ArticleNature communications2015
Asparagine requirement in Plasmodium berghei as a target to prevent malaria transmission and liver infections.
Article in Nature communications, 2015. 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.
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Who cites it
10 citing papers in PubMed, 23 citations in OpenAlex.
- Structural and functional insights from detailed computational analysis ofJournal of genetics · 2026Article
- An Unusually Mild Imported Case of Falciparum Malaria That Was Diagnosed and Successfully Treated during Concurrent Acute Leukemia Chemotherapy in Japan.The American journal of tropical medicine and hygiene · 2025Article
- Distinct evolution of type I glutamine synthetase in Plasmodium and its species-specific requirement.Nature communications · 2023Article
- Characterization of Apicomplexan Amino Acid Transporters (ApiATs) in the Malaria Parasite Plasmodium falciparum.mSphere · 2021Article
- Amino Acid Metabolism in Apicomplexan Parasites.Metabolites · 2021Review
- Diverse single-amino-acid repeat profiles in the genus Cryptosporidium.Parasitology · 2018Article
- Article
- Cationic amino acid transporters play key roles in the survival and transmission of apicomplexan parasites.Nature communications · 2017Article
- Potential Hemoglobin A/F role in clinical Malaria.Bioinformation · 2017Article
- Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The proteins of Plasmodium, the malaria parasite, are strikingly rich in asparagine. Plasmodium depends primarily on host haemoglobin degradation for amino acids and has a rudimentary pathway for amino acid biosynthesis, but retains a gene encoding asparagine synthetase (AS). Here we show that deletion of AS in Plasmodium berghei (Pb) delays the asexual- and liver-stage development with substantial reduction in the formation of ookinetes, oocysts and sporozoites in mosquitoes. In the absence of asparagine synthesis, extracellular asparagine supports suboptimal survival of PbAS knockout (KO) parasites. Depletion of blood asparagine levels by treating PbASKO-infected mice with asparaginase completely prevents the development of liver stages, exflagellation of male gametocytes and the subsequent formation of sexual stages. In vivo supplementation of asparagine in mice restores the exflagellation of PbASKO parasites. Thus, the parasite life cycle has an absolute requirement for asparagine, which we propose could be targeted to prevent malaria transmission and liver infections.
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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 OpenQuestion graph.