Fgf13-flox Mouse
一般名
Fgf13-flox
製品ID
S-CKO-02400
背景情報
C57BL/6JCya
系統ID
CKOCMP-14168-Fgf13-B6J-VA
状況
このマウス系統を論文で使用する場合は、「Fgf13-flox Mouse(カタログ番号S-CKO-02400)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
Fgf13-flox
系統ID
CKOCMP-14168-Fgf13-B6J-VA
遺伝子名
製品ID
S-CKO-02400
遺伝子別名
Fhf2, Fgf1c
遺伝子別名
C57BL/6JCya
NCBI ID
修正
Conditional knockout
染色体
Chr X
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
ENSMUST00000033473
NCBIトランスクリプトID
NM_010200
ターゲット領域
Exon 3
有効領域の大きさ
~1.0 kb
遺伝子研究の概要
Fgf13, a non-canonical, non-secreted fibroblast growth factor, is involved in multiple biological processes. It interacts with microtubules and is associated with pathways related to calcium signaling, ion channel regulation, and immune-related functions. Genetic models, such as KO and CKO mouse models, have been crucial for studying its functions [1,2,6].
In heart failure models, Fgf13 deficiency alleviates cardiac dysfunction by improving abnormal calcium signaling through inhibiting increased microtubule stability [1]. In dorsal root ganglion neurons, conditional knockout of Fgf13 impairs scratching behaviors in acute and chronic itch models, as it selectively regulates TRPV1 function via microtubule-stabilizing effect [2]. In AML patients, low Fgf13 expression is related to prognosis, and overexpression in xenograft models inhibits AML cell growth [3]. In diabetic nephropathy, endothelial-specific deletion of Fgf13 alleviates damage by improving mitochondrial homeostasis [4]. Obesity-induced Fgf13 in adipose tissue impairs energy and glucose homeostasis [5]. Interneuron-targeted deletion of Fgf13 leads to seizures and affects K⁺ channel currents [6]. Stable Fgf13 depletion in triple-negative breast cancer cells restricts metastasis [7]. Loss of Fgf13 in mouse DRG neurons impairs histamine-induced scratching behavior [8]. Fgf13 up-regulation in cardiac hypertrophy has a deteriorating role, and its deficiency inhibits NF-κB activation [9]. Cardiac Fgf13 knockdown alleviates fibrosis by modulating microtubule stabilization and ROCK signaling pathway [10].
In conclusion, Fgf13 plays essential roles in various biological processes including calcium homeostasis, itch sensation, cancer development, metabolic regulation, and neuronal excitability. Gene knockout and conditional knockout mouse models have significantly contributed to understanding its functions in heart failure, leukemia, diabetic nephropathy, metabolic diseases, epilepsy, and breast cancer, providing potential therapeutic targets for these diseases.
References:
1. Zhao, Ran, Yan, Yingke, Dong, Yiming, Gu, Guoqiang, Wang, Chuan. 2024. FGF13 deficiency ameliorates calcium signaling abnormality in heart failure by regulating microtubule stability. In Biochemical pharmacology, 225, 116329. doi:10.1016/j.bcp.2024.116329. https://pubmed.ncbi.nlm.nih.gov/38821375/
2. Dong, Zi-Shan, Zhang, Xue-Rou, Xue, Da-Zhong, Zhang, Hai-Lin, Wang, Chuan. . FGF13 enhances the function of TRPV1 by stabilizing microtubules and regulates acute and chronic itch. In FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 38, e23661. doi:10.1096/fj.202400096R. https://pubmed.ncbi.nlm.nih.gov/38733310/
3. Li, Ran, Xue, Kai, Li, Junmin. 2022. FGF13 suppresses acute myeloid leukemia by regulating bone marrow niches. In Frontiers of medicine, 16, 896-908. doi:10.1007/s11684-022-0944-z. https://pubmed.ncbi.nlm.nih.gov/36053411/
4. Sun, Jia, Guan, Xueqiang, Niu, Chao, Jin, Litai, Cong, Weitao. . FGF13-Sensitive Alteration of Parkin Safeguards Mitochondrial Homeostasis in Endothelium of Diabetic Nephropathy. In Diabetes, 72, 97-111. doi:10.2337/db22-0231. https://pubmed.ncbi.nlm.nih.gov/36256844/
5. Naderi, Jamal, Johnson, Amanda Kelsey, Thakkar, Himani, Pitt, Geoffrey S, Chaurasia, Bhagirath. 2025. Ceramide-induced FGF13 impairs systemic metabolic health. In Cell metabolism, 37, 1206-1222.e8. doi:10.1016/j.cmet.2025.03.002. https://pubmed.ncbi.nlm.nih.gov/40169001/
6. Lin, Susan, Gade, Aravind R, Wang, Hong-Gang, Rajadhyaksha, Anjali M, Pitt, Geoffrey S. 2024. Interneuron FGF13 regulates seizure susceptibility via a sodium channel-independent mechanism. In bioRxiv : the preprint server for biology, , . doi:10.1101/2024.04.18.590019. https://pubmed.ncbi.nlm.nih.gov/38659789/
7. Johnstone, Cameron N, Pattison, Andrew D, Harrison, Paul F, Anderson, Robin L, Beilharz, Traude H. 2020. FGF13 promotes metastasis of triple-negative breast cancer. In International journal of cancer, 147, 230-243. doi:10.1002/ijc.32874. https://pubmed.ncbi.nlm.nih.gov/31957002/
8. Dong, Fei, Shi, Haixiang, Yang, Liu, Bao, Lan, Zhang, Xu. 2020. FGF13 Is Required for Histamine-Induced Itch Sensation by Interaction with NaV1.7. In The Journal of neuroscience : the official journal of the Society for Neuroscience, 40, 9589-9601. doi:10.1523/JNEUROSCI.0599-20.2020. https://pubmed.ncbi.nlm.nih.gov/33172979/
9. Sun, Jia, Niu, Chao, Ye, Weijian, Cong, Weitao, Li, Xiaokun. 2020. FGF13 Is a Novel Regulator of NF-κB and Potentiates Pathological Cardiac Hypertrophy. In iScience, 23, 101627. doi:10.1016/j.isci.2020.101627. https://pubmed.ncbi.nlm.nih.gov/33089113/
10. Wang, Cong, Wang, Xiangchong, Zhang, Yiyi, Gu, Guoqiang, Wang, Chuan. . Inducible Fgf13 ablation alleviates cardiac fibrosis via regulation of microtubule stability. In Acta biochimica et biophysica Sinica, 56, 1802-1812. doi:10.3724/abbs.2024075. https://pubmed.ncbi.nlm.nih.gov/38818580/
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