C57BL/6JCya-Mtfr1em1flox/Cya
Common Name:
Mtfr1-flox
Product ID:
S-CKO-13711
Background:
C57BL/6JCya
Product Type
Age
Genotype
Sex
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Basic Information
Strain Name
Mtfr1-flox
Strain ID
CKOCMP-67472-Mtfr1-B6J-VA
Gene Name
Product ID
S-CKO-13711
Gene Alias
1300002C08Rik; 1700080D04Rik; 2810026O10Rik; 4930579E05Rik; Chppr; Fam54a2
Background
C57BL/6JCya
NCBI ID
Modification
Conditional knockout
Chromosome
3
Phenotype
Document
Application
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Note: When using this mouse strain in a publication, please cite “C57BL/6JCya-Mtfr1em1flox/Cya mice (Catalog S-CKO-13711) were purchased from Cyagen.”
Strain Description
Ensembl Number
ENSMUST00000130645
NCBI RefSeq
NM_026182
Target Region
Exon 4
Size of Effective Region
~1.2 kb
Detailed Document
Overview of Gene Research
MTFR1, short for mitochondrial fission regulator 1, is a nuclear gene coding for a mitochondrial protein. It plays a crucial role in regulating mitochondrial dynamics, including fission and fusion, which are essential for maintaining cellular function. MTFR1 is also associated with antioxidant activity and may be involved in various biological processes such as cell metabolism, proliferation, and apoptosis. Genetic models, like gene knockout (KO) mouse models, have been valuable in studying its functions [7,8].
In multiple cancer types, MTFR1 shows distinct roles. In tongue squamous cell carcinoma (TSCC), knockdown of MTFR1 inhibits TGFβ1-induced epithelial-mesenchymal transition (EMT), migration, and invasion [1]. In lung adenocarcinoma (LAC), overexpression of MTFR1 promotes cancer progression, drug-resistance to cisplatin, and is related to the immune microenvironment. Interfering with MTFR1 expression inhibits the proliferation, migration, and invasion of LAC cells and promotes their sensitivity to cisplatin [2]. In colon cancer, MTFR1 is highly expressed, and under glucose deprivation, it interacts with NEK1, leading to phosphorylation at serine 119, promoting mitochondrial fusion, and enhancing cellular tolerance to glucose deprivation [3]. In addition, in LUAD, MTFR1 promotes the progression and glycolysis via the AMPK/mTOR signalling pathway, and is negatively regulated by miR-29c-3p [4].
In cardiac-related studies, knocking down Mtfr1 in cardiomyocytes suppresses mitochondrial fission, apoptosis, and myocardial infarction. miR-324-5p, which is regulated by NFAT4, targets Mtfr1 to attenuate mitochondrial fission and cardiomyocyte apoptosis [5]. Also, miR-324-5p protects against oxidative stress-induced endothelial progenitor cell injury by targeting Mtfr1 [6].
In conclusion, MTFR1 is essential for regulating mitochondrial dynamics and functions, which impacts various biological processes. Its role in multiple diseases, especially in cancer progression and drug-resistance, and in cardiac-related pathologies, has been revealed through model-based research. Understanding MTFR1 functions can provide potential therapeutic targets for these diseases.
References：
1. Jia, Yonglu, Chen, Xiaojuan, Zhao, Dayong, Ma, Sancheng. 2022. SNHG1/miR-194-5p/MTFR1 Axis Promotes TGFβ1-Induced EMT, Migration and Invasion of Tongue Squamous Cell Carcinoma Cells. In Molecular biotechnology, 64, 780-790. doi:10.1007/s12033-021-00445-1. https://pubmed.ncbi.nlm.nih.gov/35107755/
2. Li, Qian-Yun, Guo, Qiang, Luo, Wei-Min, Zhang, Jun, Ke, Di. 2024. Overexpression of MTFR1 promotes cancer progression and drug-resistance on cisplatin and is related to the immune microenvironment in lung adenocarcinoma. In Aging, 16, 66-88. doi:10.18632/aging.205338. https://pubmed.ncbi.nlm.nih.gov/38170222/
3. Zhang, Nan, Dong, Lu, Liu, Sifan, Ning, Tingting, Zhu, Shengtao. 2025. MTFR1 phosphorylation-activated adaptive mitochondrial fusion is essential for colon cancer cell survival during glucose deprivation. In Neoplasia (New York, N.Y.), 63, 101159. doi:10.1016/j.neo.2025.101159. https://pubmed.ncbi.nlm.nih.gov/40121946/
4. Li, Yongmeng, Liu, Yanfei, Jin, Kai, Zhang, Huiying, Tian, Hui. 2021. Negatively Regulated by miR-29c-3p, MTFR1 Promotes the Progression and Glycolysis in Lung Adenocarcinoma via the AMPK/mTOR Signalling Pathway. In Frontiers in cell and developmental biology, 9, 771824. doi:10.3389/fcell.2021.771824. https://pubmed.ncbi.nlm.nih.gov/34926459/
5. Wang, K, Zhang, D-L, Long, B, Liu, C-Y, Li, P-F. 2015. NFAT4-dependent miR-324-5p regulates mitochondrial morphology and cardiomyocyte cell death by targeting Mtfr1. In Cell death & disease, 6, e2007. doi:10.1038/cddis.2015.348. https://pubmed.ncbi.nlm.nih.gov/26633713/
6. Chen, Peier, Zhong, Jianfeng, Ye, Jianfeng, Chen, Hao, Chen, Can. 2019. miR-324-5p protects against oxidative stress-induced endothelial progenitor cell injury by targeting Mtfr1. In Journal of cellular physiology, 234, 22082-22092. doi:10.1002/jcp.28771. https://pubmed.ncbi.nlm.nih.gov/31066044/
7. Monticone, Massimiliano, Panfoli, Isabella, Ravera, Silvia, Boitani, Carla, Castagnola, Patrizio. . The nuclear genes Mtfr1 and Dufd1 regulate mitochondrial dynamic and cellular respiration. In Journal of cellular physiology, 225, 767-76. doi:10.1002/jcp.22279. https://pubmed.ncbi.nlm.nih.gov/20568109/
8. Monticone, Massimiliano, Tonachini, Laura, Tavella, Sara, Cancedda, Ranieri, Castagnola, Patrizio. . Impaired expression of genes coding for reactive oxygen species scavenging enzymes in testes of Mtfr1/Chppr-deficient mice. In Reproduction (Cambridge, England), 134, 483-92. doi:. https://pubmed.ncbi.nlm.nih.gov/17709566/
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