Helicobacter pylori
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: GSE6531
PROVIDER: PRJNA104245 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Chronic Helicobacter pylori Infection with Sydney Strain 1 and Mouse-Adapted Sydney Strain 2000
| PRJNA94259 | ENA
Project description:Microarray based comparative genomic hybridization of mouse adapted strains: 10700 pre-mouse SS1, SS1(A.L.)Sydney strain obtained directly from Adrian Lee, NSH79 Salama lab strain labeled as SS1-now know distinct, G27 obtained from Antonello Covacci. Genomic DNA from est strain (Cy5), genomic DNA from reference strains used for array fabrication (equimolar mix of 26695 and J99 genomic DNA)
2006-12-15 | E-SMDB-3902 | biostudies-arrayexpress
Project description:Array CGH of Mexican Patient Isolates and BCS100 Strain
| PRJNA100159 | ENA
Project description:USU101 gene content determined by array CGH
| PRJNA258371 | ENA
Project description:H. pylori strain content variation after five year infection of macaques measured by array CGH
| PRJNA258372 | ENA
Project description:Helicobacter pylori colonizes the stomach of half of the world's population, causing a wide spectrum of disease ranging from asymptomatic gastritis to ulcers to gastric cancer. Although the basis for these diverse clinical outcomes is not understood, more severe disease is associated with strains harboring a pathogenicity island. To characterize the genetic diversity of more and less virulent strains, we examined the genomic content of 15 H. pylori clinical isolates by using a whole genome H. pylori DNA microarray. We found that a full 22% of H. pylori genes are dispensable in one or more strains, thus defining a minimal functional core of 1281 H. pylori genes. While the core genes encode most metabolic and cellular processes, the strain-specific genes include genes unique to H. pylori, restriction modification genes, transposases, and genes encoding cell surface proteins, which may aid the bacteria under specific circumstances during their long-term infection of genetically diverse hosts. We observed distinct patterns of the strain-specific gene distribution along the chromosome, which may result from different mechanisms of gene acquisition and loss. Among the strain-specific genes, we have found a class of candidate virulence genes identified by their coinheritance with the pathogenicity island. Keywords: other
2001-07-25 | GSE6 | GEO
Project description:Chronic infection of the human stomach with Helicobacter pylori leads to a variety of pathologic sequelae including peptic ulcer and gastric cancer, resulting in significant human morbidity and mortality. Several genes have been implicated in disease related to H. pylori infection including the vacuolating cytotoxin and the cag pathogenicity island. Other factors important for establishment and maintenance of infection include urease enzyme production, motility, iron uptake and stress response. We utilized a C57BL/6 mouse infection model to query a collection of 2400 transposon mutants in two different bacterial strain backgrounds for H. pylori genetic loci contributing to colonization of the stomach. Microarray based tracking of transposon mutants allowed us to monitor the behavior of transposon insertions in 758 different gene loci. Of the loci measured 223 (29%) had a predicted colonization defect. These include previously described H. pylori virulence genes, genes implicated in virulence in other pathogenic bacteria and 81 hypothetical proteins. We have retested 10 previously uncharacterized candidate colonization gene loci by making independent null alleles and confirmed their colonization phenotype using competition experiments and determination of the dose required for 50% infection. Of the genetic loci retested, 60% have strain specific colonization defects while 40% had phenotypes in both strain backgrounds for infection, highlighting the profound effect of H. pylori strain variation on the pathogenic potential of this organism. This SuperSeries is composed of the SubSeries listed below.
2006-12-15 | GSE6531 | GEO
Project description:Many host-adapted bacterial pathogens contain DNA methyltransferases (mod genes) that are subject to phase-variable expression (high-frequency reversible ON/OFF switching of gene expression). In Haemophilus influenzae, Neissera Meningtidis and Neisseria Gonorrhoeae, the random switching of the modA gene, associated with a phase variable type III restriction modification (R-M) system, controls expression of a phase-variable regulon of genes (a “phasevarion”), via differential methylation of the genome in the modA ON and OFF states. Phase variable type III R-M systems are also found in Helicobacter pylori, suggesting that phasevarions may also exist in this intriguing pathogen. Phylogenetic studies on the phase-variable type III modC gene revealed that there are 12 distinct alleles in H. pylori, which differ only in their DNA recognition domain, with the majority containing the C5 allele. Microarray analysis comparing the H. pylori wild-type P12modC5 ON strain to the P12(delta)modC5 mutant revealed that six genes were either up-regulated or down-regulated, some of which were virulence-associated. For example flaA, which encodes a flagella protein important in motility and hopG, which encodes an important outer membrane protein. This study, in conjunction with our previous work, indicates that phasevarions may be a common strategy used by host-adapted bacterial pathogens to randomly switch between “differentiated” cell types.
2012-01-16 | GSE26759 | GEO
Project description:We engineered a derivative of H. pylori strain 26695 that expresses an N-terminal DDK-tagged version of LolF from the endogenous locus. As controls, we also engineered strains to express DDK-tagged versions of two unrelated inner membrane proteins ExbD2 and FrdC. The tagged proteins were affinity purified and co-purifying proteins were identified by LC/MS-MS. We then performed an unbiased analysis using SAINTexpress (Significance Analysis of INTeractome) that included data from affinity purifications of test (i.e., LolF-DDK) and control (i.e., ExbD2-DDK and FrdC-DDK) bait proteins. This led to identification of HP0179 as an interaction partner of LolF. We then engineered a derivative of H. pylori strain 26695 that expresses a C-terminal HA-tagged version of HP0179. As controls, additional strains were generated that express HA-tagged versions of two unrelated proteins HP0838 and CagF. he tagged proteins were affinity purified and co-purifying proteins were identified by LC/MS-MS. We then performed an unbiased analysis using SAINTexpress that included data from affinity purifications of test (i.e., HP0179-HA) and control (i.e., HP0838-HA and CagF-HA) bait proteins. This led to identification of LolF as an interaction partner of HP0179.
2023-01-31 | MSV000091176 | MassIVE