Itprip-flox 基因敲除小鼠

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产品名称

Itprip-flox 基因敲除小鼠

产品编号

S-CKO-11211

品系全称

C57BL/6JCya-Itpripem1flox/Cya

品系背景

C57BL/6JCya

品系编号

CKOCMP-414801-Itprip-B6J-VA

品系状态

使用本品系发表的文献需注明: Itprip-flox 基因敲除小鼠 mice (Strain S-CKO-11211) 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
inositol 1,4,5-triphosphate receptor interacting protein
基因别称
4833424O12Rik,DANGER
染色体号
Chr 19 (Mouse)
转录本 ID
NCBI: NM_001001738.3 | Ensembl: ENSMUST00000095998
修饰方式
条件性基因敲除
靶向范围
Exon 2
敲除长度
~1938 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:3042776Mice homozygous for a null mutation are grossly normal, but MEF and neuronal cells show increased susceptibility to induced cell death due to increase in death-associated protein kinase (DAPK) activity.
Itprip,也称为inositol 1,4,5-trisphosphate receptor interacting protein,是一种重要的蛋白质,参与多种生物学过程。Itprip能够与inositol 1,4,5-trisphosphate receptor (IP3R)相互作用,影响细胞内钙离子的释放和信号传导。此外,Itprip还能够与肌动蛋白调节轻链9 (MYL9)结合,参与细胞骨架的调节和细胞运动。Itprip还能够在病毒感染过程中,与病毒触发型干扰素信号通路中的关键分子MDA5相互作用,促进MDA5的寡聚化和激活,从而增强先天免疫反应[1,2,3]。

在肿瘤发生和发展中,Itprip也发挥着重要作用。研究表明,Itprip在恶性胶质瘤细胞中与死亡相关蛋白激酶1 (DAPK1)相互作用,抑制DAPK1的活性,从而促进胶质瘤的进展[1]。此外,Itprip的表达与结直肠癌患者的生存预后密切相关,可以作为结直肠癌患者预后的可靠预测指标[2]。Itprip的表达还与肺腺癌患者的生存预后和免疫浸润状态相关,可以作为肺腺癌患者预后和免疫治疗的潜在指标[4,5]。在血浆淀粉样β蛋白水平的研究中,Itprip被发现与血浆β蛋白水平相关,可能影响细胞死亡和阿尔茨海默病的发生[6]。此外,Itprip的表达还与心脏捐赠后循环死亡心脏的心肌和冠状动脉转录组变化相关[7]。

综上所述,Itprip是一种重要的蛋白质,参与多种生物学过程,包括细胞内钙离子释放、信号传导、细胞骨架调节、先天免疫反应、肿瘤发生和发展等。Itprip的研究有助于深入理解其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. Cao, Changchun, He, Kang, Li, Shaoxun, Sun, Xiaoyang, Ding, Lianshu. 2021. ITPRIP promotes glioma progression by linking MYL9 to DAPK1 inhibition. In Cellular signalling, 85, 110062. doi:10.1016/j.cellsig.2021.110062. https://pubmed.ncbi.nlm.nih.gov/34111521/
2. Abdul Aziz, Nurul Ainin, Mokhtar, Norfilza M, Harun, Roslan, Wan Ngah, Wan Zurinah, Jamal, Rahman. 2016. A 19-Gene expression signature as a predictor of survival in colorectal cancer. In BMC medical genomics, 9, 58. doi:10.1186/s12920-016-0218-1. https://pubmed.ncbi.nlm.nih.gov/27609023/
3. Xie, Qinya, Chen, Shengwen, Tian, Renyun, Li, Guangdi, Zhu, Haizhen. 2018. Long Noncoding RNA ITPRIP-1 Positively Regulates the Innate Immune Response through Promotion of Oligomerization and Activation of MDA5. In Journal of virology, 92, . doi:10.1128/JVI.00507-18. https://pubmed.ncbi.nlm.nih.gov/29899107/
4. Chen, Funan, Ma, Jun, Hu, Shuqiao, Chen, Shanshan, Lin, Jiehuan. . Prognostic Cell Death Index for Lung Adenocarcinoma: A Comprehensive Transcriptome-Based Analysis of Twelve Programmed Cell Death Pattern Genes. In Frontiers in bioscience (Landmark edition), 29, 135. doi:10.31083/j.fbl2904135. https://pubmed.ncbi.nlm.nih.gov/38682187/
5. Liu, Yue, Hu, Shiqi, Teng, Meixin, Chen, Linsong, Ai, Kaixing. 2023. A novel anoikis-related prognostic signature associated with prognosis and immune infiltration landscape in lung adenocarcinoma. In The journal of gene medicine, 26, e3610. doi:10.1002/jgm.3610. https://pubmed.ncbi.nlm.nih.gov/37985130/
6. Simino, Jeannette, Wang, Zhiying, Bressler, Jan, Boerwinkle, Eric, Mosley, Thomas H. 2017. Whole exome sequence-based association analyses of plasma amyloid-β in African and European Americans; the Atherosclerosis Risk in Communities-Neurocognitive Study. In PloS one, 12, e0180046. doi:10.1371/journal.pone.0180046. https://pubmed.ncbi.nlm.nih.gov/28704393/
7. Saemann, Lars, Wächter, Kristin, Georgevici, Adrian-Iustin, Simm, Andreas, Szabó, Gábor. 2024. Transcriptomic Changes in the Myocardium and Coronary Artery of Donation after Circulatory Death Hearts following Ex Vivo Machine Perfusion. In International journal of molecular sciences, 25, . doi:10.3390/ijms25021261. https://pubmed.ncbi.nlm.nih.gov/38279260/