Disease relevance of ureA

• A polymerase chain reaction (PCR) assay for Helicobacter pylori was developed with use of primer sequences from the ureA structural gene coding for the small subunit of urease [1].
• Duodenal H. pylori ureA was significantly more frequent in patients with duodenal diseases than in those without (p <.01), cagA positive strains being mainly involved in the infection of this anatomical area (p <.01) [2].
• The aim of the present study was to correlate molecular evidence of the presence of Helicobacter pylori in gastric biopsy samples, based on analysis of 16S rDNA, vacuolating toxin (vacA), urease A (ureA) and cagA genes, with the clinical, histological and serological findings in patients with H. pylori-associated gastritis [3].

High impact information on ureA

• The transcription start point of ureI was identified by primer extension using a ureA promoter-deleted mutant, and a consensus sequence of RpoD-RNA polymerase was found in the ureI promoter [4].
• With one exception, each isolate not distinguished from the others by RFLPs in ureA-ureB was distinguished by Mbol digestion of the neighboring 1.7 kb ureC-ureD segment [5].
• Furthermore, deletion of a distal upstream ArsR binding site of the ureA promoter demonstrates its role in acid-dependent activation of the promoter [6].
• The carcinoma patients were considered to be H. pylori-positive if culture alone or 2 among preformed urease test, stained smear or histologic section, serology, polymerase chain reaction (PCR) for ureA and urea breath test were positive [7].
• Expressing sigma(54) at high levels by putting rpoN under the control of the ureA promoter restored flagellar biogenesis and motility in the hp0958:aphA3 mutant [8].

Biological context of ureA

• Plasmid-free mutagenesis was used to replace ureA and ureB with chloramphenicol acetyltransferase in Hp Strains 11637 and 11916. ureAB null Hp lacked detectable urease activity and did not express UreA or UreB as judged by immunoblotting [9].
• Here the properties of the products of the urease gene clusters, ureA, B and ureI, E, F, G and H are explored in order to explain the unique location of this pathogen [10].
• The gene complex encodes catalytic subunits (ureA/B), an acid-gated urea channel (ureI), and accessory assembly proteins (ureE-H) [11].
• The amino acid sequences of the ureA and the phylogenetic relationship of the 29 strains indicated that the strains in Taiwan are rapidly evolving into a unique clone [12].
• When 16S rRNA, ureA and cagA amplified gene sequences were aligned with H. pylori 26695 and J99 genome sequences, we obtained a percentage of alignment over 90% [13].

Anatomical context of ureA

• Incubation of nonculturable cold-starved cells with an erythrocyte lysate increased total RNA expression and ureA mRNA transcription as measured by quantitative real-time reverse transcription-PCR [14].
• In a subset of 171 patients H. pylori ureaseA (ureA) and cagA genes were amplified (PCR) using mucosal biopsies from the duodenum [2].
• DESIGN AND METHODS: Helicobacter pylori status was recorded in Group 1 (n = 187) by UBT, H. pylori stool antigen, ureA and cagA PCR in feces [15].

Associations of ureA with chemical compounds

• DNA extraction of stool specimens was done using QIAamp DNA Stool Mini Kit (QIAGEN) and PCR conditions included amplification and reamplification steps using the H. pylori ureA gene specific primers (HPU1, HPU2) and were visualized on 1% agarose gel stained with ethidium bromide [16].

Other interactions of ureA

• No statistical difference was defined in the accumulation of cagA and ureA [17].
• Helicobacter pylori: ureA, cagA and vacA expression during conversion to the coccoid form [18].
• In the isogenic mutant of rpoN, transcription of the flaB gene was severely affected, but transcription of the ureA gene (control) was intact [19].

Analytical, diagnostic and therapeutic context of ureA

• RT-PCR with ureA primers detected 16 of 25 tissue-positive and 0 of 17 tissue-negative patients (P < 0.001) [20].
• Variation was analysed at the urease genes, ureA and ureCD, by employing PCR-generated probes in genomic Southern blot hybridizations [21].
• The study was performed in 47 dyspeptic adult patients undergoing endoscopy, and infection was detected by amplification of a segment of H. pylori ureA gene [22].
• We evaluated 240 children undergoing upper gastrointestinal endoscopy for H. pylori infection by rapid urease test, culture, ureA PCR and histopathology [23].
• Helicobacter pylori binding immunomagnetic beads with H. pylori-specific goat anti-H. pylori antibody was shown by electron microscopy in both raw and pasteurized milk positive for the ureA gene [24].

References