Project description:Part of a mouse inflammation model set in order to observe the similarities and differences between the multiple options for the generation of intestinal inflammation in an animal model. Experimental samples are generated according to the standard protocol for the model. and are processes using the same set of bioinformatic tools.
Project description:Helicobacter hepaticus causes disease in the liver and lower intestinal tract of mice. It is strongly urease positive, although it does not live in an acidic environment. The H. hepaticus urease gene cluster was expressed in Escherichia coli with and without coexpression of the Helicobacter pylori nickel transporter NixA. As for H. pylori, it was difficult to obtain enzymatic activity from recombinant H. hepaticus urease; special conditions including NiCl2 supplementation were required. The H. hepaticus urease cluster contains a homolog of each gene in the H. pylori urease cluster, including the urea transporter gene ureI. Downstream genes were homologs of the nik nickel transport operon of E. coli. Nongastric H. hepaticus produces urease similar to that of H. pylori.
Project description:Differential gene regulation in Helicobacter hepaticus between wild type bacteria and fliA mutant 3 biological experiments of both wild type and fliA mutant bacteria (1-3) and 2 replicates (dye flip) of each biological experiment
Project description:The purpose of the study was to define gastric cell-specific proteomic changes, induced by H. pylori oncogenic strains, that are critical for initiation of the gastric carcinogenic cascade. Gastric cell scrapings were harvested from H. pylori-infected and uninfected animals for quantitative proteomic analyses using isobaric tags for relative and absolute quantitation (iTRAQ). Canonical and disease pathway mapping using Ingenuity Pathway Analysis (IPA) identified significantly altered inflammatory and cancer-signaling pathways that included Rab/Ras signaling proteins.