Clec4n-KO 基因敲除小鼠

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产品名称

Clec4n-KO 基因敲除小鼠

产品编号

S-KO-16753

品系全称

C57BL/6JCya-Clec4nem1/Cya

品系背景

C57BL/6JCya

品系编号

KOCMP-56620-Clec4n-B6J-VB

品系状态

使用本品系发表的文献需注明: Clec4n-KO 基因敲除小鼠 mice (Strain S-KO-16753) 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
C-type lectin domain family 4, member n
基因别称
Clec6a,Clecsf10,Nkcl
染色体号
Chr 6 (Mouse)
转录本 ID
NCBI: NM_020001.2 | Ensembl: ENSMUST00000024118
修饰方式
全身性基因敲除
靶向范围
Exon 4
敲除长度
~0.2 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:1861231Mice homozygous for a null allele have defective responses to Candida albicans.
Clec4n,也称为Dectin-2,是一种C型凝集素受体,主要表达于树突状细胞(DCs)和巨噬细胞表面。Clec4n能够识别多种病原微生物的配体,包括真菌的α-甘露聚糖和分枝杆菌的甘露糖帽脂阿拉伯甘露聚糖(Man-LAM),并通过激活下游信号通路,诱导免疫细胞产生炎症因子,参与宿主的免疫防御反应[6][9]。Clec4n的激活可以促进Th17细胞的分化,增强宿主对真菌感染的防御能力[9]。此外,Clec4n还能够促进Th2细胞的分化,参与哮喘等过敏性疾病的发生发展[7][8]。

研究发现,Clec4n在多种疾病中发挥重要作用。例如,在急性肝损伤中,Clec4n的表达上调,与巨噬细胞浸润和肝功能损伤相关[2]。在阿尔茨海默病模型小鼠中,Clec4n的表达上调,可能与神经炎症和突触损伤有关[1]。在年龄相关性听力损失中,Clec4n的表达上调,可能与炎症和免疫反应有关[4]。在皮肤炎症性疾病中,Clec4n的表达上调,可能与中性粒细胞浸润和炎症反应有关[5][8]。

Clec4n的激活可以导致下游信号通路的激活,包括Syk-NF-κB和Syk-JNK信号通路,从而促进炎症因子的产生和免疫细胞的活化[3][8]。此外,Clec4n的激活还可以影响免疫细胞的功能,例如促进DCs的活化,增强其诱导Th2和Th17细胞分化的能力[7][8]。

Clec4n作为一种重要的C型凝集素受体,在宿主的免疫防御和疾病发生发展中发挥重要作用。Clec4n的激活可以促进炎症反应和免疫细胞的活化,参与多种疾病的发生发展。因此,Clec4n可能成为治疗炎症和免疫相关疾病的重要靶点。

参考文献:
1. Wang, Yi-Ying, Zhou, Yu-Ning, Jiang, Lin, Chao, Feng-Lei, Tang, Yong. 2023. Long-term voluntary exercise inhibited AGE/RAGE and microglial activation and reduced the loss of dendritic spines in the hippocampi of APP/PS1 transgenic mice. In Experimental neurology, 363, 114371. doi:10.1016/j.expneurol.2023.114371. https://pubmed.ncbi.nlm.nih.gov/36871860/
2. Cao, Zhiwen, Lu, Peipei, Li, Li, Tan, Yong, Lu, Cheng. 2023. Bioinformatics-led discovery of liver-specific genes and macrophage infiltration in acute liver injury. In Frontiers in immunology, 14, 1287136. doi:10.3389/fimmu.2023.1287136. https://pubmed.ncbi.nlm.nih.gov/38130716/
3. Qu, Yulan, Ma, Xiaotian, Deng, Jiewen, Guo, Zhenhong, Bai, Chong. 2022. Dectin-2 promotes house dust mite-skewed Th2 response through the activation of cDC2s. In Cellular immunology, 378, 104558. doi:10.1016/j.cellimm.2022.104558. https://pubmed.ncbi.nlm.nih.gov/35717749/
4. Cheng, Yajing, Chen, Wenjin, Xu, Jia, Chen, Ting, Hu, Jun. 2023. Genetic analysis of potential biomarkers and therapeutic targets in age-related hearing loss. In Hearing research, 439, 108894. doi:10.1016/j.heares.2023.108894. https://pubmed.ncbi.nlm.nih.gov/37844444/
5. Guerrero-Juarez, Christian F, Schilf, Paul, Li, Jing, Sadik, Christian D, Amber, Kyle T. 2023. C-type lectin receptor expression is a hallmark of neutrophils infiltrating the skin in epidermolysis bullosa acquisita. In Frontiers in immunology, 14, 1266359. doi:10.3389/fimmu.2023.1266359. https://pubmed.ncbi.nlm.nih.gov/37799716/
6. Yonekawa, Akiko, Saijo, Shinobu, Hoshino, Yoshihiko, Akashi, Koichi, Yamasaki, Sho. 2014. Dectin-2 is a direct receptor for mannose-capped lipoarabinomannan of mycobacteria. In Immunity, 41, 402-413. doi:10.1016/j.immuni.2014.08.005. https://pubmed.ncbi.nlm.nih.gov/25176311/
7. Norimoto, Ayako, Hirose, Koichi, Iwata, Arifumi, Iwakura, Yoichiro, Nakajima, Hiroshi. . Dectin-2 promotes house dust mite-induced T helper type 2 and type 17 cell differentiation and allergic airway inflammation in mice. In American journal of respiratory cell and molecular biology, 51, 201-9. doi:10.1165/rcmb.2013-0522OC. https://pubmed.ncbi.nlm.nih.gov/24588637/
8. Nesterovitch, Andrew B, Arbieva, Zarema, Toth, Daniel M, Tharp, Michael D, Glant, Tibor T. 2016. A differential gene expression study: Ptpn6 (SHP-1)-insufficiency leads to neutrophilic dermatosis-like disease (NDLD) in mice. In Journal of dermatological science, 83, 17-25. doi:10.1016/j.jdermsci.2016.03.005. https://pubmed.ncbi.nlm.nih.gov/27020408/
9. Saijo, Shinobu, Ikeda, Satoshi, Yamabe, Keiko, Akira, Shizuo, Iwakura, Yoichiro. 2010. Dectin-2 recognition of alpha-mannans and induction of Th17 cell differentiation is essential for host defense against Candida albicans. In Immunity, 32, 681-91. doi:10.1016/j.immuni.2010.05.001. https://pubmed.ncbi.nlm.nih.gov/20493731/