Mtfr1-flox Mouse
一般名
Mtfr1-flox
製品ID
S-CKO-13711
背景情報
C57BL/6JCya
系統ID
CKOCMP-67472-Mtfr1-B6J-VA
状況
このマウス系統を論文で使用する場合は、「Mtfr1-flox Mouse（カタログ番号S-CKO-13711）はサイアジェンから購入しました。」と引用してください。
製品タイプ
年齢
遺伝子型
性別
数量
標準的な配送方法では、少なくとも3匹のヘテロ接合体キャリアを保証しています。ホモ接合体キャリアや指定された性別の個体の繁殖サービスも利用可能です。
基本情報
系統名
Mtfr1-flox
系統ID
CKOCMP-67472-Mtfr1-B6J-VA
遺伝子名
製品ID
S-CKO-13711
遺伝子別名
Chppr, Fam54a2, 1300002C08Rik, 1700080D04Rik, 2810026O10Rik, 4930579E05Rik
遺伝子別名
C57BL/6JCya
NCBI ID
修正
Conditional knockout
染色体
Chr 3
表現型
アプリケーション
--
さらに
系統詳細
EnsemblトランスクリプトID
ENSMUST00000130645
NCBIトランスクリプトID
NM_026182
ターゲット領域
Exon 4
有効領域の大きさ
~1.2 kb
遺伝子研究の概要
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/
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凍結前の精子濃度を測定し、精子の生存能力の判定します。
凍結後の精子では、各バッチから1本の凍結保存された精子を選び出し、体外受精に使用します。
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