Mir214-KO 基因敲除小鼠

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产品名称

Mir214-KO 基因敲除小鼠

产品编号

S-KO-19833

品系全称

C57BL/6JCya-Mir214em1/Cya

品系背景

C57BL/6JCya

品系编号

KOCMP-387210-Mir214-B6J-VA

品系状态

使用本品系发表的文献需注明: Mir214-KO 基因敲除小鼠 mice (Strain S-KO-19833) were purchased from Cyagen.
交付类型
周龄
性别
基因型
数量

基本信息

基因研究概述

质控标准

基因
基因全称
microRNA 214
基因别称
Mirn214,mir-214,mmu-mir-214
染色体号
Chr 1 (Mouse)
转录本 ID
NCBI: NR_029796 | Ensembl: ENSMUST00000083582
修饰方式
全身性基因敲除
靶向范围
Exon 1
敲除长度
~0.2 kb
品系说明
该品系是基于策略设计时的数据库信息制作而成,建议您在购买前查询最新的数据库和相关文献,以获取最准确的表型信息。
表型提示
MGI:2676890Mice homozygous for a knock-out allele exhibit increased myocyte apoptosis, fibrosis and myocyte size following cardiac ischemia and reperfusion with altered calcium transients in cardiomyocytes.
基因Mir214,也称为microRNA-214,是一种短链非编码RNA分子,属于microRNA家族。MicroRNA是一类内源性非编码RNA,它们通过与靶基因mRNA的3'非翻译区(3'-UTR)结合,介导mRNA的转录后沉默和降解,从而在基因表达调控中发挥重要作用。Mir214在多种生物学过程中发挥作用,包括细胞增殖、凋亡、分化、代谢和疾病发生等。

Mir214在多种疾病中发挥重要作用。例如,在非酒精性脂肪肝疾病(NAFLD)中,Mir214-3p的表达上调,导致自噬相关基因UlK1的表达下调,从而抑制自噬活性,加重脂肪肝病变[1]。在糖尿病肾脏病(DKD)中,p53的表达上调导致Mir214的表达上调,进而抑制ULK1的表达,降低自噬活性,导致肾小管损伤和纤维化[2]。此外,Mir214还与心肌梗死、骨质疏松、心血管疾病和癌症等疾病的发生发展密切相关[4,5,8,9]。

研究表明,Mir214可以通过多种机制发挥作用。例如,在脑缺血再灌注损伤中,lncRNA PVT1通过miR-214介导的TFR1和p53表达调控,影响铁死亡的发生[3]。在心脏修复中,过表达Mir214的间充质干细胞来源的外泌体可以促进心肌细胞存活和内皮细胞功能,改善心肌梗死后的心脏功能[6]。此外,Mir214还可以通过调节骨吸收表面的骨吸收活性,影响骨质疏松的发生发展[7]。

综上所述,Mir214是一种重要的microRNA,参与调控多种生物学过程,与多种疾病的发生发展密切相关。深入研究Mir214的功能机制和作用靶点,有助于揭示疾病的发生发展机制,为疾病的诊断和治疗提供新的思路和策略。

参考文献:
1. Lee, Da-Hye, Park, So-Hyun, Ahn, Jiyun, Jeon, Tae-Il, Jung, Chang Hwa. 2020. Mir214-3p and Hnf4a/Hnf4α reciprocally regulate Ulk1 expression and autophagy in nonalcoholic hepatic steatosis. In Autophagy, 17, 2415-2431. doi:10.1080/15548627.2020.1827779. https://pubmed.ncbi.nlm.nih.gov/33078654/
2. Ma, Zhengwei, Li, Lin, Livingston, Man J, Mei, Changlin, Dong, Zheng. . p53/microRNA-214/ULK1 axis impairs renal tubular autophagy in diabetic kidney disease. In The Journal of clinical investigation, 130, 5011-5026. doi:10.1172/JCI135536. https://pubmed.ncbi.nlm.nih.gov/32804155/
3. Lu, Jingjing, Xu, Feng, Lu, Hong. 2020. LncRNA PVT1 regulates ferroptosis through miR-214-mediated TFR1 and p53. In Life sciences, 260, 118305. doi:10.1016/j.lfs.2020.118305. https://pubmed.ncbi.nlm.nih.gov/32827544/
4. Amin, Meer M J, Trevelyan, Christopher J, Turner, Neil A. 2021. MicroRNA-214 in Health and Disease. In Cells, 10, . doi:10.3390/cells10123274. https://pubmed.ncbi.nlm.nih.gov/34943783/
5. Gupta, Shashi Kumar, Kumari, Sunaina, Singh, Sandhya, Singh, Sushil Kumar, Thum, Thomas. 2020. Non-coding RNAs: Regulators of valvular calcification. In Journal of molecular and cellular cardiology, 142, 14-23. doi:10.1016/j.yjmcc.2020.03.015. https://pubmed.ncbi.nlm.nih.gov/32247640/
6. Zhu, Wenwu, Wang, Qingjie, Zhang, Jian, Wang, Haoran, Han, Bing. 2023. Exosomes derived from mir-214-3p overexpressing mesenchymal stem cells promote myocardial repair. In Biomaterials research, 27, 77. doi:10.1186/s40824-023-00410-w. https://pubmed.ncbi.nlm.nih.gov/37563655/
7. Cai, Mingxiang, Yang, Li, Zhang, Shufan, Sun, Yao, Wang, Xiaogang. 2017. A bone-resorption surface-targeting nanoparticle to deliver anti-miR214 for osteoporosis therapy. In International journal of nanomedicine, 12, 7469-7482. doi:10.2147/IJN.S139775. https://pubmed.ncbi.nlm.nih.gov/29075114/
8. Zhao, Yanfang, Ponnusamy, Murugavel, Zhang, Lei, Wang, Kun, Li, Peifeng. 2017. The role of miR-214 in cardiovascular diseases. In European journal of pharmacology, 816, 138-145. doi:10.1016/j.ejphar.2017.08.009. https://pubmed.ncbi.nlm.nih.gov/28842125/
9. Sukmana, Bayu Indra, Al-Hawary, Sulieman Ibraheem Shelash, Abosaooda, Munther, Sapaev, I B, Mustafa, Yasser Fakri. 2023. A thorough and current study of miR-214-related targets in cancer. In Pathology, research and practice, 249, 154770. doi:10.1016/j.prp.2023.154770. https://pubmed.ncbi.nlm.nih.gov/37660658/