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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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H. pylori 26695: wild-type vs nitro-oxide (NO) treated; knockout-crdS in H. pylori 26695 vs knockout-crdS with NO treatment

ABSTRACT: There are two transcription profiles. The first profiling is comparing control untreated H. pylori with H. pylori with NO treatment. And the second profiling is comparing knockout-crdS in H. pylori untreated with knockout-crdS with NO treatment. The goal was determine the effects of NO-responsive gene and crdS-regulated genes on H. pylori gene expression. Four-condition experiment, wild-type H. pylori untreated (WT –NO), H. pylori with NO treatment (WT +NO), knockout-crdS in H. pylori untreated (ΔcrdS -NO), ΔcrdS with NO treatment (ΔcrdS +NO)

ORGANISM(S): Helicobacter pylori 26695

SUBMITTER: CHIU-LIEN HUNG

PROVIDER: E-GEOD-69846 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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H. pylori 26695: wild-type vs nitro-oxide (NO) treated; knockout-crdS in H. pylori 26695 vs knockout-crdS with NO treatment

Project description:There are two transcription profiles. The first profiling is comparing control untreated H. pylori with H. pylori with NO treatment. And the second profiling is comparing knockout-crdS in H. pylori untreated with knockout-crdS with NO treatment. The goal was determine the effects of NO-responsive gene and crdS-regulated genes on H. pylori gene expression.

2015-06-13 | GSE69846 | GEO

The CrdRS two-component system in Helicobacter pylori responds to nitrosative stress

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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Project description:Helicobacter pylori infection reprograms host gene expression and influences various cellular processes, which have been investigated by cDNA microarray in vitro culture cells and in vivo patients of the chronic abdominal complaint. In this study，the effects of H. pylori infection on host gene expression in the gastric antral mucosa of patients with chronic gastritis were examined. The gastric antral mucosa was obtained from a total of 6 untreated patients undergoing gastroscopic and pathologic confirmation of chronic superficial gastritis. Three patients infected by H. pylori and 3 patients uninfected were used to cDNA microarray experiment.

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Changes in gene expression in AGS cells in response to Helicobacter pylori lipopolysaccharide

Project description:This study set out to identify global changes in gene expression in AGS gastric epithelial cells following 8 hours stimulation with 10 μg/ml lipopolysaccharide (LPS) from the gastric pathogen H. pylori. Microarray analysis was used to compare changes in gene expression between cells treated with 10 μg/ml H. pylori LPS and untreated cells at the same time point. Total RNA was harvested from AGS cells following treatment with LPS for 8h or untreated cells at the same time-point. 2 independent experiments were carried out. RNA was labelled and hybridized to GeneChips to analyse changes in gene expression.

2011-01-12 | E-GEOD-25146 | biostudies-arrayexpress

Changes in gene expression in MKN45 cells in response to Helicobacter pylori lipopolysaccharide

Project description:This study set out to identify global changes in gene expression in MKN45 gastric epithelial cells following 8 hours stimulation with 10 μg/ml lipopolysaccharide (LPS) from the gastric pathogen H. pylori. Microarray analysis was used to compare changes in gene expression between cells treated with 10 μg/ml H. pylori LPS and untreated cells at the same time point. Total RNA was harvested from MKN45 cells following treatment with LPS for 8h or untreated cells at the same time-point. 2 independent experiments were carried out. RNA was labeled and hybridized to GeneChips to analyse changes in gene expression.

2011-01-12 | E-GEOD-25147 | biostudies-arrayexpress

Changes in gene expression in MKN45 cells in response to Helicobacter pylori lipopolysaccharide

2011-01-12 | GSE25147 | GEO

Changes in gene expression in AGS cells in response to Helicobacter pylori lipopolysaccharide

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Helicobacter pylori-mediated Epigenetic Dysregulation of FOXD3 Tumor-suppressive Cascade In Gastric Carcinogenesis [ChIP]

Project description:Forkhead box (Fox) proteins constitute an evolutionarily conserved family of transcriptional regulators whose deregulations lead to tumorigenesis. However, their regulation and function in gastric cancer are unknown. Promoter hypermethylation occurs during Helicobacter pylori (H pylori)-induced gastritis, but whether the deregulated genes contribute to the multi-step gastric carcinogenesis remains unclear. FOXD3 was found to be hypermethylated in a mouse model of H pylori infection and possess tumor-suppressive functions in gastric cancer cell lines. In order to characterize the direct targets of FOXD3 that confer its actions, we performed ChIP-chip in N87 gastric cancer cell line which express low level of FOXD3 in the nuclei of a sub-population of cells. Promoter hypermethylation occurs during Helicobacter pylori (H pylori)-induced gastritis, but whether the deregulated genes contribute to the multi-step gastric carcinogenesis remains unclear. We used MethylCap-microarray to identify hypermethylated genes in a mouse model of H pylori infection. human Samples: Human gastric tumor cell line, N87 was grown in RPMI1640 supplemented with 10% fetal bovine serum. ChIP assays were performed using anti-FOXD3 antibody. The immunoprecipitated-FOXD3 and -IgG DNA were used to probe the Agilent human ChIP-chip arrays. mouse Samples: Two-condition experiment, H pylori-infected vs. control gastric tissues. 2 dye-swap replicates.

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Gene expression profiles in gastric mucosa from a transgenic mice infected with H. pylori and immunized with BabA

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Changes in gene expression in HEK-TLR2 cells in response to Helicobacter pylori lipopolysaccharide

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2011-01-12 | E-GEOD-25148 | biostudies-arrayexpress

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