Ets2-KO 基因敲除小鼠

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产品名称

Ets2-KO 基因敲除小鼠

产品编号

S-KO-07000

品系全称

C57BL/6JCya-Ets2em1/Cya

品系背景

C57BL/6JCya

品系编号

KOCMP-23872-Ets2-B6J-VB

品系状态

使用本品系发表的文献需注明: Ets2-KO 基因敲除小鼠 mice (Strain S-KO-07000) 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
E26 avian leukemia oncogene 2, 3' domain
基因别称
Ets-2
染色体号
Chr 16 (Mouse)
转录本 ID
NCBI: NM_011809 | Ensembl: ENSMUST00000023612
修饰方式
全身性基因敲除
靶向范围
Exon 2~10
敲除长度
~14.6 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
MGI:95456Homozygotes for targeted null mutations exhibit defective trophoblast formation and die by embryonic day 8.5, but tetraploid chimeric rescue results in viable and fertile mutants with wavy hair. Mammary tumors induced in carriers are reduced in size.
基因Ets2,全称为V-ets erythroblastosis virus E26 oncogene homolog 2,属于Ets基因家族,是一类具有保守DNA结合域的转录因子。Ets基因家族成员通过调节多种细胞和病毒基因的启动子和增强子元件的转录起始,参与调控细胞生长、分化、凋亡和发育等多种生物学过程。Ets2具有转录激活和抑制的双重功能,其活性受多种信号通路的调控,包括MAPK/Erk信号通路、p53信号通路等。

Ets2在多种疾病的发生发展中发挥重要作用。例如,Ets2在心脏肥大中发挥关键作用。Ets2被Erk1/2磷酸化并激活,随后与NFAT形成复合物,共同促进心脏肥大相关基因的转录,导致心脏肥大和功能障碍[1]。此外,Ets2还与人类端粒酶逆转录酶(hTERT)基因的表达和乳腺癌细胞增殖密切相关。Ets2与c-Myc形成复合物,共同维持hTERT基因的表达和乳腺癌细胞的增殖[2]。

Ets2还与衰老相关基因的表达和急性心肌梗死(AMI)的发生发展有关。Ets2是衰老相关基因之一,其在AMI患者的循环内皮细胞中表达上调,可能成为AMI早期诊断的潜在生物标志物[3]。此外,Ets2还与突变型p53蛋白相互作用,促进肿瘤的发生发展。突变型p53蛋白与Ets2形成复合物,通过多种机制促进肿瘤的生长和转移,包括上调微小RNA(miRNA)的表达、抑制肿瘤抑制基因的表达等[4,5]。

综上所述,Ets2是一种重要的转录因子,参与调控多种生物学过程,并在多种疾病的发生发展中发挥重要作用。Ets2的活性受多种信号通路的调控,其表达异常可能导致多种疾病的发生。因此,深入研究Ets2的功能和调控机制,有助于理解相关疾病的发病机制,为疾病的治疗和预防提供新的思路和策略。

参考文献:
1. Luo, Yuxuan, Jiang, Nan, May, Herman I, Gillette, Thomas G, Hill, Joseph A. 2021. Cooperative Binding of ETS2 and NFAT Links Erk1/2 and Calcineurin Signaling in the Pathogenesis of Cardiac Hypertrophy. In Circulation, 144, 34-51. doi:10.1161/CIRCULATIONAHA.120.052384. https://pubmed.ncbi.nlm.nih.gov/33821668/
2. Xu, Dakang, Dwyer, Julie, Li, He, Duan, Wei, Liu, Jun-Ping. 2008. Ets2 maintains hTERT gene expression and breast cancer cell proliferation by interacting with c-Myc. In The Journal of biological chemistry, 283, 23567-80. doi:10.1074/jbc.M800790200. https://pubmed.ncbi.nlm.nih.gov/18586674/
3. Xiang, Jie, Shen, Jun, Zhang, Ling, Tang, Baopeng. 2022. Identification and validation of senescence-related genes in circulating endothelial cells of patients with acute myocardial infarction. In Frontiers in cardiovascular medicine, 9, 1057985. doi:10.3389/fcvm.2022.1057985. https://pubmed.ncbi.nlm.nih.gov/36582740/
4. Martinez, Luis Alfonso. 2016. Mutant p53 and ETS2, a Tale of Reciprocity. In Frontiers in oncology, 6, 35. doi:10.3389/fonc.2016.00035. https://pubmed.ncbi.nlm.nih.gov/26925389/
5. Liu, Daniel D, Kang, Yibin. . Ets2 anchors the prometastatic function of mutant p53 in osteosarcoma. In Genes & development, 31, 1823-1824. doi:10.1101/gad.307439.117. https://pubmed.ncbi.nlm.nih.gov/29051386/
6. Chapman, Laura R, Ramnarine, Isabela V P, Zemke, Dan, Majid, Arshad, Bell, Simon M. 2024. Gene Expression Studies in Down Syndrome: What Do They Tell Us about Disease Phenotypes? In International journal of molecular sciences, 25, . doi:10.3390/ijms25052968. https://pubmed.ncbi.nlm.nih.gov/38474215/
7. Macleod, K, Leprince, D, Stehelin, D. . The ets gene family. In Trends in biochemical sciences, 17, 251-6. doi:. https://pubmed.ncbi.nlm.nih.gov/1502727/
8. Chen, Shuxiang, Zhu, Xiaotong, Ou, Wenhuan, Qi, Weizhong, Ni, Songjia. 2023. ETS2 overexpression ameliorates cartilage injury in osteoarthritis by the ETS2/miR-155/STAT1/DNMT1 feedback loop pathway. In Biochimica et biophysica acta. Gene regulatory mechanisms, 1866, 194965. doi:10.1016/j.bbagrm.2023.194965. https://pubmed.ncbi.nlm.nih.gov/37524226/
9. Sacchi, N, Nalbantoglu, J, Sergovich, F R, Papas, T S. . Human ETS2 gene on chromosome 21 is not rearranged in Alzheimer disease. In Proceedings of the National Academy of Sciences of the United States of America, 85, 7675-9. doi:. https://pubmed.ncbi.nlm.nih.gov/2902635/
10. Carbone, Giuseppina M, McGuffie, Eileen M, Collier, Angela, Catapano, Carlo V. . Selective inhibition of transcription of the Ets2 gene in prostate cancer cells by a triplex-forming oligonucleotide. In Nucleic acids research, 31, 833-43. doi:. https://pubmed.ncbi.nlm.nih.gov/12560478/