Prdx3-KO 基因敲除小鼠

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产品名称

Prdx3-KO 基因敲除小鼠

产品编号

S-KO-18402

品系全称

C57BL/6JCya-Prdx3em1/Cya

品系背景

C57BL/6JCya

品系编号

KOCMP-11757-Prdx3-B6J-VB

品系状态

使用本品系发表的文献需注明: Prdx3-KO 基因敲除小鼠 mice (Strain S-KO-18402) 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
peroxiredoxin 3
基因别称
Aop1,D0Tohi1,Ef2l,Mer5,Prx3,SP22,TDXM
染色体号
Chr 19 (Mouse)
转录本 ID
NCBI: NM_007452 | Ensembl: ENSMUST00000025961
修饰方式
全身性基因敲除
靶向范围
Exon 2
敲除长度
~1.3 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:88034Homozygotes for a null allele show increased fat mass, adipocyte hypertrophy, mitochondrial dysfunction, oxidative stress, adipokine dysregulation and altered lipid and glucose metabolism. Homozygotes for a gene-trap allele show reduced weight and high susceptibility to LPS-induced oxidative stress.
Prdx3,全称为Peroxiredoxin 3,是一种定位于线粒体的过氧化还原酶,属于过氧化物酶家族成员。过氧化物酶是一类能够清除细胞内的活性氧(ROS)的抗氧化酶,对于维持细胞的氧化还原平衡和防止氧化应激损伤至关重要。Prdx3通过还原过氧化氢和其他过氧化物,保护线粒体免受氧化损伤,维持线粒体功能稳定。此外,Prdx3还参与细胞的增殖、分化、凋亡和应激反应等多种生物学过程。

研究表明,Prdx3在多种疾病的发生和发展中发挥重要作用。例如,在神经退行性疾病中,如帕金森病(PD),线粒体功能障碍和ROS增加会导致Prdx3水平下降,从而增加神经细胞的损伤和死亡[1]。而在癌症中,如胶质母细胞瘤(GBM),Prdx3的表达上调可以抑制ROS水平,促进癌细胞的生长和放疗抵抗[3]。此外,Prdx3还与遗传性疾病相关,如Spinocerebellar Ataxia(SCA),由于Prdx3基因的非标准剪接突变导致的剪接外显子跳跃,导致SCA的发生[7]。

进一步的研究表明,Prdx3的调控机制复杂多样。例如,c-Myc转录因子可以激活Prdx3基因的表达,维持线粒体功能和细胞增殖[2]。而抑制因子FOXO1可以抑制Prdx3的表达,从而抑制癌细胞的生长和转移[8]。此外,Prdx3的表达还受到其他因子如PHB、FOXO1、ASB1等的调控[4,5,6]。

综上所述,Prdx3作为一种重要的线粒体过氧化还原酶,在维持细胞的氧化还原平衡和线粒体功能稳定中发挥重要作用。Prdx3的异常表达与多种疾病的发生和发展密切相关,包括神经退行性疾病、癌症和遗传性疾病。深入研究Prdx3的生物学功能和调控机制,有助于揭示疾病的发生机制,并为疾病的治疗提供新的思路和策略。

参考文献:
1. Villa-Cedillo, Sheila Adela, Acosta-Espinoza, Esrom Jared, Soto-Domínguez, Adolfo, Valdés, Jesús, Saucedo-Cárdenas, Odila. 2024. Antioxidant PRDX3 gene therapy protects brain cells and prevents neurodegeneration in an animal model of Parkinson's disease. In Neuropeptides, 110, 102494. doi:10.1016/j.npep.2024.102494. https://pubmed.ncbi.nlm.nih.gov/39736192/
2. Wonsey, Diane R, Zeller, Karen I, Dang, Chi V. . The c-Myc target gene PRDX3 is required for mitochondrial homeostasis and neoplastic transformation. In Proceedings of the National Academy of Sciences of the United States of America, 99, 6649-54. doi:. https://pubmed.ncbi.nlm.nih.gov/12011429/
3. Huang, Haohao, Zhang, Songyang, Li, Yuanyuan, Xia, Qing, Man, Jianghong. 2021. Suppression of mitochondrial ROS by prohibitin drives glioblastoma progression and therapeutic resistance. In Nature communications, 12, 3720. doi:10.1038/s41467-021-24108-6. https://pubmed.ncbi.nlm.nih.gov/34140524/
4. Zhao, Zhou, Cai, Zhaolun, Zhang, Su, Han, Junhong, Zhang, Bo. 2024. Activation of the FOXM1/ASF1B/PRDX3 axis confers hyperproliferative and antioxidative stress reactivity to gastric cancer. In Cancer letters, 589, 216796. doi:10.1016/j.canlet.2024.216796. https://pubmed.ncbi.nlm.nih.gov/38537775/
5. Wang, Hong, Dey, Kaushik Kumar, Chen, Ping-Chung, Beach, Thomas G, Peng, Junmin. 2020. Integrated analysis of ultra-deep proteomes in cortex, cerebrospinal fluid and serum reveals a mitochondrial signature in Alzheimer's disease. In Molecular neurodegeneration, 15, 43. doi:10.1186/s13024-020-00384-6. https://pubmed.ncbi.nlm.nih.gov/32711556/
6. Liu, Zhilei, Hu, Yadong, Liang, Haisha, Feng, Shan, Deng, Haiteng. 2016. Silencing PRDX3 Inhibits Growth and Promotes Invasion and Extracellular Matrix Degradation in Hepatocellular Carcinoma Cells. In Journal of proteome research, 15, 1506-14. doi:10.1021/acs.jproteome.5b01125. https://pubmed.ncbi.nlm.nih.gov/26983019/
7. Wang, Guangyu, Wang, Bin, Qin, Qingtao, Zhao, Yuying, Lin, Pengfei. 2023. Exon Skipping Caused by Noncanonical Splicing Mutation in PRDX3-Related Spinocerebellar Ataxia. In Movement disorders : official journal of the Movement Disorder Society, 38, 1968-1970. doi:10.1002/mds.29575. https://pubmed.ncbi.nlm.nih.gov/37553955/
8. Rafeeq, Misbahuddin M, Umair, Muhammad, Bilal, Muhammad, Alam, Mohammad Zubair, Ali, Raja Hussain. 2022. A novel biallelic variant further delineates PRDX3-related autosomal recessive cerebellar ataxia. In Neurogenetics, 24, 55-60. doi:10.1007/s10048-022-00701-9. https://pubmed.ncbi.nlm.nih.gov/36190665/