Generation of a mouse model for arginase II deficiency by targeted disruption of the arginase II gene

被引:120
作者
Shi, O
Morris, SM
Zoghbi, H
Porter, CW
O'Brien, WE [1 ]
机构
[1] Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA
[2] Baylor Coll Med, Dept Pediat, Houston, TX 77030 USA
[3] Univ Pittsburgh, Dept Mol Genet & Biochem, Pittsburgh, PA 15261 USA
[4] Roswell Pk Canc Inst, Grace Canc Drug Ctr, Buffalo, NY 14263 USA
关键词
D O I
10.1128/MCB.21.3.811-813.2001
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:811 / 813
页数:3
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