Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Francisella tularensis LVS MSMS spectral library for SRM design

ABSTRACT: This analysis was performed in order to collect a library of MSMS spectra for tryptic peptides derived from Francisella tularensis LVS proteins. Such MSMS library facilities the design and refinement of LC-SRM assays.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Francisella Tularensis Subsp. Holarctica (strain Lvs)

SUBMITTER: Juraj Lenco

LAB HEAD: Jiri Stulik

PROVIDER: PXD001069 | Pride | 2019-06-04

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Publications

Changes in proteome of the Δhfq strain derived from Francisella tularensis LVS correspond with its attenuated phenotype.

Lenco Juraj J Tambor Vojtech V Link Marek M Klimentova Jana J Dresler Jiri J Peterek Miroslav M Charbit Alain A Stulik Jiri J

Proteomics 20140922 21-22

The posttranscriptional regulatory protein Hfq was shown to be an important determinant of the stress resistance and full virulence in the dangerous human pathogen Francisella tularensis. Transcriptomics brought rather limited clues to the precise contribution of Hfq in virulence. To reveal the molecular basis of the attenuation caused by hfq inactivation, we employed iTRAQ in the present study and compared proteomes of the parent and isogenic Δhfq strains. We show that Hfq modulates the level o ...[more]

PMID: 25156581

Similar Datasets

Microarray analysis of human monocytes infected with Francisella tularensis

2008-08-13 | GSE12108 | GEO

An AraC/XylS Family Transcriptional Regulator Modulates the Oxidative Stress Response of Francisella tularensis

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

The role and mechanism of erythrocyte invasion by Francisella tularensis

Project description:Francisella tularensis, is an extremely virulent bacterium that can be transmitted naturally by blood sucking arthropods. During mammalian infection, F. tularensis infects numerous types of host cells, including erythrocytes. As erythrocytes do not undergo phagocytosis or endocytosis, it remains unknown how F. tularensis invades these cells. Furthermore, the consequence of inhabiting the intracellular space of red blood cells has not been determined. Here, we provide evidence indicating that residing within an erythrocyte enhances the ability of F. tularensis to colonize ticks following a blood meal.

2017-05-24 | GSE93233 | GEO

Intra-macrophage Expression data of Francisella tularensis novicida U112

Project description:These samples are part of an experiment comparing the expression profiles of Francisella tularensis novicida grown in chemically defined medium and bacteria isolated 24 hours post infection of J774 macrophages to identify virulence factors

2017-05-02 | GSE75689 | GEO

Inflammatory gene expression in response to Francisella tularensis exposure in Balb/c mice

Project description:Francisella tularensis may enter the body thorugh the lungs and cause fatal infection. In this study the inflammatory response to the virulent strain of Francisella (Schu4) was mapped over a 96h time-course using a custom microarray.

2011-03-01 | GSE17248 | GEO

Transcription profiling of human monocytes infected with Francisella tularensis

Project description:Differential expression in human peripheral blood monocytes between F. novicida-infected and uninfected, and between Francisella tularensis tularensis isolate Schu S4 and uninfected. The goal was to examine genomewide transcriptional reponses to these two strains, and identify differentially-regulated genes that may help explain the virulence of Schu S4. Experiment Overall Design: Human monocytes were infected with the Schu S4 isolate of Francisella tularensis tularensis (n=4), with F. tularensis subspecies novicida isolate U112 (n=4) or were left uninfected (n=6). Gene expression values were calculated using the gcrma package in R and BioConductor, and limma to identify differentially expressed genes. Submitted here are expression values calculated using R 2.7.1 and BioConductor 2.2 (FreeBSD/amd64) but the original were done using R 2.6.1 and BioConductor 2.1 (FreeBSD/amd64). Twelve other chips were pooled with these 14 for preprocessing.

2008-10-25 | E-GEOD-12108 | biostudies-arrayexpress

Francisella tularensis Schu4 gene expression during infection of mouse spleen

Project description:Francisella tularensis is classified as a Category A priority pathogen and causes fatal disseminated disease in humans upon inhalation of less than 50 bacteria. Although drugs are available for treatment, they are not ideal because of toxicity and delivery, and in some cases relapse upon withdrawal. We have an ongoing program in the development of novel FabI enoyl-ACP-reductase enzyme inhibitors for Francisella and other select agents. To establish ftFabI in F. tularensis as a clinically relevant drug target, we demonstrated that the enzyme is essential for growth in vitro and that ftfabI is not transcriptionally altered in the presence of exogenous fatty acids. Inhibition of ftFabI results in loss of viability that is not rescued by exogenous fatty acids supplementation. Importantly, whole-genome transcriptional profiling of F. tularensis with DNA microarrays from infected tissues revealed that ftfabI and de novo fatty acid biosynthetic genes are transcriptionally active during infection. This is the first demonstration that the FabI enoyl-ACP-reductase enzyme encoded by F. tularensis is essential and that de novo fatty acid biosynthetic components are transcriptionally active during infection in the mouse model tularemia.

2012-08-04 | GSE39871 | GEO

Francisella tularensis subsp. tularensis

Project description:Francisella tularensis subsp. tularensis Multiisolate

| PRJNA217354 | ENA

Transcription profiling of Francisella tularensis to spermine

Project description:Francisella tularensis LVS was grown in MH broth in the presence or absence of 200uM spermine. RNA was harvasted from overnight (16 hour) cultures and processed for microarray hybridization.

2009-11-20 | E-MEXP-2327 | biostudies-arrayexpress

Francisella tularensis subsp. tularensis Induces a Unique Pulmonary Inflammatory Response: Role of Bacterial Gene Expression in Temporal Regulation of Host Defense Responses

Project description:Virulent Francisella tularensis induces a unique pulmonary inflammatory response characterized by temporal regulation of innate immune pathways correlating with altered bacterial gene expression patterns.

2013-04-15 | GSE44320 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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