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C57BL/6JCya-Kmoem1flox/Cya
Common Name:
Kmo-flox
Product ID:
S-CKO-18676
Background:
C57BL/6JCya
Product Type
Age
Genotype
Sex
Quantity
Price:
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Basic Information
Strain Name
Kmo-flox
Strain ID
CKOCMP-98256-Kmo-B6J-VB
Gene Name
Kmo
Product ID
S-CKO-18676
Gene Alias
-
Background
C57BL/6JCya
NCBI ID
98256
Modification
Conditional knockout
Chromosome
1
Phenotype
MGI:2138151
Document
Click here to download >>
Application
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Rare Disease Data Center >>
Note
Note: When using this mouse strain in a publication, please cite “C57BL/6JCya-Kmoem1flox/Cya mice (Catalog S-CKO-18676) were purchased from Cyagen.”
Strain Description
Ensembl Number
ENSMUST00000040250
NCBI RefSeq
NM_133809
Target Region
Exon 5
Size of Effective Region
~0.8 kb
Detailed Document
Click here to download >>
Overview of Gene Research
Kmo, short for kynurenine-3-monooxygenase, is a mitochondrial enzyme. It is a key rate-limiting enzyme in the eukaryotic kynurenine pathway (KP), which is the major catabolic route of tryptophan. Kmo can convert kynurenine into the neurotoxin 3-hydroxykynurenine and quinolinic acid, influencing the balance of toxic and neuroprotective metabolites in the body [1].

In various disease models, the role of Kmo has been explored. In myocardial ischemia (MI) mouse models, pharmacological or heart-specific inhibition of Kmo suppressed the elevation of xanthurenic acid (XA) and ameliorated OGD-induced cardiomyocytes injury and ligation-induced MI injury, by maintaining mitochondrial fusion and fission balance [2]. In hepatocellular carcinoma (HCC) cell experiments, low expression of Kmo promoted HCC proliferation, invasion, metastasis, EMT, and cell apoptosis [3]. In atherosclerotic plaque studies, lentivirus-mediated KMO silencing in high-fat-fed ApoE-/-mice attenuated plaque formation and promoted plaque stability [4]. In a stroke mouse model, suppression of Kmo expression by circSCMH1 enhanced mitochondrial fusion and inhibited mitophagy, promoting post-stroke brain repair [5]. In kmo-/-mice, they were vulnerable to pathogenic viral challenge, indicating Kmo and its enzymatic product QUIN have antiviral functions [6]. Inhibition of Kmo may also mitigate colitis and protect against colorectal cancer [7]. In Huntington's disease (HD) model systems, inhibition of Kmo shifted the flux in the KP towards the formation of the neuroprotectant kynurenic acid (KYNA), ameliorating disease-relevant phenotypes [8].

In conclusion, Kmo is a crucial enzyme in the kynurenine pathway, significantly affecting multiple biological processes and disease conditions. Studies using gene knockout or conditional knockout mouse models have revealed its roles in diseases such as myocardial ischemia, hepatocellular carcinoma, atherosclerotic plaque instability, stroke, viral infections, colitis, colorectal cancer, and Huntington's disease. These findings provide potential therapeutic directions for these diseases by targeting Kmo.

References:
1. Chen, Yanmei, Zhang, Jiahui, Yang, Yueying, Sun, Dejuan, Chen, Lixia. 2022. Kynurenine-3-monooxygenase (KMO): From its biological functions to therapeutic effect in diseases progression. In Journal of cellular physiology, 237, 4339-4355. doi:10.1002/jcp.30876. https://pubmed.ncbi.nlm.nih.gov/36088660/
2. Lai, Qiong, Wu, Lingling, Dong, Shuhong, Yu, Boyang, Li, Fang. 2023. Inhibition of KMO Ameliorates Myocardial Ischemia Injury via Maintaining Mitochondrial Fusion and Fission Balance. In International journal of biological sciences, 19, 3077-3098. doi:10.7150/ijbs.83392. https://pubmed.ncbi.nlm.nih.gov/37416768/
3. Xu, Jun, Song, Jianping, Zeng, Xinmin, Hu, Yanqin, Kuang, Jingru. . KMO in the promotion of tumor development and progression in hepatocellular carcinoma. In Journal of gastrointestinal oncology, 14, 516-532. doi:10.21037/jgo-23-147. https://pubmed.ncbi.nlm.nih.gov/37201083/
4. Liao, Fu-Jun, Shen, Shao-Liang, Bao, Hai-Long, Li, Wei, Liu, Da-Nan. 2024. Identification and experimental validation of KMO as a critical immune-associated mitochondrial gene in unstable atherosclerotic plaque. In Journal of translational medicine, 22, 668. doi:10.1186/s12967-024-05464-5. https://pubmed.ncbi.nlm.nih.gov/39026250/
5. Wang, Yu, Bai, Ying, Cai, Yang, Han, Bing, Yao, Honghong. 2024. Circular RNA SCMH1 suppresses KMO expression to inhibit mitophagy and promote functional recovery following stroke. In Theranostics, 14, 7292-7308. doi:10.7150/thno.99323. https://pubmed.ncbi.nlm.nih.gov/39659575/
6. Zhao, Jin, Chen, Jiaoshan, Wang, Congcong, Cheng, Genhong, Sun, Caijun. 2022. Kynurenine-3-monooxygenase (KMO) broadly inhibits viral infections via triggering NMDAR/Ca2+ influx and CaMKII/ IRF3-mediated IFN-β production. In PLoS pathogens, 18, e1010366. doi:10.1371/journal.ppat.1010366. https://pubmed.ncbi.nlm.nih.gov/35235615/
7. Ala, Moein. 2021. Tryptophan metabolites modulate inflammatory bowel disease and colorectal cancer by affecting immune system. In International reviews of immunology, 41, 326-345. doi:10.1080/08830185.2021.1954638. https://pubmed.ncbi.nlm.nih.gov/34289794/
8. Thevandavakkam, Mathuravani A, Schwarcz, Robert, Muchowski, Paul J, Giorgini, Flaviano. . Targeting kynurenine 3-monooxygenase (KMO): implications for therapy in Huntington's disease. In CNS & neurological disorders drug targets, 9, 791-800. doi:. https://pubmed.ncbi.nlm.nih.gov/20942784/
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
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