C57BL/6JCya-Uoxem1flox/Cya
Common Name:
Uox-flox
Product ID:
S-CKO-06551
Background:
C57BL/6JCya
Product Type
Age
Genotype
Sex
Quantity
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Basic Information
Strain Name
Uox-flox
Strain ID
CKOCMP-22262-Uox-B6J-VA
Gene Name
Product ID
S-CKO-06551
Gene Alias
-
Background
C57BL/6JCya
NCBI ID
Modification
Conditional knockout
Chromosome
3
Phenotype
Document
Application
--
Note: When using this mouse strain in a publication, please cite “C57BL/6JCya-Uoxem1flox/Cya mice (Catalog S-CKO-06551) were purchased from Cyagen.”
Strain Description
Ensembl Number
ENSMUST00000029837
NCBI RefSeq
NM_009474
Target Region
Exon 3~4
Size of Effective Region
~1.7 kb
Detailed Document
Overview of Gene Research
Uox, also known as urate oxidase, is an enzyme that metabolizes poorly-soluble uric acid (UA) to highly-soluble allantoin. Most mammals maintain normal serum uric acid levels via Uox. This process is crucial in purine metabolism pathways [4].
Uox-knockout (KO) mouse models have been widely used to study the role of Uox. Uox-KO mice spontaneously develop hyperuricemia, which is associated with multiple complications such as severe renal insufficiency, hypertension, left-ventricular remodeling, aortic endothelial dysfunction, hepatic steatosis, hyperglycemia, and hypercholesteremia [3]. These mice also exhibit systemic inflammation, impairment of intestinal integrity, and dysregulation of amino acids transportation that impacts serum uric acid level and CD4+ Th17-driven inflammation [1]. Additionally, in Urat1-Uox double-knockout (DKO) mice, which serve as models for hereditary renal hypouricemia type 1 (RHUC1), there are uricosuric effects, elevated renal injury markers, and increased NLRP3 inflammasome activity [2,5].
In conclusion, Uox is essential for maintaining normal uric acid metabolism. The study of Uox-KO and related double-knockout mouse models has significantly contributed to understanding the pathophysiology of hyperuricemia, gout, renal hypouricemia, and associated comorbidities, providing insights into potential therapeutic strategies for these diseases.
References:
1. Song, Siyue, Lou, Yu, Mao, Yingying, Wen, Chengping, Shao, Tiejuan. 2022. Alteration of Gut Microbiome and Correlated Amino Acid Metabolism Contribute to Hyperuricemia and Th17-Driven Inflammation in Uox-KO Mice. In Frontiers in immunology, 13, 804306. doi:10.3389/fimmu.2022.804306. https://pubmed.ncbi.nlm.nih.gov/35197978/
2. Hosoya, Takuji, Uchida, Shunya, Shibata, Shigeru, Matsumoto, Koji, Hosoyamada, Makoto. 2021. Xanthine Oxidoreductase Inhibitors Suppress the Onset of Exercise-Induced AKI in High HPRT Activity Urat1-Uox Double Knockout Mice. In Journal of the American Society of Nephrology : JASN, 33, 326-341. doi:10.1681/ASN.2021050616. https://pubmed.ncbi.nlm.nih.gov/34799437/
3. Zeng, Linzi, Shali, Shalaimaiti, Gao, Yabiao, Dai, Yuxiang, Zhou, Ping. 2024. Nuclease technology Mediated Deletion of the Uox Gene Generates a Mouse Model of Hyperuricemia with Multiple Complications. In Journal of cardiovascular translational research, 17, 1455-1465. doi:10.1007/s12265-024-10526-6. https://pubmed.ncbi.nlm.nih.gov/38856882/
4. Zhang, Mengjie, Hussain, Abid, Hu, Bo, Qin, Cheng-Feng, Huang, Yuanyu. 2024. Atavistic strategy for the treatment of hyperuricemia via ionizable liposomal mRNA. In Nature communications, 15, 6463. doi:10.1038/s41467-024-50752-9. https://pubmed.ncbi.nlm.nih.gov/39085241/
5. Hosoyamada, Makoto, Tsurumi, Yu, Hirano, Hidenori, Morisaki, Takayuki, Uchida, Shunya. . Urat1-Uox double knockout mice are experimental animal models of renal hypouricemia and exercise-induced acute kidney injury. In Nucleosides, nucleotides & nucleic acids, 35, 543-549. doi:. https://pubmed.ncbi.nlm.nih.gov/27906636/
Quality Control Standard
Sperm Test
Pre-cryopreservation: Measurement of sperm concentration, determination of sperm viability.
Post-cryopreservation: A vial of cryopreserved sperms is selected for in-vitro fertilization from each batch.
Environmental Standards:SPF
Available Region:Global
Source:Cyagen