title: An intact urease assembly pathway is required to compete with NikR for nickel ions in Helicobacter pylori.
abstract: We examined the effects of urease and hydrogenase assembly gene deletions on NikR activation in H. pylori strains 26695 and G27. The loss of any component of urease assembly increased NikR activity under Ni2+-limiting conditions, as measured by reduced transcript levels and 63Ni accumulation. Additionally, SlyD functioned in urease assembly in strain 26695.
authors.affiliation: Department of Biochemistry and Molecular Biophysics, Washington University School of Medicine, St. Louis, MO 63110, USA.
authors.forename: Erin L
authors.initials: EL
authors.lastname: Benanti
authors.forename: Peter T
authors.initials: PT
authors.lastname: Chivers
mesh_terms: D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism*; D017353:Gene Deletion; D016480:Helicobacter pylori / Q000235:genetics / Q000378:metabolism*; D009532:Nickel / Q000378:metabolism*; D012097:Repressor Proteins / Q000235:genetics / Q000378:metabolism*; D014158:Transcription, Genetic; D014510:Urease / Q000235:genetics / Q000378:metabolism*
chemical_list: D001426:Bacterial Proteins; C523724:NikR protein, Helicobacter pylori; D012097:Repressor Proteins; D009532:Nickel; D014510:Urease