Trypanosoma rangeli
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA18957 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| AUPL01.dat.gz | Other | |||
| AUPL01.fasta.gz | Fasta.gz | |||
| AUPL01.master.dat | Other |
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Similar Datasets
Project description:A non-pathogenic human parasite in Latin America
| PRJNA18959 | ENA
Project description:A non-pathogenic human parasite in Latin America
| PRJNA18945 | ENA
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: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: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
Project description:Genetic diversity of Human Metapneumovirus in Latin America
| PRJNA237298 | ENA
Project description:Trypanosoma cruzi is the protozoan that causes Chagas disease, an endemic parasitosis in Latin America that has spread around the globe. Recently, a series of studies indicate that the gastrointestinal tract represents an important reservoir for T. cruzi in the chronic phase. It is also known that, during contact between T. cruzi and host cells, there is a release of extracellular vesicles (EVs) that modulates the immune system and enhances the infection, but the dynamics of secretion of host and parasite molecules through these EVs is not understood. In this study, we used two cell lines to simulate the environments found by the parasite in the host: C2C12 cell (myoblast) and Caco-2 cell (intestinal epithelium). We isolated large EVs (LEVs) from the interaction of T. cruzi culture-derived trypomastigotes (TCTs) belonging to two distinct strains (CL Brener, DTU Tc VI and Dm28c DTU Tc I) in contact with C2C12 and Caco-2 cells to 2 hours and after 24 hours of infection. The interaction of the parasite with the host cell induces a switch in the functionality of proteins carried by LEVs and a varied tissue answer. Protein-protein interaction analysis indicates that LEVs carry key proteins for host-pathogen interaction that could participate in the pathogenesis of Chagas Disease.
2024-05-17 | PXD046906 | Pride
Project description:Chagas disease is one of the most lethal diseases in Latin America, but currently it has become a global health problem because of migration. It is caused by the parasite Trypanosoma cruzi (T. cruzi), an intracellular flagellated protist whose life cycle has been defined in detail, although the immunopathology of its infection is still quite unknown. Moreover, there are differences in pathogenicity between the strains in mice, Y produces a high lethality while VFRA remains in the host in a most chronic manner. Comparative proteomics studies between T. cruzi strains have not been performed extensively, they should allow the detection of relevant virulent factors or distinctive functions. We focused on the proteome analysis of trypomastigotes of Y and VFRA strains by mass spectrometry followed by gene ontology analysis to display similarities or differences in cellular components, biological processes and molecular functions. Also, we performed metabolic pathways enrichment analysis to see the most relevant pathways in each strain. There were a 20% of different proteins showing that Y strain has specific proteins for replication and growth, while VFRA for localization or transport, among others. We found a very similar profile in the different ontology groups, but with some punctual differences. We detected enriched antioxidant defenses in VFRA that could correlate with its behavior of chronic infection in mice controlling the ROS production, while Y strain displayed a great enrichment of pathways related with nucleotides and protein production, explaining the high parasite load and lethality of this strain.
2019-09-25 | PXD012536 | Pride
Project description:Trypanosoma cruzi is the causal agent of Chagas’ disease, which is one of the biggest public health problems in Latin America. Several post-translational modifications (PTM) have been studied in T. cruzi but there is no work focused on the O-GlcNAcylation, which is a highly conserved monosaccharide PTM found on serine and threonine residues of proteins mainly from the nucleus, cytoplasm and mitochondria. It is thought to regulate proteins in a manner analogous to protein phosphorylation, even their crosstalk allows the regulation of cellular functions in response to nutrients and stress. In the present work we demonstrate O-GlcNacylation in T. cruzi epimastigotes using two different methods: western blot with specific antibodies and click chemistry labelling. Then, we identify 2033 O-GlcNAcilated proteins and 48 modification sequences by mass spectrometry. Most of this proteins are part of structures, functions and pathways that are essentials for the parasite survival and evolution. For the first time O-GlcNacylation is idenytified in T. cruzi proteins and due to the many biological processes in which they participate, this study opens a new research field in Trypanosomatids biology, infection processes and potential identification of therapeutic targets.
2019-04-18 | PXD010285 | Pride