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Uox KO Mouse
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Uox KO Mouse
製品名
Uox KO Mouse
製品ID
C001232
系統名
C57BL/6JCya-Uoxem1/Cya
背景情報
C57BL/6JCya
状況
このマウス系統を論文で使用する場合は、「Uox KO Mouse(カタログ番号C001232)はサイアジェンから購入しました。」と引用してください。
Disease Animal Models
Hyperuricemia
製品タイプ
年齢
遺伝子型
性別
数量
標準的な配送方法では、少なくとも3匹のヘテロ接合体キャリアを保証しています。ホモ接合体キャリアや指定された性別の個体の繁殖サービスも利用可能です。
お見積もりについてはこちらまでご連絡ください
Disease Animal Models
Hyperuricemia
基本情報
検証 Data
関連リソース
基本情報
系統詳細
Uricase, which is encoded by the urate oxidase (UOX) gene, has an important role in the purine metabolic pathway, and most mammals contain UOX, which breaks down uric acid, a metabolite of purine nucleotides, into allantoin, which is more soluble than uric acid. Unlike other mammals, humans lack UOX, and purine catabolism can only produce uric acid, which is subsequently excreted by the kidneys, resulting in higher serum uric acid concentrations in humans than in other mammals. When the rate of uric acid production exceeds the excretory capacity of the kidneys, the serum uric acid level increases significantly, resulting in hyperuricemia.UOX can dramatically reduce plasma uric acid levels and treat gout and kidney disease secondary to hyperuricemia, among others [1].
This strain is a uricase-deficient mouse line generated by knocking out the mouse Uox gene. Due to impaired uricase synthesis, these mice spontaneously exhibit a hyperuricemic phenotype. Heterozygous Uox KO mice are viable and fertile. Homozygous Uox KO mice require allopurinol or similar drugs for postnatal survival [2].
参考文献
Lu J , Dalbeth N, Yin H , et al. Mouse models for human hyperuricaemia: a critical review. Nature Reviews Rheumatology, 2019, 15(Suppl. 10):1.
Wu X . Hyperuricemia and urate nephropathy in urate oxidase-deficient mice. Proc Natl Acad Sci U S A, 1994, 91.
系統作製戦略
The Uox gene is located on mouse chromosome 3. Using gene editing technology, Exons 2-4 of the Uox gene were deleted to generate this strain.
適用分野
Hyperuricemia Research;
Gout and Related Disease Research;
Other Metabolic and Renal Disease Research.
検証 Data
1. Survival Curve

Figure 1. Survival curves of homozygous Uox KO mice under different concentrations of allopurinol maintenance*. Pregnant surrogate mice and their offspring were provided with drinking water containing varying concentrations of allopurinol from 3 days post-embryo transfer to postnatal day 28 (postnatal week 4). Allopurinol administration was discontinued on postnatal day 28, and normal drinking water was introduced. Following complete cessation of allopurinol administration, offspring mice were group-housed on postnatal day 33. The data indicated that the survival rate of offspring mice was dose-dependent on allopurinol concentration, with the death phenomenon essentially ceasing after group housing. Group G3 exhibited the highest survival rate, approximately 50%, and demonstrated the best overall survival status. Group G2 showed a survival rate of approximately 44%, while Group G1 had a survival rate of approximately 23%.
*Experimental Group Information:
G1: Uox KO mice + 100mg/L allopurinol, n=46; G2: Uox KO mice + 150mg/L allopurinol, n=25; G3: Uox KO mice + 200mg/L allopurinol, n=30; G4: Uox KO mice + No allopurinol added, n=6; Sexes were not distinguished across groups.
*Experimental Group Information:
G1: Uox KO mice + 100mg/L allopurinol, n=46; G2: Uox KO mice + 150mg/L allopurinol, n=25; G3: Uox KO mice + 200mg/L allopurinol, n=30; G4: Uox KO mice + No allopurinol added, n=6; Sexes were not distinguished across groups.
2. Uric Acid (UA) Levels

Figure 2. Comparison of uric acid (UA) levels in homozygous Uox KO mice under different concentrations of allopurinol maintenance. During the 6 to 14 weeks of age, uric acid (UA) levels in Uox KO mice exhibited a slow, overall downward trend with increasing age. UA levels were similar between male and female mice. (Females: nG1=4, nG2=9, nG3=8, nG4=1; Males: nG1=7, nG2=2, nG3=6; Data presented as Mean ± SD).
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