ArticleProceedings of the National Academy of Sciences of the United States of America2001
Trypanosoma cruzi trans-sialidase: a potent and specific survival factor for human Schwann cells by means of phosphatidylinositol 3-kinase/Akt signaling.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 88 citations in OpenAlex.
- PI3K/AKT signaling in parasites and parasite diseases: Role and therapeutic potential.Virulence · 2025Review
- The pathogenicity and virulence of Leishmania - interplay of virulence factors with host defenses.Virulence · 2022Review
- Immune and Genomic Analysis of Boxer Dog Breed and Its Relationship withVeterinary sciences · 2022Article
- Modulation of miR-145-5p and miR-146b-5p levels is linked to reduced parasite load in H9C2 Trypanosoma cruzi infected cardiomyoblasts.Scientific reports · 2022Article
- Complementary crosstalk between palmitoylation and phosphorylation events in MTIP regulates its role duringFrontiers in cellular and infection microbiology · 2022Article
- All Roads Lead to Cytosol:Frontiers in cellular and infection microbiology · 2021Review
- Transcriptional Studies onFrontiers in cellular and infection microbiology · 2021Review
- Article
- Search of Allosteric Inhibitors and Associated Proteins of an AKT-International journal of molecular sciences · 2018Article
- EarlyFrontiers in microbiology · 2018Article
- Role of Inactive and ActiveFrontiers in microbiology · 2017Article
- Transcriptome Remodeling in Trypanosoma cruzi and Human Cells during Intracellular Infection.PLoS pathogens · 2016Article
- Mir-190b negatively contributes to the Trypanosoma cruzi-infected cell survival by repressing PTEN protein expression.Memorias do Instituto Oswaldo Cruz · 2015Article
- PTEN inhibitor bisperoxovanadium protects oligodendrocytes and myelin and prevents neuronal atrophy in adult rats following cervical hemicontusive spinal cord injury.Neuroscience letters · 2014Article
- Mechanisms of cellular invasion by intracellular parasites.Cellular and molecular life sciences : CMLS · 2014Review
- Host metabolism regulates intracellular growth of Trypanosoma cruzi.Cell host & microbe · 2013Article
- Multigene families in Trypanosoma cruzi and their role in infectivity.Infection and immunity · 2012Review
- Toll-like receptor-2 and interleukin-6 mediate cardiomyocyte protection from apoptosis during Trypanosoma cruzi murine infection.Medical microbiology and immunology · 2012Article
- Current understanding of the Trypanosoma cruzi-cardiomyocyte interaction.Frontiers in immunology · 2012Article
- Sialic acid: a sweet swing between mammalian host and Trypanosoma cruzi.Frontiers in immunology · 2012Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Patients infected with Trypanosoma cruzi may remain asymptomatic for decades and show signs of neuroregeneration in the peripheral nervous system (PNS). In the absence of such neuroregeneration, patients may die in part by extensive neuronal destruction in the gastrointestinal tract. Thus, T. cruzi may, despite their invasion of the PNS, directly prevent cell death to keep nerve destruction in check. Indeed, T. cruzi invasion of Schwann cells, their prime target in PNS, suppressed host-cell apoptosis caused by growth-factor deprivation. The trans-sialidase (TS) of T. cruzi and the Cys-rich domain of TS reproduced the antiapoptotic activity of the parasites at doses (> or =3.0 nM) comparable or lower than those of bona fide mammalian growth factors. This effect was blocked by LY294002, an inhibitor of phosphatidylinositol 3-kinase (PI3K). TS also activated Akt, a downstream effector of PI3K. Ectopic expression of TS in an unrelated parasite, Leishmania major, turned those parasites into activators of Akt in Schwann cells. In contrast, the Cys-rich domain of TS did not block apoptosis in Schwann cells overexpressing dominant-negative Akt or constitutively active PTEN, a negative regulator of PI3K/Akt signaling. The results demonstrate that T. cruzi, through its TS, triggers the survival of host Schwann cells via the PI3K/Akt pathway, suggesting a role for PI3K/Akt in the pathogenesis of Chagas' disease.
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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.