Helicobacter pylori 26695
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ABSTRACT:
PROVIDER: PRJNA286939 | ENA |
REPOSITORIES: ENA
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Project description:Helicobacter pylori 26695 Genome sequencing
| PRJNA175543 | ENA
Project description:Helicobacter pylori 26695-1 Genome sequencing
| PRJNA270700 | ENA
Project description:Dear Sir or Madam, we report an in-depth proteogenomics study of Helicobacter pylori strain 26695 and provide the supporting MS data via ProteomExchange. The study includes 2 biological replicates with 6 different datasets: G1: in-gel digestion with trypsin, replicate 1 G2: in-gel digestion with trypsin, replicate 2 T1: SEC fractionation of low molecular weight (LMW) proteins and subsequent trypsin digestion, replicate 1 T2: SEC fractionation of LMW proteins and subsequent trypsin digestion, replicate 2 A1: SEC fractionation of LMW proteins and subsequent AspN digestion, replicate 1 A2: SEC fractionation of LMW proteins and subsequent AspN digestion, replicate 2 L1: SEC fractionation of LMW proteins and subsequent LysC digestion, replicate 1 L2: SEC fractionation of LMW proteins and subsequent LysC digestion, replicate 2 In our proteogenomics approach, we could identify four previously missing protein annotations and were able to correct sequences of six protein coding regions. Furthermore we identified signal peptidase cleavage sites for 72 different proteins. MGFs were generated by Maxquant 1.1 [1] using recalibration of peptide parent masses. For PRIDE (http://www.ebi.ac.uk/pride) submission, we made an additional database search with Mascot and X!Tandem using the SearchGUI [2]. Therefore we searched against a NCBI database of H. pylori strain 26695 complemented with the sequence corrections, signal peptide cleavage sites and missing annotations with the same configurations as described in materials and methods. For pride xml export we used the software PeptideShaker (http://code.google.com/p/peptide-shaker/). The complemented database has entries which will be submitted to the UniProtKB via SPIN. The entries have the according SPIN number as accession number. The NCBI accession numbers for the shortened sequences due to signal peptide cleavage are extended with “_1”. The fasta database is added to the submission. For additional information, please contact me: stephan.mueller@ufz.de Yours sincerely, Stephan Mueller References: [1] Cox J, Neuhauser N, Michalski A, Scheltema RA, Olsen JV, Mann M. Andromeda: a peptide search engine integrated into the MaxQuant environment. Journal of proteome research. 2011;10:1794-805. [2] Vaudel M, Barsnes H, Berven FS, Sickmann A, Martens L. SearchGUI: An open-source graphical user interface for simultaneous OMSSA and X!Tandem searches. Proteomics. 2011;11:996-9.
2013-08-01 | PXD000054 | Pride
Project description:Purpose: Next-generation sequencing (NGS) was used to analyze pH-responsive gene expression in H. pylori. The goals of this study are to compare H. pylori pH-responsive gene expression in H. pylori strain 26695 and 26695 dervatives containing mutations to the ArsRS two component system.
2021-01-19 | GSE165055 | GEO
Project description:Helicobacter pylori strain:26695-1MET Genome sequencing
| PRJNA270699 | ENA
Project description:Purpose: Next-generation sequencing (NGS) was used to analyze pH-responsive gene expression in H. pylori. The goals of this study are to compare H. pylori pH-responsive gene expression in H. pylori strain 26695 and 26695 dervatives containing mutations to the ArsS, CrdS and FlgS sensor kinases.
2021-01-19 | GSE165056 | GEO
Project description:RNA-seq to investigate regulatory roles of DNA methyltransferases in Helicobacter pylori strain 26695.
| PRJDB3908 | ENA
Project description:Background: Helicobacter pylori has been shown to alter the secretion of gastric hormones that modulate body fat deposition. Since cag-positive H. pylori strains interact intimately with the host gastric epithelial cells and trigger higher inflammation than cag-negative strains, we hypothesized that gastric colonization with H. pylori strains without functional cagA ameliorates obesity and its complications by modulating gastric gene expression and inflammation. Methodology/Principal Findings: To test this hypothesis we examined the effects of gastric colonization on metabolic and inflammatory markers in mice infected with two isogenic strains of H. pylori: 26695 strain 98-325 (cagA+ wild-type) and its cag pathogenicity island (cagPAI) mutant strain 99-305, a knockout made by inserting a chloramphenicol resistance cassette. Only the cagPAI mutant decreased fasting blood glucose levels, improved glucose tolerance and suppressed weight gain in db/db mice and mice with diet-induced obesity. These effects were associated with increased gastric leptin levels, suppressed infiltration of macrophages, enhanced influx of regulatory T cells (Treg) in adipose tissue and suppressed gastric inflammation. Gene set enrichment analyses of gastric mucosal samples identified six differentially modulated pathways, including the Hedgehog signaling pathway that is associated with control of cellular proliferation and gastric carcinogenesis as well as the insulin signaling pathway. Conclusions/Significance: Gastric colonization with cagPAI-negative strains of H. pylori ameliorate obesity and inflammation by modulating gastric gene expression, suggesting that cag-negative H. pylori strains might be beneficial in ameliorating obesity and its co-morbidities. Gastric mucosa from three groups of mice: uninfected, infected with H. pylori 26695 strain 98-325 (cagA+ wild-type) or infected with H. pylori mutant strain 99-305 (lacking cag pathogenicity island; cagA-)
2010-11-13 | E-GEOD-21833 | biostudies-arrayexpress
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. 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)
2015-06-13 | E-GEOD-69846 | biostudies-arrayexpress
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