ArticleScientific reports2014
Antisense oligonucleotides targeting parasite inositol 1,4,5-trisphosphate receptor inhibits mammalian host cell invasion by Trypanosoma cruzi.
Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 22 citations in OpenAlex.
- Investigating the impact of HIS-1 and HSP-70 genes on drug response and pathology of Leishmania major using antisense oligonucleotides.Antonie van Leeuwenhoek · 2025Article
- Development of Antisense Tools to Study Bodo saltans and Its Intracellular Symbiont.MicrobiologyOpen · 2025Article
- Antisense Therapy for Infectious Diseases.Cells · 2023Review
- Interaction With the Extracellular Matrix Triggers Calcium Signaling inFrontiers in cellular and infection microbiology · 2021Article
- InsP3 Signaling in Apicomplexan Parasites.Current topics in medicinal chemistry · 2017Review
- Inositol 1,4,5-trisphosphate receptor determines intracellular CaFEBS open bio · 2016Article
- Antisense antimicrobial therapeutics.Current opinion in microbiology · 2016Review
- Neglected tropical diseases in the genomics era: re-evaluating the impact of new drugs and mass drug administration.Genome biology · 2016Article
- Calcium signaling in trypanosomatid parasites.Cell calcium · 2015Review
- The role of antisense oligonucleotide therapy in patients with familial hypercholesterolemia: risks, benefits, and management recommendations.Current atherosclerosis reports · 2015Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chagas disease is caused by an intracellular parasitic protist, Trypanosoma cruzi. As there are no highly effective drugs against this agent that also demonstrate low toxicity, there is an urgent need for development of new drugs to treat Chagas disease. We have previously demonstrated that the parasite inositol 1,4,5-trisphosphate receptor (TcIP3R) is crucial for invasion of the mammalian host cell by T. cruzi. Here, we report that TcIP3R is a short-lived protein and that its expression is significantly suppressed in trypomastigotes. Treatment of trypomastigotes, an infective stage of T. cruzi, with antisense oligonucleotides specific to TcIP3R deceased TcIP3R protein levels and impaired trypomastigote invasion of host cells. Due to the resulting instability and very low expression level of TcIP3R in trypomastigotes indicates that TcIP3R is a promising target for antisense therapy in Chagas disease.
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Registered trials
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