Trim38-flox 基因敲除小鼠

下单100%中奖,最高可得千元京东卡
复苏/繁育服务
产品名称

Trim38-flox 基因敲除小鼠

产品编号

S-CKO-05807

品系全称

C57BL/6JCya-Trim38em1flox/Cya

品系背景

C57BL/6JCya

品系编号

CKOCMP-214158-Trim38-B6J-VA

品系状态

使用本品系发表的文献需注明: Trim38-flox 基因敲除小鼠 mice (Strain S-CKO-05807) 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
tripartite motif-containing 38
基因别称
Gm23
染色体号
Chr 13 (Mouse)
转录本 ID
NCBI: NM_001029935 | Ensembl: ENSMUST00000074067
修饰方式
条件性基因敲除
靶向范围
Exon 3~5
敲除长度
~2.3 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:2684869Mice homozygous for a knock-out allele exhibit increased poly(I:C) and LPS-induced IFN-beta, TNFalpha and IL6 with increased induced mortality induced by poly(I:C), LPS or S. typhimurium infection,
TRIM38,也称为三重基序蛋白38,是一种重要的E3泛素连接酶,属于TRIM家族。TRIM蛋白是一类具有三重基序(RING finger、B-box和Coiled-coil)的蛋白质,参与多种生物学过程,包括细胞增殖、分化、凋亡和抗病毒防御[3]。TRIM38在多种细胞类型中表达,包括神经元、星形胶质细胞、肝细胞、骨细胞和免疫细胞。TRIM38具有多种生物学功能,包括调节细胞因子和趋化因子的表达、抑制病毒复制和基因表达、调节NF-κB信号通路和影响骨代谢[1,2,3,4,5,6,7,8]。

TRIM38在病毒感染中发挥重要作用。研究发现,TRIM38可以抑制多种DNA和RNA病毒的复制和基因表达,包括乙型肝炎病毒(HBV)、呼吸道合胞病毒(RSV)和流感病毒。TRIM38的抑制病毒复制和基因表达的功能与其E3泛素连接酶活性有关,它可以泛素化并降解病毒蛋白或病毒复制所需的宿主蛋白[1,4,5]。此外,TRIM38还可以调节I型干扰素(IFN-I)的表达。IFN-I是宿主抗病毒免疫应答的关键因子,可以抑制病毒复制和基因表达。TRIM38可以与RIG-I和TRIF等IFN-I信号通路的蛋白相互作用,抑制IFN-I的表达[4,6,7]。TRIM38在骨代谢中也发挥重要作用。研究发现,TRIM38可以抑制破骨细胞的形成和功能,促进成骨细胞的分化和功能。TRIM38的这些功能与其调节NF-κB信号通路有关[3]。此外,TRIM38还可以抑制葡萄糖转运蛋白1(GLUT1)的表达,从而限制肿瘤的进展[5]。

TRIM38在病毒感染、骨代谢和肿瘤进展中发挥重要作用。TRIM38的抑制病毒复制和基因表达的功能有助于宿主抵御病毒感染。TRIM38的调节骨代谢的功能有助于维持骨稳态。TRIM38的抑制肿瘤进展的功能为治疗肿瘤提供了新的思路和策略。

参考文献:
1. Selinger, Martin, Věchtová, Pavlína, Tykalová, Hana, Štěrba, Ján, Grubhoffer, Libor. 2022. Integrative RNA profiling of TBEV-infected neurons and astrocytes reveals potential pathogenic effectors. In Computational and structural biotechnology journal, 20, 2759-2777. doi:10.1016/j.csbj.2022.05.052. https://pubmed.ncbi.nlm.nih.gov/35685361/
2. Luo, Haiying, Hu, Xiaoxia, Li, Yadi, Zeng, Yueying, Qin, Bo. 2022. The antiviral activity of tripartite motif protein 38 in hepatitis B virus replication and gene expression and its association with treatment responses during PEG-IFN-α antiviral therapy. In Virology, 579, 84-93. doi:10.1016/j.virol.2022.12.014. https://pubmed.ncbi.nlm.nih.gov/36623352/
3. Kim, Kabsun, Kim, Jung Ha, Kim, Inyoung, Seong, Semun, Kim, Nacksung. 2018. TRIM38 regulates NF-κB activation through TAB2 degradation in osteoclast and osteoblast differentiation. In Bone, 113, 17-28. doi:10.1016/j.bone.2018.05.009. https://pubmed.ncbi.nlm.nih.gov/29753717/
4. Sun, Qingqing, Han, Xiao, Meng, Lingtong, Wei, Lin, Ma, Cuiqing. 2024. TRIM38 Induced in Respiratory Syncytial Virus-infected Cells Downregulates Type I Interferon Expression by Competing with TRIM25 to Bind RIG-I. In Inflammation, 47, 1328-1343. doi:10.1007/s10753-024-01979-7. https://pubmed.ncbi.nlm.nih.gov/38630167/
5. Wang, Xiaojing, He, Hongchao, Rui, Wenbin, Zhu, Yu, Xie, Xin. 2021. TRIM38 triggers the uniquitination and degradation of glucose transporter type 1 (GLUT1) to restrict tumor progression in bladder cancer. In Journal of translational medicine, 19, 508. doi:10.1186/s12967-021-03173-x. https://pubmed.ncbi.nlm.nih.gov/34906161/
6. Xue, Qinghua, Zhou, Zhuo, Lei, Xiaobo, Wang, Jianwei, Hung, Tao. 2012. TRIM38 negatively regulates TLR3-mediated IFN-β signaling by targeting TRIF for degradation. In PloS one, 7, e46825. doi:10.1371/journal.pone.0046825. https://pubmed.ncbi.nlm.nih.gov/23056470/
7. Hu, Ming-Ming, Xie, Xue-Qin, Yang, Qing, Lin, Heng, Shu, Hong-Bing. 2015. TRIM38 Negatively Regulates TLR3/4-Mediated Innate Immune and Inflammatory Responses by Two Sequential and Distinct Mechanisms. In Journal of immunology (Baltimore, Md. : 1950), 195, 4415-25. doi:10.4049/jimmunol.1500859. https://pubmed.ncbi.nlm.nih.gov/26392463/
8. Jia, Xiuzhi, Zhao, Chunyuan, Zhao, Wei. 2021. Emerging Roles of MHC Class I Region-Encoded E3 Ubiquitin Ligases in Innate Immunity. In Frontiers in immunology, 12, 687102. doi:10.3389/fimmu.2021.687102. https://pubmed.ncbi.nlm.nih.gov/34177938/