Map3k2-KO 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

Map3k2-KO 基因敲除小鼠

产品编号

S-KO-08487

品系全称

C57BL/6JCya-Map3k2em1/Cya

品系背景

C57BL/6JCya

品系编号

KOCMP-26405-Map3k2-B6J-VA

品系状态

使用本品系发表的文献需注明: Map3k2-KO 基因敲除小鼠 mice (Strain S-KO-08487) were purchased from Cyagen.
交付类型
周龄
性别
基因型
数量
KO小鼠库模型
MAPK信号通路

基本信息

基因研究概述

质控标准

基因
基因全称
mitogen-activated protein kinase kinase kinase 2
基因别称
9630061B06Rik,Mekk2,Mekk2b
染色体号
Chr 18 (Mouse)
转录本 ID
NCBI: NM_011946.3 | Ensembl: ENSMUST00000096575
修饰方式
全身性基因敲除
靶向范围
Exon 3~6
敲除长度
~6300 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:1346873Mice homozygous for disruptions in this gene are grossly normal and fertile.
MAP3K2,也称为Mitogen-activated protein kinase kinase kinase 2,是一种丝氨酸/苏氨酸激酶,属于丝裂原活化蛋白激酶(MAPK)信号通路的上游调控因子。MAPK信号通路是细胞内重要的信号转导途径,参与调控细胞的生长、分化、凋亡和炎症等多种生物学过程。MAP3K2通过磷酸化激活下游的MAPK激酶(MAP2Ks),进而激活MAPKs,最终影响细胞内多种转录因子的活性,从而调节基因表达和生物学过程。

MAP3K2在多种疾病的发生和发展中发挥重要作用。例如,在非小细胞肺癌中,KIAA1429通过激活JNK/MAPK通路,促进肿瘤的发生和耐药性[1]。在癌症中,SMYD3介导的MAP3K2的甲基化,可以增强Ras驱动的ERK1/2信号通路,导致肺癌和胰腺癌的发生[2]。此外,MAP3K2在静脉血栓栓塞(VTE)的发生中也有重要作用,其基因变异与VTE的风险相关[6]。

MAP3K2的活性受到多种因素的调控。例如,转录因子XBP1s可以促进子宫内膜炎引起的上皮-间质转化(EMT),其机制是通过靶向MAP3K2,激活MAPK/ERK通路[3]。在前列腺癌中,SMYD3-MAP3K2信号轴可以促进肿瘤的侵袭和转移,其机制是通过改变中间丝蛋白vimentin的表达[4]。此外,microRNA(miRNA)也可以调控MAP3K2的表达。例如,miR-93-5p可以激活MAP3K2的翻译,其机制是通过与MAP3K2 3'非翻译区(3'UTR)的ARE2相互作用[5]。miR-106a-5p可以促进氧化应激损伤的修复,其机制是通过靶向MAP3K2,调节基因表达[7]。miR-338-3p可以抑制肺癌细胞的迁移、侵袭和增殖,其机制是通过靶向MAP3K2,调节ERK1/2信号通路[8]。

综上所述,MAP3K2是一种重要的MAPK信号通路的调控因子,参与调控细胞的生长、分化、凋亡和炎症等多种生物学过程。MAP3K2在多种疾病的发生和发展中发挥重要作用,其活性受到多种因素的调控。深入研究MAP3K2的生物学功能和调控机制,有助于我们更好地理解疾病的发病机制,为疾病的诊断和治疗提供新的思路和策略。

参考文献:
1. Lin, Xi, Ye, Rongyi, Li, Zhiming, Zhong, Yizhou, Huang, Zhenlie. 2022. KIAA1429 promotes tumorigenesis and gefitinib resistance in lung adenocarcinoma by activating the JNK/ MAPK pathway in an m6A-dependent manner. In Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy, 66, 100908. doi:10.1016/j.drup.2022.100908. https://pubmed.ncbi.nlm.nih.gov/36493511/
2. Colón-Bolea, Paula, Crespo, Piero. 2014. Lysine methylation in cancer: SMYD3-MAP3K2 teaches us new lessons in the Ras-ERK pathway. In BioEssays : news and reviews in molecular, cellular and developmental biology, 36, 1162-9. doi:10.1002/bies.201400120. https://pubmed.ncbi.nlm.nih.gov/25382779/
3. Gao, Kangkang, Si, Mengqi, Qin, Xinxi, Wang, Aihua, Jin, Yaping. 2025. Transcription factor XBP1s promotes endometritis-induced epithelial-mesenchymal transition by targeting MAP3K2, a key gene in the MAPK/ERK pathway. In Cell communication and signaling : CCS, 23, 72. doi:10.1186/s12964-025-02050-0. https://pubmed.ncbi.nlm.nih.gov/39930412/
4. Ikram, Sabeen, Rege, Apurv, Negesse, Maraki Y, Reynoird, Nicolas, Green, Erin M. 2023. The SMYD3-MAP3K2 signaling axis promotes tumor aggressiveness and metastasis in prostate cancer. In Science advances, 9, eadi5921. doi:10.1126/sciadv.adi5921. https://pubmed.ncbi.nlm.nih.gov/37976356/
5. Shi, Xuan, Qi, Zhuoran, Huang, Dongbo, Shen, Xizhong, Liu, Taotao. 2024. HuR facilitates miR-93-5p-induced activation of MAP3K2 translation via MAP3K2 3'UTR ARE2 in hepatocellular carcinoma. In Biochemical and biophysical research communications, 722, 150152. doi:10.1016/j.bbrc.2024.150152. https://pubmed.ncbi.nlm.nih.gov/38795452/
6. He, Xiao-Yu, Wu, Bang-Sheng, Yang, Liu, Dong, Qiang, Yu, Jin-Tai. 2024. Genetic associations of protein-coding variants in venous thromboembolism. In Nature communications, 15, 2819. doi:10.1038/s41467-024-47178-8. https://pubmed.ncbi.nlm.nih.gov/38561338/
7. Zhang, Li, Luo, Xiang, Tang, Rui, Pi, Jinsong, Zhang, Hao. 2024. MiR-106a-5p by Targeting MAP3K2 Promotes Repair of Oxidative Stress Damage to the Intestinal Barrier in Prelaying Ducks. In Animals : an open access journal from MDPI, 14, . doi:10.3390/ani14071037. https://pubmed.ncbi.nlm.nih.gov/38612276/
8. Zhang, Bo, Wang, Dongchang, Wang, Yuanyuan, Chen, Gang. 2022. miRNA-338-3p inhibits the migration, invasion and proliferation of human lung adenocarcinoma cells by targeting MAP3K2. In Aging, 14, 6094-6110. doi:10.18632/aging.204198. https://pubmed.ncbi.nlm.nih.gov/35929837/