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Uox KO Mouse
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Uox KO Mouse
제품명
Uox KO Mouse
제품 ID
C001232
품종 계통
C57BL/6JCya-Uoxem1/Cya
Backgroud
C57BL/6JCya
상태
이 마우스 계통을 논문에서 사용할 경우, “Uox KO Mouse (카탈로그 번호 C001232)은 Cyagen에서 구입하였습니다.”라고 명시해 주시기 바랍니다.
Disease Animal Models
Hyperuricemia
구매 가능한 제품 종류
연령
Genotype
성별
수량
표준 제공 조건은 최소 3마리의 이형접합(heterozygous) 보균자를 보장합니다. 동형접합(homozygous) 보균자 및/또는 특정 성별에 대한 브리딩 서비스도 제공됩니다.
가격 문의
Disease Animal Models
Hyperuricemia
기본 정보
검증 데이터
관련 자료
기본 정보
유전자명
유전자 별칭
--
NCBI ID
염색체
Chr 3
MGI ID
Datasheet
품종 계통 설명
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].
Reference
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.
변형 전략
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.
응용 분야
Hyperuricemia Research;
Gout and Related Disease Research;
Other Metabolic and Renal Disease Research.
검증 데이터
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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