Dffa-flox 基因敲除小鼠

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产品名称

Dffa-flox 基因敲除小鼠

产品编号

S-CKO-02031

品系全称

C57BL/6JCya-Dffaem1flox/Cya

品系背景

C57BL/6JCya

品系编号

CKOCMP-13347-Dffa-B6J-VA

品系状态

使用本品系发表的文献需注明: Dffa-flox 基因敲除小鼠 mice (Strain S-CKO-02031) were purchased from Cyagen.
交付类型
周龄
性别
基因型
数量
cKO小鼠库模型

基本信息

基因研究概述

质控标准

基因
基因全称
DNA fragmentation factor, alpha subunit
基因别称
A330085O09Rik,DFF35,Dff45,ICAD,ICAD-L,ICAD-S
染色体号
Chr 4 (Mouse)
转录本 ID
NCBI: NM_001025296.2 | Ensembl: ENSMUST00000030816
修饰方式
条件性基因敲除
靶向范围
Exon 2~3
敲除长度
~2260 bp
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:1196227Mice homozygous for a knock-out allele show increased resistance to apoptosis in response to several apoptotic stimuli, enhanced spatial learning and memory, higher granule cell density and total granule cell number in the dentate gyrus, and resistance to kainic acid-induced CA3 neuronal cell death.
Dffa基因,也称为细胞死亡诱导的DFFA样效应蛋白A,是一种与细胞凋亡和脂滴代谢相关的蛋白质。Dffa基因在多种生物学过程中发挥重要作用,包括细胞分化、发育、代谢和疾病发生。

Dffa基因在多种疾病中发挥重要作用,包括动脉粥样硬化、糖尿病心肌病、结直肠癌和Wilms瘤。在动脉粥样硬化中,Dffa通过NF-κB/IL-6信号通路介导巨噬细胞的炎症反应,促进动脉粥样硬化斑块的形成[1]。在糖尿病心肌病中,Dffa通过下调lncRNA TINCR抑制焦亡和糖尿病心肌病的发生[2]。在结直肠癌中,Dffa通过m6A修饰抑制SOX4 mRNA的表达,从而抑制肿瘤的转移[3]。此外,Dffa的基因多态性与中国儿童Wilms瘤的易感性降低相关[4]。

高风险神经母细胞瘤(NB)患者中,Dffa表达显著上调,与不良预后有强相关性。Dffa通过m6A-YTHDF1依赖机制抑制YWHAH表达,激活PI3K/AKT信号通路,促进NB细胞活性[5]。Dffa通过促进PRC2和KDM5B在二价结构域上的结合,影响组蛋白修饰,进而调控二价结构基因的表达[6]

Dffa不仅在RNA修饰中发挥作用,还具有独立的染色质调控功能。Dffa可以与H3K27me3结合,招募KDM6B诱导H3K27me3的去甲基化,从而影响基因表达和干细胞的多能性维持[7]。此外,Dffa还可以通过下调lncRNA XIST的表达抑制结直肠癌的增殖和转移[8]。

综上所述,Dffa是一种重要的蛋白质,参与调控RNA的稳定性和功能,影响基因表达和生物学过程。Dffa在多种疾病中发挥重要作用,包括动脉粥样硬化、糖尿病心肌病、结直肠癌和Wilms瘤。此外,Dffa还具有独立的染色质调控功能,影响基因表达和干细胞的多能性维持。Dffa的研究有助于深入理解RNA表观遗传修饰的生物学功能和疾病发生机制,为疾病的治疗和预防提供新的思路和策略。

参考文献:
1. Yamada, Osamu, Na Nan, Suthamas, Akao, Takeshi, Enei, Hitoshi, Akita, Osamu. . dffA gene from Aspergillus oryzae encodes L-ornithine N5-oxygenase and is indispensable for deferriferrichrysin biosynthesis. In Journal of bioscience and bioengineering, 95, 82-8. doi:. https://pubmed.ncbi.nlm.nih.gov/16233371/
2. Zhou, Hui-Min, Ti, Yun, Wang, Hui, Zhang, Wei, Zhong, Ming. . Cell death-inducing DFFA-like effector C/CIDEC gene silencing alleviates diabetic cardiomyopathy via upregulating AMPKa phosphorylation. In FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 35, e21504. doi:10.1096/fj.202002562R. https://pubmed.ncbi.nlm.nih.gov/33913563/
3. Watanabe, Hisayuki, Hatakeyama, Makoto, Sakurai, Hiroshi, Uchimiya, Hirofumi, Sato, Toshitsugu. . Isolation of industrial strains of Aspergillus oryzae lacking ferrichrysin by disruption of the dffA gene. In Journal of bioscience and bioengineering, 106, 488-92. doi:10.1263/jbb.106.488. https://pubmed.ncbi.nlm.nih.gov/19111645/
4. Wu, Jing, Bu, Dandan, Wang, Haiquan, Xue, Bin, Li, Chao-Jun. 2023. The rhythmic coupling of Egr-1 and Cidea regulates age-related metabolic dysfunction in the liver of male mice. In Nature communications, 14, 1634. doi:10.1038/s41467-023-36775-8. https://pubmed.ncbi.nlm.nih.gov/36964140/
5. Yang, Xuping, Liu, Qinhui, Li, Yanping, Wang, Rui, He, Jinhan. . The diabetes medication canagliflozin promotes mitochondrial remodelling of adipocyte via the AMPK-Sirt1-Pgc-1α signalling pathway. In Adipocyte, 9, 484-494. doi:10.1080/21623945.2020.1807850. https://pubmed.ncbi.nlm.nih.gov/32835596/
6. Wang, Jing, Cao, Xiukai, Pan, Hong, Lan, Xianyong, Chen, Hong. 2013. Cell death-inducing DFFA-like effector c (CIDEC/Fsp27) gene: molecular cloning, sequence characterization, tissue distribution and polymorphisms in Chinese cattles. In Molecular biology reports, 40, 6765-74. doi:10.1007/s11033-013-2793-y. https://pubmed.ncbi.nlm.nih.gov/24065549/
7. Yang, Yangjun, Li, Xi, Liu, Zonghan, Chen, Yinghong, Sun, Yi. 2022. Moderate Treadmill Exercise Alleviates NAFLD by Regulating the Biogenesis and Autophagy of Lipid Droplet. In Nutrients, 14, . doi:10.3390/nu14224910. https://pubmed.ncbi.nlm.nih.gov/36432597/
8. Slayton, Mark, Gupta, Abhishek, Balakrishnan, Bijinu, Puri, Vishwajeet. 2019. CIDE Proteins in Human Health and Disease. In Cells, 8, . doi:10.3390/cells8030238. https://pubmed.ncbi.nlm.nih.gov/30871156/