Trypanosoma cruzi
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REPOSITORIES: ENA
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Project description:Trypanosoma cruzi is a protozoan parasite that causes Chagas’ disease in humans and throughout its life cycle faces different environment changes. Protein methylation is an important post-translational modification by which cells respond and adapt to the environment. To understand the importance of protein methylation in T.cruzi biology, we applied mass spectrometry-based proteomics and report the first proteomic analysis of both arginine and lysine methylproteome in T. cruzi.
2023-05-15 | PXD034140 | Pride
Project description:Trypanosoma cruzi is an obligate intracellular protozoan parasite that causes human Chagas’ disease, a leading cause of heart failure in Latin America. Using Affymetrix oligonucleotide arrays we screened phenotypically diverse human cells (foreskin fibroblasts, microvascular endothelial cells and vascular smooth muscle cells) for a common transcriptional response signature to T. cruzi. A common feature was a prominent type I interferon response, indicative of a secondary response to secreted cytokines. Using transwell plates to distinguish cytokine-dependent and -independent gene expression profiles in T. cruzi-infected cells, a core cytokine-independent response was identified in fibroblasts and endothelial cells that featured metabolic and signaling pathways involved in cell proliferation, amino acid catabolism and response to wounding. Significant downregulation of genes involved in mitotic cell cycle and cell division predicted that T. cruzi infection impedes cell cycle progression in the host cell.
2009-06-04 | GSE13791 | GEO
Project description:This laboratory is focusing on to clarify the biologic relevance of a virulence factor known as trans-sialidase from Trypanosoma cruzi, the agent of the Chagas disease (American trypanosomiasis).
2011-02-04 | GSE27054 | GEO
Project description:This laboratory is focusing on to clarify the biologic relevance of a virulence factor known as trans-sialidase from Trypanosoma cruzi, the agent of the Chagas disease (American trypanosomiasis).
2011-02-17 | GSE27353 | GEO
Project description:Trypanosoma cruzi is a protozoan parasite and the etiologic agent of Chagas disease, an important public health problem in Latin America. T. cruzi is diploid, almost exclusively asexual, and displays an extraordinarily diverse population structure both genetically and phenotypically. Yet, to date the genotypic diversity of T. cruzi and its relationship, if any, to biological diversity have not been studied at the whole genome level. In this study, we used whole genome oligonucleotide tiling arrays to compare gene content in biologically disparate T. cruzi strains by comparative genomic hybridization (CGH). We observed that T. cruzi strains display widespread and focal copy number variations (CNV) and a substantially greater level of diversity than can be adequately defined by the current genetic typing methods. As expected, CNV were particularly frequent in gene family-rich regions containing mucins and trans-sialidases but were also evident in core genes. Gene groups that showed little variation in copy numbers among the strains tested included those encoding protein kinases and ribosomal proteins, suggesting these loci were less permissive to CNV. Moreover, frequent variation in chromosome copy numbers were observed, and chromosome-specific CNV signatures were shared by genetically divergent T. cruzi strains, suggesting a greater degree of chromosome exchange than previously thought.
2011-08-06 | GSE23576 | GEO
Project description:This laboratory is focusing on to clarify the biologic relevance of a virulence factor known as trans-sialidase from Trypanosoma cruzi, the agent of the Chagas disease (American trypanosomiasis). We are working with an enzyme able to directly transfer sialyl residues among macromolecules known as the trans-sialidase. It constitutes a virulence factor from Trypanosoma cruzi, the agent of the Chagas' Disease the American trypanosomiasis. We described the ability of this virulence factor to induce thymocyte apoptosis in vivo that happens after silayl residue mobilization. The apoptosis is mediated by the thymic epithelial cells in the nurse cell complex. By employing the microarray approach we wish to analyze the gene expression induced in the thymus after TS treatment. Examination of differential expression in thymocytes between male and female mice of genes related to glycosylation. RNA samples (in triplicate) purified from thymocytes were analyzed by Glyco-gene Chip analysis.
2011-02-04 | E-GEOD-27054 | biostudies-arrayexpress
Project description:The short non-coding transcriptome of the protozoan parasite Trypanosoma cruzi
| PRJDB2604 | ENA
Project description:Chagas disease is a parasitic infection originally endemic to latinamerican countries but now spreaded worldwide that can be transmitted congenitally. Current specific therapy involves benznidazole, however, other therapies may modify gene expression that can change genetic expression profile, allowing cell programming to provide a more unfavorable environment for intracellular parasite development. Herein, microarray analysis was performed to Human Umbilical Vein Endothelial Cells (HUVEC), treated with benznidazole and the anti-inflammatory drugs aspirin or simvastatin, and infected with T. cruzi, the causative agent of Chagas disease.
2019-03-14 | GSE128270 | GEO
Project description:Chagas’ disease, one of the major public health concerns in Latin America, is caused by the haemophlagelated protozoan Trypanosoma cruzi (T. cruzi). In the past few years congenital transmission of T. cruzi has become more important, and partly responsible for the “globalization of Chagas’ disease”. The congenital transmission, although with low rates, represents the main route of transmission in non-endemic countries and endemic countries without vectorial transmission, and represents one third of the new cases each year. Diverse pathogens, including T. cruzi, are able to cross the placental barrier and infect both the placenta and fetus. However, the exact cellular and molecular mechanisms of host-pathogen interaction between T. cruzi and the placenta has been scarcely studied. The use of microarray analysis to determine expression profiles constitutes a powerful tool in order to identify genes and pathways related to the host response to infections. Here, we analyzed the transcriptomic response of human placental chorionic villi explants (HPCVE) challenged with T. cruzi trypomastigotes at low (105) and high (106) concentrations for 2 and 24 hours
2018-04-17 | GSE113155 | GEO
Project description:Trypanosoma cruzi is a protozoan parasite and the etiologic agent of Chagas disease, an important public health problem in Latin America. T. cruzi is diploid, almost exclusively asexual, and displays an extraordinarily diverse population structure both genetically and phenotypically. Yet, to date the genotypic diversity of T. cruzi and its relationship, if any, to biological diversity have not been studied at the whole genome level. In this study, we used whole genome oligonucleotide tiling arrays to compare gene content in biologically disparate T. cruzi strains by comparative genomic hybridization (CGH). We observed that T. cruzi strains display widespread and focal copy number variations (CNV) and a substantially greater level of diversity than can be adequately defined by the current genetic typing methods. As expected, CNV were particularly frequent in gene family-rich regions containing mucins and trans-sialidases but were also evident in core genes. Gene groups that showed little variation in copy numbers among the strains tested included those encoding protein kinases and ribosomal proteins, suggesting these loci were less permissive to CNV. Moreover, frequent variation in chromosome copy numbers were observed, and chromosome-specific CNV signatures were shared by genetically divergent T. cruzi strains, suggesting a greater degree of chromosome exchange than previously thought. Genomic DNA samples from 16 T. cruzi strains were compared to genomic DNA from the CL Brener strain by competitive hybridizations on whole genome oligonucleotide tiling arrays.
2011-08-05 | E-GEOD-23576 | biostudies-arrayexpress