ArticleTraffic (Copenhagen, Denmark)2014
Host PI(3,5)P2 activity is required for Plasmodium berghei growth during liver stage infection.
Article in Traffic (Copenhagen, Denmark), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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.
The trial behind it
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
10 citing papers in PubMed.
- PIKfyve mediates the maturation of mycobacteria-containing vesicles.Frontiers in cellular and infection microbiology · 2026Article
- Autophagy in protists and their hosts: When, how and why?Autophagy reports · 2023Article
- Plasmodium's fight for survival: escaping elimination while acquiring nutrients.Trends in parasitology · 2022Review
- Plasmodium berghei sporozoites in nonreplicative vacuole are eliminated by a PI3P-mediated autophagy-independent pathway.Cellular microbiology · 2021Article
- Host cell cytosolic immune response during Plasmodium liver stage development.FEMS microbiology reviews · 2018Review
- Malaria Parasite Liver Infection and Exoerythrocytic Biology.Cold Spring Harbor perspectives in medicine · 2017Review
- Shedding of host autophagic proteins from the parasitophorous vacuolar membrane of Plasmodium berghei.Scientific reports · 2017Article
- Sequestration of cholesterol within the host late endocytic pathway restricts liver-stageMolecular biology of the cell · 2017Article
- Article
- Selection and refinement: the malaria parasite's infection and exploitation of host hepatocytes.Current opinion in microbiology · 2015Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Malaria parasites go through an obligatory liver stage before they infect erythrocytes and cause disease symptoms. In the host hepatocytes, the parasite is enclosed by a parasitophorous vacuole membrane (PVM). Here, we dissected the interaction between the Plasmodium parasite and the host cell late endocytic pathway and show that parasite growth is dependent on the phosphoinositide 5-kinase (PIKfyve) that converts phosphatidylinositol 3-phosphate [PI(3)P] into phosphatidylinositol 3,5-bisphosphate [PI(3,5)P2 ] in the endosomal system. We found that inhibition of PIKfyve by either pharmacological or non-pharmacological means causes a delay in parasite growth. Moreover, we show that the PI(3,5)P2 effector protein TRPML1 that is involved in late endocytic membrane fusion, is present in vesicles closely contacting the PVM and is necessary for parasite growth. Thus, our studies suggest that the parasite PVM is able to fuse with host late endocytic vesicles in a PI(3,5)P2 -dependent manner, allowing the exchange of material between the host and the parasite, which is essential for successful infection.
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What OpenQuestion holds
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 OpenQuestion graph.