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Hyperuricemia and urate nephropathy in urate oxidase-deficient mice.

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Wu, X, Wakamiya, M, Vaishnav, S, Geske, R, Montgomery, C, Jones, P, Bradley, A, Caskey, C T·1994·Proceedings of the National Academy of Sciences

Abstract

Urate oxidase, or uricase (EC 1.7.3.3), is a purine metabolic enzyme that catalyzes the conversion of uric acid to allantoin in most mammals except humans and certain other primates. The loss of urate oxidase in the human during primate evolution predisposes man to hyperuricemia, a metabolic disturbance that can lead to gouty arthritis and renal stones. To create a mouse model for hyperuricemia and gout, and to address the question of whether urate oxidase is essential in lower mammalian species, we have disrupted the urate oxidase gene in the mouse by homologous recombination in embryonic stem cells. Unlike the human situation, urate oxidase deficiency in mice causes pronounced hyperuricemia and urate nephropathy. More than half of the mutant mice died before 4 weeks of age, indicating that urate oxidase is essential in mice. These mutant mice may also serve as animal models for hyperuricemia and its related nephropathy in humans.

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Metadata

Authors
Wu, X., Wakamiya, M., Vaishnav, S., Geske, R., Montgomery, C., Jones, P., Bradley, A., & Caskey, C. T.
Venue
Proceedings of the National Academy of Sciences
Published
1994-01-18
Volume
91
Issue
2
Pages
742-746
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
OpenAlex
W1968290904
Cited by
291
References
0
FWCI
3.67
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Hyperuricemia and urate nephropathy in urate oxidase-deficient mice. https://app.cochat.ai/papers/10.1073/pnas.91.2.742
The paper
Wu, X., Wakamiya, M., Vaishnav, S., Geske, R., Montgomery, C., Jones, P., Bradley, A., & Caskey, C. T. (1994). Hyperuricemia and urate nephropathy in urate oxidase-deficient mice. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.91.2.742

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