Mapkapk3-KO 基因敲除小鼠

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产品名称

Mapkapk3-KO 基因敲除小鼠

产品编号

S-KO-00260

品系全称

C57BL/6JCya-Mapkapk3em1/Cya

品系背景

C57BL/6JCya

品系编号

KOCMP-102626-Mapkapk3-B6J-VA

品系状态

使用本品系发表的文献需注明: Mapkapk3-KO 基因敲除小鼠 mice (Strain S-KO-00260) 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-activated protein kinase 3
基因别称
3PK,MAPKAP-K3,MAPKAP3,MK-3,MK3,MapkKapk3
染色体号
Chr 9 (Mouse)
转录本 ID
NCBI: NM_178907 | Ensembl: ENSMUST00000035194
修饰方式
全身性基因敲除
靶向范围
Exon 3~8
敲除长度
~5.4 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:2143163Mice homozygous for a knock-out allele are viable and fertile and display normal tissue morphology, behavior, and LPS-induced production of cytokines. Eyes of homozygous null mice show defects in Bruch's membrane, with disorganized architecture and variability in thickness.
Mapkapk3,也称为Mitogen-activated protein kinase-activated protein kinase 3,是一种重要的丝氨酸/苏氨酸蛋白激酶,属于p38信号通路家族。Mapkapk3参与多种生物学过程,包括细胞应激反应、基因调控、细胞生长和发育等。Mapkapk3通过磷酸化下游底物,如Beclin 1、CREB等,影响细胞的生物学功能。

Mapkapk3在多种疾病中发挥重要作用。例如,在小鼠模型中,Mapkapk3的缺失会导致Bruch's膜不规则,出现异常增厚和变薄的区域[1]。此外,Mapkapk3的基因多态性与慢性丙型肝炎病毒感染患者对干扰素治疗的反应相关[2]。Mapkapk3在胶质瘤细胞中表达上调,抑制其表达可以降低细胞增殖和迁移能力[3]。Mapkapk3还与肥胖的发生发展相关,GLP-1可以下调Mapkapk3的表达,抑制食欲和体重增加[4]。

此外,Mapkapk3还与免疫相关。例如,Mapkapk3的表达与结直肠癌患者的预后相关,可以作为一种可靠的预后指标[5]。Mapkapk3还可以通过激活CREB,促进血管平滑肌细胞的增殖和迁移,导致血管内膜增生[6]。

综上所述,Mapkapk3是一种重要的丝氨酸/苏氨酸蛋白激酶,参与多种生物学过程,包括细胞应激反应、基因调控、细胞生长和发育等。Mapkapk3在多种疾病中发挥重要作用,包括视网膜病变、慢性丙型肝炎病毒感染、胶质瘤、肥胖、结直肠癌和血管内膜增生等。此外,Mapkapk3还与免疫相关,可以作为结直肠癌患者的预后指标。因此,Mapkapk3的研究有助于深入理解细胞应激反应、基因调控和细胞生长等生物学过程,为疾病的治疗和预防提供新的思路和策略。

参考文献:
1. Meunier, Isabelle, Lenaers, Guy, Bocquet, Béatrice, Gaestel, Matthias, Hamel, Christian P. 2016. A dominant mutation in MAPKAPK3, an actor of p38 signaling pathway, causes a new retinal dystrophy involving Bruch's membrane and retinal pigment epithelium. In Human molecular genetics, 25, 916-26. doi:10.1093/hmg/ddv624. https://pubmed.ncbi.nlm.nih.gov/26744326/
2. Tsukada, Hironobu, Ochi, Hidenori, Maekawa, Toshiro, Nakamura, Yusuke, Chayama, Kazuaki. 2009. A polymorphism in MAPKAPK3 affects response to interferon therapy for chronic hepatitis C. In Gastroenterology, 136, 1796-805.e6. doi:10.1053/j.gastro.2009.01.061. https://pubmed.ncbi.nlm.nih.gov/19208361/
3. Wang, Jingya, Ren, Peng, Zeng, Zhirui, Zhang, Hongmei, Guo, Wenzhi. . Inhibition of translocator protein 18 kDa suppressed the progression of glioma via the ELAV-like RNA-binding protein 1/MAPK-activated protein kinase 3 axis. In Bioengineered, 13, 7457-7470. doi:10.1080/21655979.2022.2048992. https://pubmed.ncbi.nlm.nih.gov/35285415/
4. Shao, Yuwei, Tian, Jun, Yang, Yanan, Zhu, Ye, Shu, Qing. 2022. Identification of key genes and pathways revealing the central regulatory mechanism of brain-derived glucagon-like peptide-1 on obesity using bioinformatics analysis. In Frontiers in neuroscience, 16, 931161. doi:10.3389/fnins.2022.931161. https://pubmed.ncbi.nlm.nih.gov/35992905/
5. Dai, Siqi, Xu, Shuang, Ye, Yao, Ding, Kefeng. 2020. Identification of an Immune-Related Gene Signature to Improve Prognosis Prediction in Colorectal Cancer Patients. In Frontiers in genetics, 11, 607009. doi:10.3389/fgene.2020.607009. https://pubmed.ncbi.nlm.nih.gov/33343640/
6. Nakanishi, Keisuke, Saito, Yukihiro, Azuma, Nobuyoshi, Sasajima, Tadahiro. 2012. Cyclic adenosine monophosphate response-element binding protein activation by mitogen-activated protein kinase-activated protein kinase 3 and four-and-a-half LIM domains 5 plays a key role for vein graft intimal hyperplasia. In Journal of vascular surgery, 57, 182-93, 193.e1-10. doi:10.1016/j.jvs.2012.06.082. https://pubmed.ncbi.nlm.nih.gov/23127979/