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Molecular and Cellular Biology, February 2001, p. 811-813, Vol. 21, No. 3
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.3.811-813.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Generation of a Mouse Model for Arginase II Deficiency by Targeted Disruption of the Arginase II Gene

Ou Shi,1 Sidney M. Morris Jr.,2 Huda Zoghbi,1,3 Carl W. Porter,4 and William E. O'Brien1,*

Department of Molecular and Human Genetics1 and Department of Pediatrics,3 Baylor College of Medicine, Houston, Texas 77030; Department of Molecular Genetics and Biochemistry, University of Pittsburgh, Pittsburgh, Pennsylvania 152612; and Grace Cancer Drug Center, Roswell Park Cancer Institute, Buffalo, New York 142634

Received 6 September 2000/Accepted 8 November 2000

Mammals express two isoforms of arginase, designated types I and II. Arginase I is a component of the urea cycle, and inherited defects in arginase I have deleterious consequences in humans. In contrast, the physiologic role of arginase II has not been defined, and no deficiencies in arginase II have been identified in humans. Mice with a disruption in the arginase II gene were created to investigate the role of this enzyme. Homozygous arginase II-deficient mice were viable and apparently indistinguishable from wild-type mice, except for an elevated plasma arginine level which indicates that arginase II plays an important role in arginine homeostasis.

* Corresponding author. Mailing address: Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030. Phone: (713) 798-5484. Fax: (713) 798-8937. E-mail: wobrien{at}bcm.tmc.edu.

Molecular and Cellular Biology, February 2001, p. 811-813, Vol. 21, No. 3
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.3.811-813.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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