ArticleThe Journal of eukaryotic microbiology
Inositolphosphoceramide metabolism in Trypanosoma cruzi as compared with other trypanosomatids.
Article in The Journal of eukaryotic microbiology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Article
- Changes in lipid abundance are associated with disease progression and treatment response in chronic Trypanosoma cruzi infection.Parasites & vectors · 2024Article
- The Glycosylphosphatidylinositol Anchor: A Linchpin for Cell Surface Versatility of Trypanosomatids.Frontiers in cell and developmental biology · 2021Review
- Extracellular Vesicles: Potential Role in Remote Signaling and Inflammation inFrontiers in cell and developmental biology · 2021Review
- Genome-scale metabolic models highlight stage-specific differences in essential metabolic pathways in Trypanosoma cruzi.PLoS neglected tropical diseases · 2020Article
- Article
- Everybody needs sphingolipids, right! Mining for new drug targets in protozoan sphingolipid biosynthesis.Parasitology · 2018Review
- Comparative sphingolipidomics of disease-causing trypanosomatids reveal unique lifecycle- and taxonomy-specific lipid chemistries.Scientific reports · 2017Article
- Identification and functional analysis of Trypanosoma cruzi genes that encode proteins of the glycosylphosphatidylinositol biosynthetic pathway.PLoS neglected tropical diseases · 2013Article
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Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
Abstract
Chagas disease is caused by Trypanosoma cruzi and is endemic to North, Central and South American countries. Current therapy against this disease is only partially effective and produces adverse side effects. Studies on the metabolic pathways of T. cruzi, in particular those with no equivalent in mammalian cells, might identify targets for the development of new drugs. Ceramide is metabolized to inositolphosphoceramide (IPC) in T. cruzi and other kinetoplastid protists whereas in mammals it is mainly incorporated into sphingomyelin. In T. cruzi, in contrast to Trypanosoma brucei and Leishmania spp., IPC functions as lipid anchor constituent of glycoproteins and free glycosylinositolphospholipids (GIPLs). Inhibition of IPC and GIPLs biosynthesis impairs differentiation of trypomastigotes into the intracellular amastigote forms. The gene encoding IPC synthase in T. cruzi has been identified and the enzyme has been expressed in a cell-free system. The enzyme involved in IPC degradation and the remodelases responsible for the incorporation of ceramide into free GIPLs or into the glycosylphosphatidylinositols anchoring glycoproteins, and in fatty acid modifications of these molecules of T. cruzi have been understudied. Inositolphosphoceramide metabolism and remodeling could be exploited as targets for Chagas disease chemotherapy.
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