Ontology highlight
ABSTRACT:
PROVIDER: PRJEB88581 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR9741968_cleaned.contigs.fa.gz | Other | |||
| ERR9741513_cleaned.contigs.fa.gz | Other | |||
| ERR9742694_cleaned.contigs.fa.gz | Other | |||
| ERR9742695_cleaned.contigs.fa.gz | Other | |||
| ERR9743228_cleaned.contigs.fa.gz | Other |
Items per page: 5 1 - 5 of 186 |
Similar Datasets
Project description:Oral-gut microbiome interactions in advanced cirrhosis: characterisation of pathogenic enterotypes and salivatypes, virulence factors and antimicrobial resistance
| PRJEB52891 | ENA
Project description:Gene profiling of hepatocytes in early and advanced cirrhotic Rats Two-condition experiment, Advanced cirrhosis vs Control liver, Advanced cirrhosis vs Early cirrhosis. Biological replicates: 5 Advanced cirrhosis, 5 Early cirrhosis, 5 control liver. Each hepatocyte was isolated independently. One replicate per array.
2011-11-02 | E-GEOD-22977 | biostudies-arrayexpress
Project description:Rat hepatocytes: Advanced cirrhosis vs Control liver, Advanced cirrhosis vs Early cirrhosis
| PRJNA127753 | ENA
Project description:Objective: To evaluate gene expression profiles in patients with advanced cirrhosis compared with healthy controls (HC). Results: Patients with advanced cirrhosis exhibit an unbalanced systemic response involving pro-fibrotic / protective signatures that could be contributing to the pathogenesis of cirrhosis and also to that of the extra-hepatic complications of this disease.
2016-02-14 | E-MTAB-3338 | biostudies-arrayexpress
Project description:PhoP is considered a regulator of virulence despite being conserved in both pathogenic and non-pathogenic Enterobacteriaceae. While Escherichia coli strains represent both non-pathogenic commensal isolates and numerous virulent pathotypes, the PhoP virulence regulator has only been studied in commensal E. coli. To better understand how conserved transcription factors contribute to virulence, we characterized PhoP in pathogenic E. coli. Loss of phoP significantly attenuated E. coli during extraintestinal infection. This was not surprising since we demonstrated that PhoP differentially regulated the transcription of >600 genes. In addition to survival at acidic pH and resistance to polymyxin B, PhoP was required for repression of motility and oxygen-independent changes in the expression of primary dehydrogenase and terminal reductase respiratory chain components. All phenotypes have in common a reliance on an energized membrane. Thus, we hypothesized that PhoP mediated these effects by regulating genes that generate a proton motive force. Indeed, bacteria lacking PhoP exhibited a hyper-polarized membrane, and dissipation of the transmembrane electrochemical gradient increased the susceptibility of the phoP mutant to acidic pH, while inhibiting respiratory generation of the proton gradient restored resistance to antimicrobial peptides independent of lipopolysaccharide modification. These findings demonstrate a connection between PhoP, virulence, and the energized state of the membrane. Comparison of gene expression between wild-type CFT073 and a CFT073 phoP deletion mutant during logarithmic phase growth in LB medium. Three biological replicates were compared from each strain.
2011-07-28 | E-GEOD-31029 | biostudies-arrayexpress
Project description:Pathogenic determinants in the Cryptococcus genus have been extensively studied, often using standard laboratory isolates. Here, we analyzed the virulence of ten Cryptococcus isolates from diverse sources, species, and genotypes. These isolates exhibited marked differences in their ability to colonize and kill the invertebrate host Galleria mellonella, as well as in their interactions with hemocytes. Capsule formation also varied widely among isolates, with no clear correlation between virulence in G. mellonella and source of isolation, species, fungal burden, capsule size, or interaction with larval hemocytes. To further investigate the basis of this pathogenic diversity, we selected two hypervirulent isolates (C. deuterogattii and C. neoformans) and two hypovirulent isolates (C. gattii and C. neoformans) for in-depth analysis. Differences in the induction of antimicrobial peptides during infection did not account for the observed variation in virulence. Genomic analysis of capsule- related genes, scanning electron microscopy of capsule morphology in vitro and in vivo, and nuclear magnetic resonance of the major capsular polysaccharide all revealed high variability among isolates, but none of these features correlated with virulence. Proteomic profiling of cellular extracts showed that virulent strains were enriched in proteins associated with oxidative processes. Supplementation with an antioxidant during infection increased the virulence of hypovirulent isolates in G. mellonella. These results reveal a high pathogenic diversity in Cryptococcus that goes beyond its classical virulence factors.
2025-10-20 | PXD065863 | Pride
Project description:PhoP is considered a regulator of virulence despite being conserved in both pathogenic and non-pathogenic Enterobacteriaceae. While Escherichia coli strains represent both non-pathogenic commensal isolates and numerous virulent pathotypes, the PhoP virulence regulator has only been studied in commensal E. coli. To better understand how conserved transcription factors contribute to virulence, we characterized PhoP in pathogenic E. coli. Loss of phoP significantly attenuated E. coli during extraintestinal infection. This was not surprising since we demonstrated that PhoP differentially regulated the transcription of >600 genes. In addition to survival at acidic pH and resistance to polymyxin B, PhoP was required for repression of motility and oxygen-independent changes in the expression of primary dehydrogenase and terminal reductase respiratory chain components. All phenotypes have in common a reliance on an energized membrane. Thus, we hypothesized that PhoP mediated these effects by regulating genes that generate a proton motive force. Indeed, bacteria lacking PhoP exhibited a hyper-polarized membrane, and dissipation of the transmembrane electrochemical gradient increased the susceptibility of the phoP mutant to acidic pH, while inhibiting respiratory generation of the proton gradient restored resistance to antimicrobial peptides independent of lipopolysaccharide modification. These findings demonstrate a connection between PhoP, virulence, and the energized state of the membrane.
2011-07-29 | GSE31029 | GEO
Project description:Analysis of Antimicrobial Resistance and Virulence genes of Pathogenic E. coli
| PRJEB77416 | ENA
Project description:With the rise in antimicrobial resistance, understanding the virulence factors utilized by pathogenic E. coli is essential for the development of alternative therapeutics. While previous work has shown that disruption of the rhomboid protease gene glpG leads to defects in bacterial colonization, here we provide mechanistic insight into the loss of fitness. We show GlpG is essential for the formation of virulence factors, namely type 1 pili, required for the colonization of eukaryotic cells. As adhesion is critical for biofilm formation and bacterial persistence, the absence of GlpG proteolytic activity also reduces the production of biofilm. Working towards new potential antimicrobial targets for treating infections, we show that biofilm formation is hampered by GlpG inhibition. Our data demonstrates that GlpG plays a key role in protein quality control of virulence factors and alters the paradigm for GlpG proteolysis, previously implicated in the cleavage of only membrane embedded substrates.
2025-03-06 | MSV000097249 | MassIVE