Irf2-KO 基因敲除小鼠

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产品名称

Irf2-KO 基因敲除小鼠

产品编号

S-KO-18938

品系全称

C57BL/6JCya-Irf2em1/Cya

品系背景

C57BL/6JCya

品系编号

KOCMP-16363-Irf2-B6J-VB

品系状态

使用本品系发表的文献需注明: Irf2-KO 基因敲除小鼠 mice (Strain S-KO-18938) 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
interferon regulatory factor 2
基因别称
9830146E22Rik,Irf-2
染色体号
Chr 8 (Mouse)
转录本 ID
NCBI: NM_008391 | Ensembl: ENSMUST00000034041
修饰方式
全身性基因敲除
靶向范围
Exon 3
敲除长度
~1.1 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:96591Mice homozygous for a knock-out allele exhibit abnormalities in B lymphopoiesis and hematopoiesis, often die prematurely, show increased mortality following lymphocytic choriomeningitis virus infection, and develop an inflammatory skin disease involving CD8+ Tcells.
Irf2,即干扰素调节因子2,是一种转录因子,属于IRF家族成员。IRF家族是一组具有螺旋-转角-螺旋DNA结合基序的转录因子,在细胞对干扰素信号的反应中发挥着重要作用。Irf2与IRF1具有相反的功能,IRF1是肿瘤抑制基因,而Irf2通常被认为是原癌基因。Irf2在调节免疫反应、细胞增殖和凋亡等方面发挥着重要作用。

Irf2在多种癌症中发挥着重要作用。在结直肠癌中,Irf2的表达水平与对免疫检查点阻断疗法的反应性有关。研究表明,Irf2的表达水平升高可以增加对免疫治疗的敏感性[1]。在胶质瘤中,Irf2的表达水平与肿瘤的分级和预后相关。过表达Irf2可以保护胶质瘤细胞免受铁死亡,并增强其侵袭和迁移能力[2]。在鼻咽癌中,Irf2通过调节CENP-N的表达,进而影响葡萄糖代谢、细胞增殖、细胞周期和凋亡,促进鼻咽癌细胞的恶性生物学行为[3]。

除了在癌症中的作用外,Irf2还参与其他生物学过程。Irf2是宿主防御的重要调节因子,参与调节先天性和适应性免疫反应[4]。Irf2还参与调节多巴胺受体D2基因的转录,与猪的攻击性行为相关[5]。Irf2的缺失与MHC I途径的转录水平降低有关,导致对免疫检查点阻断疗法的抵抗[6]。Irf2在心肌梗死中发挥作用,通过调节GSDMD诱导的细胞焦亡,导致心脏损伤和功能障碍[7]。此外,Irf2还通过调节IRG1的表达,影响巨噬细胞的炎症反应、细胞存活、迁移和凋亡[8]。

综上所述,Irf2是一种重要的转录因子,参与调节免疫反应、细胞增殖和凋亡等生物学过程。在癌症中,Irf2的表达水平与肿瘤的分级、预后和对免疫治疗的反应性相关。此外,Irf2还参与其他生物学过程,如宿主防御、行为调节和心肌梗死等。研究Irf2的功能和机制有助于深入理解其在疾病发生和发展中的作用,为疾病的治疗和预防提供新的思路和策略。

参考文献:
1. Liao, Wenting, Overman, Michael J, Boutin, Adam T, Wang, Y Alan, DePinho, Ronald A. 2019. KRAS-IRF2 Axis Drives Immune Suppression and Immune Therapy Resistance in Colorectal Cancer. In Cancer cell, 35, 559-572.e7. doi:10.1016/j.ccell.2019.02.008. https://pubmed.ncbi.nlm.nih.gov/30905761/
2. Tong, Shiao, Ye, Liguo, Xu, Yang, Tian, Daofeng, Chen, Qianxue. 2022. IRF2-ferroptosis related gene is associated with prognosis and EMT in gliomas. In Translational oncology, 26, 101544. doi:10.1016/j.tranon.2022.101544. https://pubmed.ncbi.nlm.nih.gov/36156371/
3. Qi, Cheng-Lin, Huang, Mao-Ling, Zou, You, Bu, Li-Hong, Chen, Shi-Ming. 2021. The IRF2/CENP-N/AKT signaling axis promotes proliferation, cell cycling and apoptosis resistance in nasopharyngeal carcinoma cells by increasing aerobic glycolysis. In Journal of experimental & clinical cancer research : CR, 40, 390. doi:10.1186/s13046-021-02191-3. https://pubmed.ncbi.nlm.nih.gov/34893086/
4. Taniguchi, T, Ogasawara, K, Takaoka, A, Tanaka, N. . IRF family of transcription factors as regulators of host defense. In Annual review of immunology, 19, 623-55. doi:. https://pubmed.ncbi.nlm.nih.gov/11244049/
5. Zhao, Jing, Gao, Siyuan, Guo, Yanli, Schinckel, Allan P, Zhou, Bo. 2022. Functionally Antagonistic Transcription Factors IRF1 and IRF2 Regulate the Transcription of the Dopamine Receptor D2 Gene Associated with Aggressive Behavior of Weaned Pigs. In Biology, 11, . doi:10.3390/biology11010135. https://pubmed.ncbi.nlm.nih.gov/35053133/
6. Choo, Ailyn, Palladinetti, Patricia, Passioura, Toby, Symonds, Geoff, Dolnikov, Alla. . The role of IRF1 and IRF2 transcription factors in leukaemogenesis. In Current gene therapy, 6, 543-50. doi:. https://pubmed.ncbi.nlm.nih.gov/17073600/
7. Sari, G, Dhatchinamoorthy, K, Orellano-Ariza, L, Brehm, M A, Rock, K. 2024. IRF2 loss is associated with reduced MHC I pathway transcripts in subsets of most human cancers and causes resistance to checkpoint immunotherapy in human and mouse melanomas. In Journal of experimental & clinical cancer research : CR, 43, 276. doi:10.1186/s13046-024-03187-5. https://pubmed.ncbi.nlm.nih.gov/39354629/
8. Hayashi, Hideki, Kohno, Tomoko, Yasui, Kiyoshi, Mak, Tak Wah, Matsuyama, Toshifumi. 2011. Characterization of dsRNA-induced pancreatitis model reveals the regulatory role of IFN regulatory factor 2 (Irf2) in trypsinogen5 gene transcription. In Proceedings of the National Academy of Sciences of the United States of America, 108, 18766-71. doi:10.1073/pnas.1116273108. https://pubmed.ncbi.nlm.nih.gov/22042864/