| First Author | Shi O | Year | 2001 |
| Journal | Mol Cell Biol | Volume | 21 |
| Issue | 3 | Pages | 811-3 |
| PubMed ID | 11154268 | Mgi Jnum | J:67353 |
| Mgi Id | MGI:1930421 | Doi | 10.1128/MCB.21.3.811-813.2001 |
| Citation | Shi O, et al. (2001) Generation of a mouse model for arginase II deficiency by targeted disruption of the arginase II gene. Mol Cell Biol 21(3):811-3 |
| abstractText | 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. |
