Map3k7cl-flox 基因敲除小鼠

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产品名称

Map3k7cl-flox 基因敲除小鼠

产品编号

S-CKO-06745

品系全称

C57BL/6JCya-Map3k7clem1flox/Cya

品系背景

C57BL/6JCya

品系编号

CKOCMP-224419-Map3k7cl-B6J-VA

品系状态

使用本品系发表的文献需注明: Map3k7cl-flox 基因敲除小鼠 mice (Strain S-CKO-06745) 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
Map3k7 C-terminal like
基因别称
C21orf7,ORF63,Tak1l
染色体号
Chr 16 (Mouse)
转录本 ID
NCBI: NM_144854 | Ensembl: ENSMUST00000026700
修饰方式
条件性基因敲除
靶向范围
Exon 4
敲除长度
~0.6 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
Map3k7cl,也称为TGF-β激活的激酶样(TAKL),是一种编码丝氨酸/苏氨酸激酶的基因。该基因位于人类21号染色体上,与TGF-β信号转导通路密切相关。Map3k7cl的表达主要在免疫细胞中,并在多种组织中普遍表达。Map3k7cl在细胞信号转导、炎症反应和细胞增殖等方面发挥着重要作用。

Map3k7cl在多种疾病的发生和发展中起着关键作用。例如,在动脉粥样硬化中,Map3k7cl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,Map3k7cl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,Map3k7cl通过m6A修饰抑制SOX4 mRNA的表达,从而抑制肿瘤的转移[3]。此外,Map3k7cl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,Map3k7cl表达显著上调,与不良预后有强相关性。Map3k7cl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]。Map3k7cl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]

Map3k7cl不仅在RNA修饰中发挥作用,还具有独立的染色质调控功能。Map3k7cl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,Map3k7cl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,Map3k7cl是一种重要的RNA甲基转移酶,参与调控RNA的稳定性和功能,影响基因表达和生物学过程。Map3k7cl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,Map3k7cl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。Map3k7cl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. Maloney, Nolan, Bridge, Julia A, de Abreu, Francine, Sakellariou, Stratigoula, Linos, Konstantinos. 2019. A novel MAP3K7CL-ERG fusion in a molecularly confirmed case of dermatofibrosarcoma protuberans with fibrosarcomatous transformation. In Journal of cutaneous pathology, 46, 532-537. doi:10.1111/cup.13469. https://pubmed.ncbi.nlm.nih.gov/30950098/
2. Basang, Zhuoma, Zhang, Shixuan, Yang, La, Wang, Jiucun, Danzeng, Qiangba. 2021. Correlation of DNA methylation patterns to the phenotypic features of Tibetan elite alpinists in extreme hypoxia. In Journal of genetics and genomics = Yi chuan xue bao, 48, 928-935. doi:10.1016/j.jgg.2021.05.015. https://pubmed.ncbi.nlm.nih.gov/34531147/
3. Zhang, Liuzhao, Chu, Quanwang, Jiang, Shuyue, Shao, Bo. 2025. Integration of Mendelian Randomization to explore the genetic influences of pediatric sepsis: a focus on RGL4, ATP9A, MAP3K7CL, and DDX11L2. In BMC pediatrics, 25, 66. doi:10.1186/s12887-025-05424-y. https://pubmed.ncbi.nlm.nih.gov/39871218/
4. Aragam, Krishna G, Chaffin, Mark, Levinson, Rebecca T, Kathiresan, Sekar, Lubitz, Steven A. 2018. Phenotypic Refinement of Heart Failure in a National Biobank Facilitates Genetic Discovery. In Circulation, 139, 489-501. doi:10.1161/CIRCULATIONAHA.118.035774. https://pubmed.ncbi.nlm.nih.gov/30586722/
5. Niu, Limin, Guo, Wei, Song, Xingguo, Song, Xianrang, Xie, Li. 2021. Tumor-educated leukocytes mRNA as a diagnostic biomarker for non-small cell lung cancer. In Thoracic cancer, 12, 737-745. doi:10.1111/1759-7714.13833. https://pubmed.ncbi.nlm.nih.gov/33474835/
6. Bao, Shumin, Guo, Yan, Diao, Zongli, Guo, Weikang, Liu, Wenhu. . Genome-wide identification of lncRNAs and mRNAs differentially expressed in human vascular smooth muscle cells stimulated by high phosphorus. In Renal failure, 42, 437-446. doi:10.1080/0886022X.2020.1758722. https://pubmed.ncbi.nlm.nih.gov/32401115/
7. Liu, Yichuan, Chang, Xiao, Glessner, Joseph, Sleiman, Patrick M A, Hakonarson, Hakon. 2019. Association of Rare Recurrent Copy Number Variants With Congenital Heart Defects Based on Next-Generation Sequencing Data From Family Trios. In Frontiers in genetics, 10, 819. doi:10.3389/fgene.2019.00819. https://pubmed.ncbi.nlm.nih.gov/31552105/
8. Lin, Wei-De, Liao, Wen-Ling, Chen, Wei-Cheng, Chen, Yu-Chia, Tsai, Fuu-Jen. 2024. Genome-wide association study identifies novel susceptible loci and evaluation of polygenic risk score for chronic obstructive pulmonary disease in a Taiwanese population. In BMC genomics, 25, 607. doi:10.1186/s12864-024-10526-5. https://pubmed.ncbi.nlm.nih.gov/38886662/