The raw iTRAQ proteomics data of Entamoeba histolytica
Ontology highlight
ABSTRACT:
ORGANISM(S): Entamoeba Histolytica Hm-1:imss
SUBMITTER: Meng Feng
PROVIDER: PXD022686 | JPOST Repository | Tue Nov 24 00:00:00 GMT 2020
REPOSITORIES: jPOST
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| iTRAQ-01.raw | Raw | |||
| iTRAQ-02.raw | Raw | |||
| iTRAQ-03.raw | Raw | |||
| iTRAQ-04.raw | Raw | |||
| iTRAQ-05.raw | Raw |
Items per page: 5 1 - 5 of 17 |
Similar Datasets
Project description:Interventions: Case series:None
Primary outcome(s): exon genes;transcriptional expression;proteome;protein phosphorylation group
Study Design: Sequential
| 2739647 | ecrin-mdr-crc
Project description:Most B cell lymphomas arise in the germinal center (GC), where humoral immune responses evolve from potentially oncogenic cycles of mutation, proliferation, and clonal selection. Although lymphoma gene expression diverges significantly from GC-B cells, underlying mechanisms that alter the activities of corresponding regulatory elements (REs) remain elusive. Here we define the complete pathogenic circuitry of human follicular lymphoma (FL), which activates or decommissions transcriptional circuits from normal GC-B cells and commandeers enhancers from other lineages. Moreover, independent sets of transcription factors, whose expression is deregulated in FL, target commandeered versus decommissioned REs. Our approach reveals two distinct subtypes of low-grade FL, whose pathogenic circuitries resemble GC-B or activated B cells. Remarkably, FL-altered enhancers also are enriched for sequence variants, including somatic mutations, which disrupt transcription factor binding and expression of circuit-linked genes. Thus, the pathogenic regulatory circuitry of FL reveals distinct genetic and epigenetic etiologies for GC-B transformation. Expression profiles of follicular lymphoma, centrocyte and peripheral blood B cells were generated by deep sequencing, using Illumina Hi-Seq 2000.
2015-01-15 | E-GEOD-62241 | biostudies-arrayexpress
Project description:The Aspergillus fumigatus sterol regulatory element binding protein (SREBP) SrbA belongs to the basic Helix-Loop-Helix (bHLH) family of transcription factors and is crucial for antifungal drug resistance and virulence. The latter phenotype is especially striking, as loss of SrbA results in complete loss of virulence in murine models of invasive pulmonary aspergillosis (IPA). How fungal SREBPs mediate fungal virulence is unknown, though it has been suggested that lack of growth in hypoxic conditions accounts for the attenuated virulence. To further understand the role of SrbA in fungal infection site pathobiology, chromatin immunoprecipitation followed by massively parallel DNA sequencing (ChIP-seq) was used to identify genes under direct SrbA transcriptional regulation in hypoxia. These results confirmed the direct regulation of ergosterol biosynthesis and iron uptake by SrbA in hypoxia and revealed new roles for SrbA in nitrate assimilation and heme biosynthesis. Moreover, functional characterization of an SrbA target gene with sequence similarity to SrbA identified a new transcriptional regulator of the fungal hypoxia response and virulence, SrbB. SrbB co-regulates genes involved in heme biosynthesis and demethylation of C4 sterols with SrbA in hypoxic conditions. However, SrbB also has regulatory functions independent of SrbA including regulation of carbohydrate metabolism. Loss of SrbB markedly attenuates A. fumigatus virulence, and loss of both SREBPs further reduces in vivo fungal growth. These data suggest that both A. fumigatus SREBPs are critical for hypoxia adaptation and virulence and reveals new insights into SREBPM-bM-^@M-^Ys complex role in infection site adaptation and fungal virulence. 4 hour and 12 hour ChIP experiments were completed. Input control samples for each set were collected.
2014-10-03 | E-GEOD-61974 | biostudies-arrayexpress
Project description:Purpose: Key steps in understanding a biological process include identifying genes that are involved and determining how they are regulated. We developed a novel method for identifying TFs involved in a specific process and used it to map regulation of the key virulence factor of Cryptococcus neoformans, its capsule. Results: The map, built from expression profiles of 41 TF mutants, includes 20 TFs not previously known to regulate virulence attributes. It also reveals a hierarchy comprising executive, mid-level, and “foreman” TFs. When grouped by temporal expression pattern, these TFs explain much of the transcriptional dynamics of capsule induction. Phenotypic analysis of 41 TF deletion mutants revealed complex relationships among virulence factors and virulence in mice. Conclusions: These data resources and analyses provide the first integrated, systems level view of capsule regulation and biosynthesis. Our methods dramatically improve the efficiency with which transcriptional networks can be analyzed, making genomic approaches accessible to labs focused on specific physiological processes.
2015-01-14 | GSE60398 | GEO
Project description:Francisella tularensis is a Gram-negative bacterium that causes a fatal human disease known as tularemia. The Centers for Disease Control have classified F. tularensis as Category A Tier-1 Select Agent. The virulence mechanisms of Francisella are not entirely understood. Francisella possesses very few transcription regulators, and most of these regulate the expression of genes involved in intracellular survival and virulence. The F. tularensis genome sequence analysis reveals an AraC (FTL_0689) transcriptional regulator homologous to the AraC/XylS family of transcriptional regulators. In Gram-negative bacteria, AraC activates genes required for L-arabinose utilization and catabolism. The role of the FTL_0689 regulator in F. tularensis is not known. In this study, we characterized the role of FTL_0689 in gene regulation of F. tularensis and investigated its contribution to intracellular survival and virulence. The results demonstrate that FTL_0689 in Francisella is not required for L-arabinose utilization. Instead, FTL_0689 specifically regulates the expression of the oxidative and global stress response, virulence, metabolism, and other key pathways genes required by Francisella when exposed to oxidative stress. The FTL_0689 mutant is attenuated for intramacrophage growth, and mice infected with the FTL_0689 mutant survive better than wild-type F. tularensis LVS infected mice. Based on the deletion mutant phenotype, FTL_0689 was termed osrR (oxidative stress response regulator). Altogether, this study elucidates the role of the osrR transcriptional regulator in tularemia pathogenesis.
2021-10-13 | GSE183001 | GEO
Project description:The Aspergillus fumigatus sterol regulatory element binding protein (SREBP) SrbA belongs to the basic Helix-Loop-Helix (bHLH) family of transcription factors and is crucial for antifungal drug resistance and virulence. The latter phenotype is especially striking, as loss of SrbA results in complete loss of virulence in murine models of invasive pulmonary aspergillosis (IPA). How fungal SREBPs mediate fungal virulence is unknown, though it has been suggested that lack of growth in hypoxic conditions accounts for the attenuated virulence. To further understand the role of SrbA in fungal infection site pathobiology, chromatin immunoprecipitation followed by massively parallel DNA sequencing (ChIP-seq) was used to identify genes under direct SrbA transcriptional regulation in hypoxia. These results confirmed the direct regulation of ergosterol biosynthesis and iron uptake by SrbA in hypoxia and revealed new roles for SrbA in nitrate assimilation and heme biosynthesis. Moreover, functional characterization of an SrbA target gene with sequence similarity to SrbA identified a new transcriptional regulator of the fungal hypoxia response and virulence, SrbB. SrbB co-regulates genes involved in heme biosynthesis and demethylation of C4 sterols with SrbA in hypoxic conditions. However, SrbB also has regulatory functions independent of SrbA including regulation of carbohydrate metabolism. Loss of SrbB markedly attenuates A. fumigatus virulence, and loss of both SREBPs further reduces in vivo fungal growth. These data suggest that both A. fumigatus SREBPs are critical for hypoxia adaptation and virulence and reveals new insights into SREBP’s complex role in infection site adaptation and fungal virulence.
2014-10-03 | GSE61974 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below. Manuscript title: Fraxinus excelsior updated long-read genome reveals the importance of MADS-box genes in tolerance mechanisms against ash dieback, G3:Genes|Genomes|Genetics
2025-03-03 | GSE214554 | GEO
Project description:A compendium of antibiotic-induced transcription profiles reveals broad regulation of P. multocida virulence genes
| PRJNA108625 | ENA
Project description:Purpose: Key steps in understanding a biological process include identifying genes that are involved and determining how they are regulated. We developed a novel method for identifying TFs involved in a specific process and used it to map regulation of the key virulence factor of Cryptococcus neoformans, its capsule. Results: The map, built from expression profiles of 41 TF mutants, includes 20 TFs not previously known to regulate virulence attributes. It also reveals a hierarchy comprising executive, mid-level, and “foreman” TFs. When grouped by temporal expression pattern, these TFs explain much of the transcriptional dynamics of capsule induction. Phenotypic analysis of 41 TF deletion mutants revealed complex relationships among virulence factors and virulence in mice. Conclusions: These data resources and analyses provide the first integrated, systems level view of capsule regulation and biosynthesis. Our methods dramatically improve the efficiency with which transcriptional networks can be analyzed, making genomic approaches accessible to labs focused on specific physiological processes. A total of 288 expression profiles were generated by RNA-Seq analysis of Mutant and wildtype cells grown in capsule inducing conditions for 90 minutes. In addition, 3 replicate expression profiles were generated for wildtype cells grown in : a capsule non-inducing condition, a capsule inducing condition for 180 minutes, a capsule inducing condition for 480 minutes, and a capsule inducing condition for 1440 minutes. In addition, ChIP-seq of NRG1(CNAG_05222) in capsule inducing conditions, and USV101(CNAG_05420) in both capsule inducing and non-inducing conditions were generated.
2015-01-14 | E-GEOD-60398 | biostudies-arrayexpress
Project description:The microarrays for the three time course experiments described in the publication titled "Gene expression profiling of Helicobacter pylori reveals a growth phase dependent switch in virulence gene expression". TC1 refers to the first time course investigating gene expression changes over the time course of growth while TC2 refers to the second time course. TC Motility_broth refers to the third time course described in the manuscript used to investigate the concurrent changes in motility and the expression of the genes in the flagellar regulon. Detailed description of the growth of H. pylori for these 3 time courses can be found in the Materials and Methods section of the manuscript along with the exact filtering criteria used to download the data from these arrays. Note that in all three time courses the data for each array were transformed after download such that the abundance of each gene's transcript represented by a given spot was relative to the level of that transcript at the 6 h time point. Also duplicate spots for each ORF on the microarray were averaged for analysis after transformation. Groups of assays that are related as part of a time series. Computed
2005-11-21 | E-GEOD-3636 | biostudies-arrayexpress