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Infection and Immunity, September 2001, p. 5914-5920, Vol. 69, No. 9
Department of Veterinary Pathobiology,
University of Missouri, Columbia, Missouri
65211,1 and Department of Microbiology
and Immunology, University of Maryland, Baltimore, Maryland
212012
Received 2 February 2001/Returned for modification 18 April
2001/Accepted 15 June 2001
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.
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.9.5914-5920.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Cloning, Expression, and Catalytic Activity of
Helicobacter hepaticus Urease

*
Corresponding author. Present address: Department of
Comparative Medicine, Stanford University School of Medicine, Stanford, CA 94305-5410. Phone: (650) 723-5305. Fax: (650) 725-0940. E-mail: CBeckwith{at}Stanford.edu.
Present address: Department of Microbiology and Immunology, College
of Medicine, University of South Alabama, Mobile, AL 36688.
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