ArticleCommunications biology2020
Disrupting Plasmodium UIS3-host LC3 interaction with a small molecule causes parasite elimination from host cells.
Article in Communications biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 19 citations in OpenAlex.
- Article
- Hepatocyte Autophagy in Malaria: Current Concepts, Emerging Mechanisms, and Future Therapeutic Directions.Pathogens (Basel, Switzerland) · 2026Review
- The role of autophagy in protozoan infections.Frontiers in cellular and infection microbiology · 2026Review
- Elimination of intra-hepatocytic malaria parasites is driven by non-canonical autophagy but not nitric oxide production.iScience · 2025Article
- Article
- Theileria parasites sequester host eIF5A to escape elimination by host-mediated autophagy.Nature communications · 2024Article
- Drug discovery by targeting the protein-protein interactions involved in autophagy.Acta pharmaceutica Sinica. B · 2023Review
- Autophagy in protists and their hosts: When, how and why?Autophagy reports · 2023Article
- Article
- Plasmodium's fight for survival: escaping elimination while acquiring nutrients.Trends in parasitology · 2022Review
- Article
- Maria M. Mota: BringingFrontiers in cellular and infection microbiology · 2022Article
- The interplay between pathogens and Atg8 family proteins: thousand-faced interactions.FEBS open bio · 2021Review
- Targeting the Mitochondria-Proteostasis Axis to Delay Aging.Frontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The malaria parasite Plasmodium obligatorily infects and replicates inside hepatocytes surrounded by a parasitophorous vacuole membrane (PVM), which is decorated by the host-cell derived autophagy protein LC3. We have previously shown that the parasite-derived, PVM-resident protein UIS3 sequesters LC3 to avoid parasite elimination by autophagy from hepatocytes. Here we show that a small molecule capable of disrupting this interaction triggers parasite elimination in a host cell autophagy-dependent manner. Molecular docking analysis of more than 20 million compounds combined with a phenotypic screen identified one molecule, C4 (4-{[4-(4-{5-[3-(trifluoromethyl) phenyl]-1,2,4-oxadiazol-3-yl}benzyl)piperazino]carbonyl}benzonitrile), capable of impairing infection. Using biophysical assays, we established that this impairment is due to the ability of C4 to disrupt UIS3-LC3 interaction, thus inhibiting the parasite's ability to evade the host autophagy response. C4 impacts infection in autophagy-sufficient cells without harming the normal autophagy pathway of the host cell. This study, by revealing the disruption of a critical host-parasite interaction without affecting the host's normal function, uncovers an efficient anti-malarial strategy to prevent this deadly disease.
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Registered trials
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