Trim25-KO 基因敲除小鼠

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产品名称

Trim25-KO 基因敲除小鼠

产品编号

S-KO-05245

品系全称

C57BL/6JCya-Trim25em1/Cya

品系背景

C57BL/6JCya

品系编号

KOCMP-217069-Trim25-B6J-VA

品系状态

使用本品系发表的文献需注明: Trim25-KO 基因敲除小鼠 mice (Strain S-KO-05245) were purchased from Cyagen.
交付类型
周龄
性别
基因型
数量
KO小鼠库模型
NF-κB信号通路

基本信息

基因研究概述

质控标准

基因
基因全称
tripartite motif-containing 25
基因别称
EFP,Zfp147
染色体号
Chr 11 (Mouse)
转录本 ID
NCBI: NM_009546 | Ensembl: ENSMUST00000107896
修饰方式
全身性基因敲除
靶向范围
Exon 2~8
敲除长度
~11.1 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:102749Engineered mutations result in a compromised response to estrogen resulting in functional but small uteri.
Trim25,也称为Tripartite motif-containing protein 25,是一种重要的E3泛素连接酶,属于TRIM家族。TRIM家族蛋白包含一个或多个TRIM结构域,包括RING finger、B-box/coiled-coil和SPRY结构域,参与多种细胞过程,包括细胞增殖、分化、凋亡和免疫反应。Trim25在多种生物学过程中发挥重要作用,包括抗病毒免疫、细胞应激反应和肿瘤发生发展。

Trim25在抗病毒免疫中发挥重要作用。Trim25能够与RIG-I相互作用,促进RIG-I的泛素化,进而激活I型干扰素信号通路,诱导抗病毒免疫反应[5]。此外,Trim25还能够与IRF3和IRF7相互作用,促进它们的核转位和转录活性,进一步激活I型干扰素信号通路[6]。

Trim25在细胞应激反应中也发挥重要作用。Trim25能够与Keap1相互作用,促进Keap1的泛素化和降解,进而激活Nrf2信号通路,增强细胞抗氧化防御能力,保护细胞免受氧化应激损伤[1]。此外,Trim25还能够与IRE1相互作用,促进ERAD途径,减少未折叠蛋白反应的激活,维持内质网稳态[1]。

Trim25在肿瘤发生发展中发挥重要作用。Trim25能够促进多种肿瘤细胞的生长和侵袭,包括肝细胞癌、乳腺癌和胶质母细胞瘤[8,9]。Trim25能够通过多种机制促进肿瘤细胞生长和侵袭,包括促进细胞增殖、抑制细胞凋亡、促进细胞迁移和侵袭、调节细胞代谢等[1,2,3,4,7,8,9]。

Trim25在多种疾病中发挥重要作用,包括抗病毒免疫、细胞应激反应和肿瘤发生发展。Trim25的研究有助于深入理解TRIM家族蛋白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. Liu, Yanfeng, Tao, Shishi, Liao, Lijuan, Yang, Xiaolu, Chen, Liang. 2020. TRIM25 promotes the cell survival and growth of hepatocellular carcinoma through targeting Keap1-Nrf2 pathway. In Nature communications, 11, 348. doi:10.1038/s41467-019-14190-2. https://pubmed.ncbi.nlm.nih.gov/31953436/
2. Wu, Song-Fang, Xia, Li, Shi, Xiao-Dong, Wang, Yue-Ying, Chen, Saijuan. 2020. RIG-I regulates myeloid differentiation by promoting TRIM25-mediated ISGylation. In Proceedings of the National Academy of Sciences of the United States of America, 117, 14395-14404. doi:10.1073/pnas.1918596117. https://pubmed.ncbi.nlm.nih.gov/32513696/
3. Zheng, Bowen, Qian, Fengyuan, Wang, Xuehui, Zhou, Baian, Fang, Lin. 2024. Neddylation activated TRIM25 desensitizes triple-negative breast cancer to paclitaxel via TFEB-mediated autophagy. In Journal of experimental & clinical cancer research : CR, 43, 177. doi:10.1186/s13046-024-03085-w. https://pubmed.ncbi.nlm.nih.gov/38926803/
4. Liu, Jinlu, Gu, Tiantian, Chen, Jianzhou, Chen, Guohong, Xu, Qi. 2022. The TRIM25 Gene in Ducks: Cloning, Characterization and Antiviral Immune Response. In Genes, 13, . doi:10.3390/genes13112090. https://pubmed.ncbi.nlm.nih.gov/36360326/
5. Gack, Michaela U, Shin, Young C, Joo, Chul-Hyun, Inoue, Satoshi, Jung, Jae U. . TRIM25 RING-finger E3 ubiquitin ligase is essential for RIG-I-mediated antiviral activity. In Nature, 446, 916-920. doi:. https://pubmed.ncbi.nlm.nih.gov/17392790/
6. Rahimi-Tesiye, Maryam, Zaersabet, Mona, Salehiyeh, Sajad, Jafari, Seyedeh Zahra. 2023. The role of TRIM25 in the occurrence and development of cancers and inflammatory diseases. In Biochimica et biophysica acta. Reviews on cancer, 1878, 188954. doi:10.1016/j.bbcan.2023.188954. https://pubmed.ncbi.nlm.nih.gov/37437700/
7. Yan, Yuanliang, Zhou, Shangjun, Chen, Xi, Li, Zhi, Sun, Lunquan. 2024. Suppression of ITPKB degradation by Trim25 confers TMZ resistance in glioblastoma through ROS homeostasis. In Signal transduction and targeted therapy, 9, 58. doi:10.1038/s41392-024-01763-x. https://pubmed.ncbi.nlm.nih.gov/38438346/
8. Tecalco-Cruz, Angeles C, Abraham-Juárez, María Jazmin, Solleiro-Villavicencio, Helena, Ramírez-Jarquín, Josué Orlando. . TRIM25: A central factor in breast cancer. In World journal of clinical oncology, 12, 646-655. doi:10.5306/wjco.v12.i8.646. https://pubmed.ncbi.nlm.nih.gov/34513598/
9. Chen, Yike, Xu, Xiaohui, Ding, Kaikai, Ji, Jianxiong, Zhang, Jianmin. 2024. TRIM25 promotes glioblastoma cell growth and invasion via regulation of the PRMT1/c-MYC pathway by targeting the splicing factor NONO. In Journal of experimental & clinical cancer research : CR, 43, 39. doi:10.1186/s13046-024-02964-6. https://pubmed.ncbi.nlm.nih.gov/38303029/