ArticleMolecular biology of the cell2000
A trypanosomal protein synergizes with the cytokines ciliary neurotrophic factor and leukemia inhibitory factor to prevent apoptosis of neuronal cells.
Article in Molecular biology of the cell, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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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
29 citing papers in PubMed, 76 citations in OpenAlex.
- PI3K/AKT signaling in parasites and parasite diseases: Role and therapeutic potential.Virulence · 2025Review
- Apoptosis and its pathways as targets for intracellular pathogens to persist in cells.Parasitology research · 2023Review
- Effects of the PI3K/Akt signaling pathway on the apoptosis of early host cells infected with Eimeria tenella.Parasitology research · 2020Article
- Article
- Parasite-derived neurotrophic factor/trans-sialidase of Trypanosoma cruzi links neurotrophic signaling to cardiac innate immune response.Infection and immunity · 2014Article
- Trypanosoma cruzi highjacks TrkC to enter cardiomyocytes and cardiac fibroblasts while exploiting TrkA for cardioprotection against oxidative stress.Cellular microbiology · 2013Article
- Trypanosoma cruzi coaxes cardiac fibroblasts into preventing cardiomyocyte death by activating nerve growth factor receptor TrkA.PloS one · 2013Article
- Multigene families in Trypanosoma cruzi and their role in infectivity.Infection and immunity · 2012Review
- Sialic acid: a sweet swing between mammalian host and Trypanosoma cruzi.Frontiers in immunology · 2012Article
- Neurotrophin receptor TrkC is an entry receptor for Trypanosoma cruzi in neural, glial, and epithelial cells.Infection and immunity · 2011Article
- Protein kinase A catalytic subunit interacts and phosphorylates members of trans-sialidase super-family in Trypanosoma cruzi.Microbes and infection · 2010Article
- Trypanosoma cruzi-Derived Neurotrophic Factor: Role in Neural Repair and Neuroprotection.Journal of neuroparasitology · 2010Article
- Trypanosoma cruzi targets Akt in host cells as an intracellular antiapoptotic strategy.Science signaling · 2009Article
- The surface-anchored NanA protein promotes pneumococcal brain endothelial cell invasion.The Journal of experimental medicine · 2009Article
- Perspectives on the Trypanosoma cruzi-host cell receptor interactions.Parasitology research · 2009Review
- Trypanosoma cruzi promotes neuronal and glial cell survival through the neurotrophic receptor TrkC.Infection and immunity · 2009Article
- Human autoantibodies specific for neurotrophin receptors TrkA, TrkB, and TrkC protect against lethal Trypanosoma cruzi infection in mice.The American journal of pathology · 2008Article
- A novel immunoprecipitation strategy identifies a unique functional mimic of the glial cell line-derived neurotrophic factor family ligands in the pathogen Trypanosoma cruzi.Infection and immunity · 2008Article
- Chagas' disease parasite-derived neurotrophic factor activates cholinergic gene expression in neuronal PC12 cells.Brain research · 2008Article
- Auto-antibodies to receptor tyrosine kinases TrkA, TrkB and TrkC in patients with chronic Chagas' disease.Scandinavian journal of immunology · 2008Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Despite the neuronal degeneration in the chronic stage of Chagas' disease, neuron counts actually increase in the preceding, asymptomatic stage, in contrast to the age-related decrease in neuron counts in age-matched normal individuals. Relevant to this observation, we found that the trans-sialidase (TS) of Trypanosoma cruzi, the etiologic agent of Chagas' disease, induces neurite outgrowth and rescues PC12 cells from apoptotic death caused by growth factor deprivation. These properties, novel for a parasite protein, were independent of catalytic activity and were mapped to the C terminus of the catalytic domain of TS. TS activated protein kinase Akt in a phosphoinositide-3 kinase-inhibitable manner, suggesting a molecular mechanism for the TS-induced neuroprotection. TS also triggered bcl-2 gene expression in growth factor-deprived cells, an effect consistent with TS protecting against apoptosis. Ciliary neurotrophic factor and leukemia inhibitory factor, two cytokines critical to the repair of injured motor neurons, specifically potentiated the TS action. The results suggest that TS acts in synergy with host ciliary neurotrophic factor or leukemia inhibitory factor to promote neuronal survival in T. cruzi-infected individuals.
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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.