chagas disease/tyrosine

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Structure of the Trypanosoma cruzi protein tyrosine phosphatase TcPTP1, a potential therapeutic target for Chagas' disease.

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Chagas' disease, a neglected tropical affliction transmitted by the flagellated protozoan Trypanosoma cruzi, is prevalent in Latin America and affects nearly 18 million people worldwide, yet few approved drugs are available to treat the disease. Moreover, the currently available drugs exhibit severe

Auto-antibodies to receptor tyrosine kinases TrkA, TrkB and TrkC in patients with chronic Chagas' disease.

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The Chagas' disease parasite Trypanosoma cruzi promotes survival and differentiation of neurones by binding and activating nerve growth factor (NGF) receptor TrkA. The functional mimic of NGF in T. cruzi is a surface-bound and shed immunogenic protein [neurotrophic factor/trans-sialidase (TS)],

The Chagas' disease parasite Trypanosoma cruzi exploits nerve growth factor receptor TrkA to infect mammalian hosts.

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Trypanosoma cruzi, the agent of Chagas' disease, is an obligate intracellular parasite that invades various organs including several cell types in the nervous system that express the Trk receptor tyrosine kinase. Activation of Trk is a major cell-survival and repair mechanism, and parasites could

Trypanosoma cruzi-induced tyrosine phosphorylation in murine peritoneal macrophages.

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Trypanosoma cruzi, the etiological agent of Chagas' disease, binds to and invades macrophages and other cells (fibroblasts, muscle cells) via a complicated set of interactions, but the changes induced by parasite-to-cell interactions are largely unknown. This report investigates the ability of T.

The Non-Canonical Substrates of Trypanosoma cruzi Tyrosine and Aspartate Aminotransferases: Branched-Chain Amino Acids.

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Trypanosoma cruzi, the etiological agent of Chagas disease, lacks genes that encode canonical branched-chain aminotransferases. However, early studies showed that when epimastigotes were grown in the presence of 14 C1 -DL-leucine, the label was incorporated into various intermediates. More recently,

Trypanosoma cruzi: characterisation of the gene encoding tyrosine aminotransferase in benznidazole-resistant and susceptible populations.

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Various biochemical differences exist between mammalian tyrosine aminotransferase (TAT) and its analogue in Trypanosoma cruzi (TcTAT), the causative agent of Chagas disease. Moreover, TcTAT is over-expressed in strains of the parasite that are resistant to benznidazole (BZ), a drug currently used in

Enhancement of tyrosine hydroxylase expression and activity by Trypanosoma cruzi parasite-derived neurotrophic factor.

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A parasite-derived protein, PDNF, produced by the Chagas' disease agent Trypanosoma cruzi, functionally mimics mammalian neurotrophic factors by delaying apoptotic death and promoting survival and differentiation of neurons, including dopaminergic cells, through the activation of nerve growth factor

Human autoantibodies specific for neurotrophin receptors TrkA, TrkB, and TrkC protect against lethal Trypanosoma cruzi infection in mice.

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Patients with Chagas' disease remain asymptomatic for many years, presumably by keeping the etiological agent Trypanosoma cruzi in check through protective immunity against. Recently, we found that T. cruzi uses TrkA, a receptor tyrosine kinase responsive to neurotrophin nerve growth factor in

Chagas' disease parasite-derived neurotrophic factor activates cholinergic gene expression in neuronal PC12 cells.

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A parasite-derived neurotrophic factor (PDNF) produced by the Chagas' disease parasite Trypanosoma cruzi binds nerve growth factor (NGF) receptor TrkA, increasing receptor autophosphorylation, and activating phosphatidylinositol 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK/Erk)

Comprehensive analysis of three TYK2 gene variants in the susceptibility to Chagas disease infection and cardiomyopathy.

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Tyrosine kinase 2 (TYK2) is a member of the Janus kinases family implicated in the signal transduction of type I interferons and several interleukins. It has been described that genetic mutations within TYK2 lead to multiple deleterious effects in the immune response. In this work, we have analyzed

Neurodegeneration and neuroregeneration in Chagas disease.

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Autonomic dysfunction plays a significant role in the development of chronic Chagas disease (CD). Destruction of cardiac parasympathetic ganglia can underlie arrhythmia and heart failure, while lesions of enteric neurons in the intestinal plexuses are a direct cause of aperistalsis and

Association study of PTPN22 C1858T polymorphism in Trypanosoma cruzi infection.

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In this study we investigated a possible role for the single nucleotide polymorphism C1858T of the PTPN22 (protein tyrosine phosphatase nonreceptor 22) gene in determining the susceptibility to Trypanosoma cruzi infection, as well as in development of chagasic heart disease. This study included 316

Differential expression of Trypanosoma cruzi I associated with clinical forms of Chagas disease: overexpression of oxidative stress proteins in acute patient isolate.

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Chagas disease has a variable clinical course with different manifestations and heterogenous geographical distribution. Some studies suggest that this clinical variability could be influenced by the genetic variability of T. cruzi. Here we present the differential protein expression among

Biochemical characterization of a protein tyrosine phosphatase from Trypanosoma cruzi involved in metacyclogenesis and cell invasion.

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Protein tyrosine phosphatases (PTPs) form a large family of enzymes involved in the regulation of numerous cellular functions in eukaryotes. Several protein tyrosine phosphatases have been recently identified in trypanosomatides. Here we report the purification and biochemical characterization of

Global metabolomic profiling of acute myocarditis caused by Trypanosoma cruzi infection.

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Chagas disease is caused by Trypanosoma cruzi infection, being cardiomyopathy the more frequent manifestation. New chemotherapeutic drugs are needed but there are no good biomarkers for monitoring treatment efficacy. There is growing evidence linking immune response and metabolism in inflammatory

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