Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

EPEC1

ABSTRACT: EPEC1 effector mutant from EPEC E2348/69 variety 2

PROVIDER: PRJEB18717 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	GCA_900149875.1_sequence_report.txt	Txt

Items per page:

1 - 1 of 1

Similar Datasets

EPEC-E2348/69-V2

Project description:EPEC E2348/69 variety 2. Wild-type strain.

| PRJEB18716 | ENA

Transcriptional response induced by enteropathogenic Escherichia coli (EPEC) in mouse intestinal epithelial cells in vivo

Project description:In order to identify genes that were differentally regulated upon oral infection with EPEC, we isolated 8 days post-infection intestinal epithelial cells (IECs) from the small intestine of C57BL/6 neonate mice that were left untreated or orally infected with 5x104 WT EPEC E2348/69 or with 5x104 of the isogenic mutant ΔescV on their first day of life.

2016-04-20 | GSE71685 | GEO

Comparative genomics provides insight into the diversity of the attaching and effacing Escherichia coli (AEEC) virulence plasmids

Project description:Global transcriptional analysis of the EPEC prototype strain E2348/69 and its plasmid mutants containing a deletion of perABC, or missing the entire EAF plasmid (strain JPN15).

2015-08-11 | GSE69375 | GEO

Highly-conserved regulatory activity of the ANR family in the virulence of diarrheagenic bacteria through interaction with Master and Global regulators

Project description:To gain mechanistic insights into this phenomenon, we characterized the regulatory role of Rnr in the virulence of prototype EPEC strain E2348-69 by genetic, biochemical, and human organoid-based approaches. Accordingly, RNA-seq analysis revealed more than 500 genes differentially regulated by Rnr, including the type-3 secretion system (T3SS).

2023-05-03 | GSE225626 | GEO

Cell type dependent comparison and strain specific comparison

Project description:Enterohemorrhagic Escherichia coli (EHEC) is a gram negative enteric bacterial pathogen that can cause hemorrhagic colitis and heamolytic uremic syndrome (HUS) in humans and is the cause of bloody diarrhoea and acute renal failure in children. We have studied the transcriptional response of a colon cell line (CaCo2) to infection by EHEC and another closely related enteric pathogen Enteropathogenic Escherichia coli (EPEC) and compared its response to a cervical cell line (Hela). We carried out microarray analysis on CaCo2 infected with EHEC O157H:7 EDL933 and EPEC E2348/69 at 4 hours of infection and analysis on Hela infected with EHEC also at 4 hours of infection CaCo2 cells and Hela cells were grown to 80% confluency and infected with the bacteria for 4 hours before samples were collected for microarray analysis.

2016-09-01 | E-GEOD-13403 | biostudies-arrayexpress

Cell type dependent comparison and strain specific comparison

2016-09-01 | GSE13403 | GEO

Metabolome and transcriptome-wide effects of the carbon storage regulator A in enteropathogenic Escherichia coli.

Project description:The carbon storage regulator A (CsrA) is a conserved swivel of a global regulatory system known to regulate central carbon pathways, biofilm formation, motility, and pathogenicity. The aim of this study was to characterize changes in major metabolic pathways induced by CsrA in the human enteropathogenic Escherichia coli (EPEC) strain E2348/69. The EPEC strain E2348/69 and a csrA deletion mutant were grown under virulence factor inducing conditions and characterized by a combined analysis of their metabolomes and transcriptomes. Of the 159 metabolites identified from untargeted GC/MS and LC/MS data, 70 were significantly (fold change ≥ 1.5; p-value ≤ 0.05) regulated between the knockout and the wildtype strain. A lack of csrA led to an upregulation of upper glycolysis and glycogen synthesis pathways, whereas lower glycolysis and the citric acid cycle were downregulated. Associated pathways from the citric acid cycle like aromatic amino acid and siderophore biosynthesis were also negatively influenced. The nucleoside salvage pathways were featured by an accumulation of nucleosides and nucleobases, and a downregulation of nucleotides. In addition, a pronounced downregulation of lyso-lipid metabolites was observed. A drastic change in the morphology in the form of vesicle-like structures of the csrA knockout strain was visible by electron microscopy, which is supposed to be a consequence of a strong upregulation of colanic acid synthesis. The findings expand the scope of pathways affected by the csrA regulon and emphasize its importance as a global regulator.

2018-12-15 | GSE103415 | GEO

RIL-seq of EPEC E2348/69 hfq-flag, in virulence activating and non-activating conditions.

Project description:RIL-seq of EPEC E2348/69 hfq-flag, in virulence activating and non-activating conditions.

| PRJEB36843 | ENA

RNA-seq of EPEC E2348/69 in virulence activating and non-activating conditions. Comparison of wt and dhfq strains.

Project description:RNA-seq of EPEC E2348/69 in virulence activating and non-activating conditions. Comparison of wt and dhfq strains.

| PRJEB36845 | ENA

The E. coli type III secreted effectors NleB and EspL interact with the microtubule associated protein ensconsin to disrupt vesicle trafficking, part 1

Project description:Enteropathogenic and enterohaemorrhagic E. coli (EPEC and EHEC) translocate a set of type III effector proteins into host cells that are critical for bacterial virulence. These effectors subvert normal host pathways by interacting with a variety of targets within the cell, but the binding partners and mechanism of action of the majority of effectors are not understood. We identified the microtubule associated protein, ensconsin, as a novel target for two EPEC/EHEC effectors. We found that the secreted effectors NleB and EspL bind host ensconsin and work synergistically to paralyze kinesin-based intracellular vesicular transport. Our findings demonstrate that EPEC/EHEC encode multiple effectors that control intracellular vesicle movement and suggest a simple strategy for broad-based immobilization of host cells by pathogens.

2016-12-22 | PXD002933 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data