ArticleScientific reports2016
Biliverdin targets enolase and eukaryotic initiation factor 2 (eIF2α) to reduce the growth of intraerythrocytic development of the malaria parasite Plasmodium falciparum.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- The first de novo genome assembly and annotation of a green-blooded skink (Prasinohaema aff. flavipes) from a historic museum sample.The Journal of heredity · 2025Article
- A metabolite-based resistance mechanism against malaria.Science (New York, N.Y.) · 2025Article
- Babesia, Theileria, Plasmodium and Hemoglobin.Microorganisms · 2022Article
- Discovery and evaluation of inhibitory activity and mechanism of arylcoumarin derivatives on Theileria annulata enolase by in vitro and molecular docking studies.Molecular diversity · 2020Article
- Article
- Porphyrin Derivative Nanoformulations for Therapy and Antiparasitic Agents.Molecules (Basel, Switzerland) · 2020Review
- Evidence for Regulation of Hemoglobin Metabolism and Intracellular Ionic Flux by the Plasmodium falciparum Chloroquine Resistance Transporter.Scientific reports · 2018Article
- Multiple origins of green blood in New Guinea lizards.Science advances · 2018Article
- Functions of tryptophan residues in EWGWS insert ofFEBS open bio · 2017Article
- Immunolocation and enzyme activity analysis of Cryptosporidium parvum enolase.Parasites & vectors · 2017Article
- Complete Molecular and Immunoprotective Characterization ofFrontiers in microbiology · 2017Article
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
In mammals, haem degradation to biliverdin (BV) through the action of haem oxygenase (HO) is a critical step in haem metabolism. The malaria parasite converts haem into the chemically inert haemozoin to avoid toxicity. We discovered that the knock-out of HO in P. berghei is lethal; therefore, we investigated the function of biliverdin (BV) and haem in the parasite. Addition of external BV and haem to P. falciparum-infected red blood cell (RBC) cultures delays the progression of parasite development. The search for a BV molecular target within the parasites identified P. falciparum enolase (Pf enolase) as the strongest candidate. Isothermal titration calorimetry using recombinant full-length Plasmodium enolase suggested one binding site for BV. Kinetic assays revealed that BV is a non-competitive inhibitor. We employed molecular modelling studies to predict the new binding site as well as the binding mode of BV to P. falciparum enolase. Furthermore, addition of BV and haem targets the phosphorylation of Plasmodium falciparum eIF2α factor, an eukaryotic initiation factor phosphorylated by eIF2α kinases under stress conditions. We propose that BV targets enolase to reduce parasite glycolysis rates and changes the eIF2α phosphorylation pattern as a molecular mechanism for its action.
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