Pbyop1∆-infected mice. Pbyop1∆ sporozoites have reduced speed, are slower to invade host cells but give rise to equal numbers of infected HepG2 cells, as WT sporozoites. We propose that PbYOP1's disruption may lead to defects in trafficking and secretion of a subset of proteins required for parasite development and invasion of erythrocytes. Furthermore, the maintenance of ER morphology in different parasite stages is likely to depend on different proteins.
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Registered trials
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