C57BL/6JCya-Fmo2em1/Cya
Common Name
Fmo2-KO
Product ID
S-KO-19413
Backgroud
C57BL/6JCya
Strain ID
KOCMP-55990-Fmo2-B6J-VC
Status
When using this mouse strain in a publication, please cite “Fmo2-KO Mouse (Catalog S-KO-19413) were purchased from Cyagen.”
Product Type
Age
Genotype
Sex
Quantity
The standard delivery applies for a guaranteed minimum of three heterozygous carriers. Breeding services for homozygous carriers and/or specified sex are available.
Basic Information
Strain Name
Fmo2-KO
Strain ID
KOCMP-55990-Fmo2-B6J-VC
Gene Name
Product ID
S-KO-19413
Gene Alias
2310008D08Rik, 2310042I22Rik
Background
C57BL/6JCya
Gene Full Name
flavin containing monooxygenase 2
Modification
Conventional knockout
NCBI ID
Phenotype
Chromosome
Chr 1 (Mouse)
Application
--
Datasheet
Strain Description
Ensembl Transcript ID
ENSMUST00000045902
NCBI Transcript ID
NM_018881
Target Region
Exon 4
Size of Effective Region
~0.8 kb
Overview of Gene Research
Fmo2, or flavin-containing monooxygenase 2, is involved in multiple biological processes and disease-related pathways. It has been shown to play roles in processes such as lipogenesis regulation, immune-related responses, and cell protection mechanisms. Genetic models, like gene knockout (KO) and conditional knockout (CKO) mouse models, have been crucial for studying its functions [1,3,5].
In the context of non-alcoholic fatty liver disease (NAFLD), both global and hepatocyte-specific knockout of Fmo2 in mice led to increased lipogenesis, severe hepatic steatosis, inflammation, and fibrosis. In contrast, FMO2 overexpression improved NAFL/NASH. Mechanistically, FMO2 directly interacts with SREBP1, inhibiting its translocation from the endoplasmic reticulum to the Golgi apparatus and subsequent activation, thus suppressing de novo lipogenesis [1].
In epithelial ovarian cancer, FMO2 is upregulated in tumor stroma, correlates with fibroblast activation, and predicts a worse clinical outcome. It also contributes to immune cell infiltration, especially of CD163 + macrophages [2].
In the heart, genetic deletion of FMO2 in cardiomyocytes reduced cell survival and enhanced cardiac dysfunction after ischemic injury, while cardiomyocyte-specific overexpression had a protective effect. FMO2 inhibits ER stress-induced apoptotic proteins through its disulfide bond catalytic activity [3].
In breast cancer, FMO2 is downregulated and is closely related to clinical indicators. Decreased FMO2 expression is associated with poor survival, and it may be related to immunotherapy sensitivity [4].
In post-myocardial infarction cardiac remodeling, CELF1 promotes remodeling by suppressing FMO2, and FMO2 overexpression can improve extracellular matrix deposition and cardiac remodeling [5].
In lung adenocarcinoma, circ_MACF1 upregulates FMO2 by targeting miR-421, suppressing paclitaxel resistance and malignant cellular behaviors [6].
In conclusion, Fmo2 plays essential roles in various biological processes and disease conditions. Studies using KO/CKO mouse models have revealed its significance in diseases such as NAFLD, epithelial ovarian cancer, ischemic heart disease, breast cancer, post-myocardial infarction cardiac remodeling, and lung adenocarcinoma. Understanding Fmo2 functions provides insights into disease mechanisms and potential therapeutic targets.
References：
1. Ke, Changle, Xiao, Changchen, Li, Jiamin, Wu, Rongrong, Hu, Xinyang. 2023. FMO2 ameliorates nonalcoholic fatty liver disease by suppressing ER-to-Golgi transport of SREBP1. In Hepatology (Baltimore, Md.), 81, 181-197. doi:10.1097/HEP.0000000000000643. https://pubmed.ncbi.nlm.nih.gov/37874228/
2. Yu, Sihui, Yang, Rui, Xu, Tianhan, Wu, Sufang, Zhang, Jiawen. 2022. Cancer-associated fibroblasts-derived FMO2 as a biomarker of macrophage infiltration and prognosis in epithelial ovarian cancer. In Gynecologic oncology, 167, 342-353. doi:10.1016/j.ygyno.2022.09.003. https://pubmed.ncbi.nlm.nih.gov/36114029/
3. Liu, Qingnian, Huang, Jiniu, Ding, Hao, Hu, Xinyang, Wang, Jian'an. 2024. Flavin-containing monooxygenase 2 confers cardioprotection in ischemia models through its disulfide bond catalytic activity. In The Journal of clinical investigation, 134, . doi:10.1172/JCI177077. https://pubmed.ncbi.nlm.nih.gov/39480513/
4. Wu, Lichun, Chu, Jie, Shangguan, Lijuan, Cao, Mingfei, Lu, Feng. 2023. Discovery and identification of the prognostic significance and potential mechanism of FMO2 in breast cancer. In Aging, 15, 12651-12673. doi:10.18632/aging.205204. https://pubmed.ncbi.nlm.nih.gov/37963835/
5. Lai, Jun, Li, Likang, Liu, Jun, Jin, Wen, Ye, Zebing. 2025. CELF1 Promotes Post-myocardial Infarction Cardiac Remodeling Via Suppression of FMO2. In Cardiovascular toxicology, 25, 441-454. doi:10.1007/s12012-024-09951-5. https://pubmed.ncbi.nlm.nih.gov/40021568/
6. Qian, Xiaoting, Chen, Chunhua, Tong, Sanxiang, Zhang, Jun. 2023. Circ_MACF1 targets miR-421 to upregulate FMO2 to suppress paclitaxel resistance and malignant cellular behaviors in lung adenocarcinoma. In Thoracic cancer, 14, 3348-3357. doi:10.1111/1759-7714.15132. https://pubmed.ncbi.nlm.nih.gov/37814902/
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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