Nlrp3-KO 基因敲除小鼠

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产品名称

Nlrp3-KO 基因敲除小鼠

产品编号

S-KO-05210

品系全称

C57BL/6NCya-Nlrp3em1/Cya

品系背景

C57BL/6NCya

品系编号

KOCMP-216799-Nlrp3-B6N-VA

品系状态

使用本品系发表的文献需注明: Nlrp3-KO 基因敲除小鼠 mice (Strain S-KO-05210) 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
NLR family, pyrin domain containing 3
基因别称
AGTAVPRL,AII/AVP,Cias1,FCAS,FCU,MWS,Mmig1,NALP3,Pypaf1
染色体号
Chr 11 (Mouse)
转录本 ID
NCBI: NM_145827 | Ensembl: ENSMUST00000101148
修饰方式
全身性基因敲除
靶向范围
Exon 3~6
敲除长度
~9.1 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:2653833Mice homozygous for null mutations exhibit attenuated inflammatory responses related to decrease secretion of IL-1beta and IL-18. Mice heterozygous for activating mutations suffer from autoinflammatory attacks that lead to organ failure and death before weaning.

发表文献

Advanced Science
2026-02-27
Sirt3 Genetically Engineered Apoptotic Bodies Alleviate Skeletal Aging by Limiting Aggravated NLRP3 Inflammasome Activation of Senescent Macrophages
Signal Transduction and Targeted Therapy
2025-09-23
Ninjurin-1 mediates cell lysis and detrimental inflammation of PANoptosis during influenza A virus infection
Nature Chemical Biology
2025-05-25
Eukaryotic ADCY7 catalyzes the production of c-di-AMP to activate the NLRP3 inflammasome
Science Advances
2025-04-25
The P2X7R/NLRP3 inflammasome axis suppresses enthesis regeneration through inflammatory and metabolic macrophage-stem cell cross-talk
Cellular & Molecular Immunology
2024-10-07
The TET3 inflammasome senses unique long HSV-1 proteins for virus particle budding from the nucleus
Cellular & Molecular Immunology
2023-11-26
Integrated NLRP3, AIM2, NLRC4, Pyrin inflammasome activation and assembly drive PANoptosis
1
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NLRP3(Nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing 3)基因编码一种重要的细胞质传感器蛋白,它在识别病原体相关分子模式(PAMPs)和损伤相关分子模式(DAMPs)中发挥着关键作用。NLRP3蛋白广泛表达于巨噬细胞和其他先天免疫细胞中,并参与NLRP3炎症小体的组装。炎症小体激活后,会激活caspase-1,进而将前炎症因子IL-1β和IL-18转化为活性形式,引发多种炎症反应和细胞信号通路。

在鸡中,NLRP3基因的表达研究显示,该基因mRNA在鸡的各个器官中均有表达,且在雄性和雌性鸡之间以及不同器官之间没有显著差异。当鸡受到细菌脂多糖(LPS)刺激时,NLRP3基因在小肠、大肠、肌胃、肝脏、肺、脾脏和派尔集合淋巴结中的表达水平显著升高,并在24小时内达到峰值,48小时后逐渐恢复正常[1]。

NLRP3炎症小体在缺血性脑卒中的发病机制中也发挥着重要作用。研究发现,抑制JAK2/STAT3信号通路可以降低NLRP3炎症小体的激活,从而减轻脑卒中的损伤和神经炎症[2]。此外,SHIP1蛋白在调节小胶质细胞吞噬功能和免疫反应中发挥重要作用,SHIP1的缺失会导致NLRP3炎症小体的过度激活,进而加重阿尔茨海默病(AD)相关的炎症反应[3]。

NLRP3炎症小体还与肥胖相关的代谢性疾病有关。研究发现,线粒体自噬缺陷会导致NLRP3炎症小体的过度激活,进而导致棕色脂肪组织(BAT)功能障碍和肥胖倾向[4]。此外,NLRP3基因多态性与急性心肌梗死(MI)的发生风险相关,且与MI患者血清NLRP3水平升高有关[5]。NLRP3炎症小体的激活还与PFAPA综合征的发病机制有关,但该综合征的遗传背景尚不清楚[6]。

Maf1蛋白可以抑制NF-κB/NLRP3炎症小体信号通路,从而减轻脓毒症相关脑病(SAE)的炎症反应和神经细胞凋亡[7]。Geniposide可以抑制NLRP3炎症小体介导的细胞焦亡,并通过AMPK信号通路减轻心肌缺血再灌注损伤(MI/RI)[8]。NLRP3基因多态性与特应性皮炎(AD)的发病风险和严重程度相关,其中G等位基因与AD的易感和病情加重有关[9]。IκBζ蛋白通过上调Nlrp3基因的表达来控制NLRP3炎症小体的激活[10]。

综上所述,NLRP3炎症小体在多种炎症相关疾病中发挥着重要作用,包括缺血性脑卒中、阿尔茨海默病、肥胖相关代谢性疾病、急性心肌梗死和特应性皮炎等。深入研究NLRP3炎症小体的激活机制和调控因素,有助于开发针对这些疾病的新型治疗策略。

参考文献:
1. Al-Ogaili, Adil Sabr, Hameed, Samer Sadeq, Noori, Noor. 2022. LPS-induced NLRP3 gene expression in chicken. In Open veterinary journal, 12, 197-203. doi:10.5455/OVJ.2022.v12.i2.7. https://pubmed.ncbi.nlm.nih.gov/35603067/
2. Zhu, Hua, Jian, Zhihong, Zhong, Yi, Gu, Lijuan, Xiong, Xiaoxing. 2021. Janus Kinase Inhibition Ameliorates Ischemic Stroke Injury and Neuroinflammation Through Reducing NLRP3 Inflammasome Activation via JAK2/STAT3 Pathway Inhibition. In Frontiers in immunology, 12, 714943. doi:10.3389/fimmu.2021.714943. https://pubmed.ncbi.nlm.nih.gov/34367186/
3. Terzioglu, Gizem, Young-Pearse, Tracy L. 2023. Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer's disease. In Molecular neurodegeneration, 18, 89. doi:10.1186/s13024-023-00674-9. https://pubmed.ncbi.nlm.nih.gov/38017562/
4. Ko, Myoung Seok, Yun, Ji Young, Baek, In-Jeoung, Koh, Eun Hee, Lee, Ki-Up. 2020. Mitophagy deficiency increases NLRP3 to induce brown fat dysfunction in mice. In Autophagy, 17, 1205-1221. doi:10.1080/15548627.2020.1753002. https://pubmed.ncbi.nlm.nih.gov/32400277/
5. M Jalil, Haider, F Ghazi, Haider. . NLRP3 Inflammasome Gene Polymorphisms Variably Associated with its Serum Levels in Acute Myocardial Infarction. In Pakistan journal of biological sciences : PJBS, 23, 612-618. doi:10.3923/pjbs.2020.612.618. https://pubmed.ncbi.nlm.nih.gov/32363817/
6. Chen, Shenglong, Tang, Chaogang, Ding, Hongguang, Han, Yongli, Zeng, Hongke. 2020. Maf1 Ameliorates Sepsis-Associated Encephalopathy by Suppressing the NF-kB/NLRP3 Inflammasome Signaling Pathway. In Frontiers in immunology, 11, 594071. doi:10.3389/fimmu.2020.594071. https://pubmed.ncbi.nlm.nih.gov/33424842/
7. Kaynak, Damla, Yildiz, Mehmet, Sahin, Sezgin, Kasapcopur, Ozgur, Dasdemir, Selcuk. 2022. NLRP3 gene variants and serum NLRP3 levels in periodic fever, aphthous stomatitis, pharyngitis, and adenitis (PFAPA) syndrome. In Clinical rheumatology, 42, 245-251. doi:10.1007/s10067-022-06370-1. https://pubmed.ncbi.nlm.nih.gov/36087224/
8. Li, Haiyan, Yang, Dong-Hua, Zhang, Yanmei, Sun, Jiajia, Shi, Ganggang. 2022. Geniposide suppresses NLRP3 inflammasome-mediated pyroptosis via the AMPK signaling pathway to mitigate myocardial ischemia/reperfusion injury. In Chinese medicine, 17, 73. doi:10.1186/s13020-022-00616-5. https://pubmed.ncbi.nlm.nih.gov/35715805/
9. El Gendy, Aya, Abo Ali, Fawzia H, Baioumy, Shereen A, El-Bassiouny, Mahy, Abdel Latif, Osama M. . NLRP3 inflammasome (rs10754558) gene polymorphism in patients with atopic dermatitis. In The Egyptian journal of immunology, 30, 102-109. doi:. https://pubmed.ncbi.nlm.nih.gov/37440332/
10. Kim, Jeongeun, Ahn, Huijeong, Yu, Sangjung, Lee, Eunsong, Lee, Geun-Shik. 2020. IκBζ controls NLRP3 inflammasome activation via upregulation of the Nlrp3 gene. In Cytokine, 127, 154983. doi:10.1016/j.cyto.2019.154983. https://pubmed.ncbi.nlm.nih.gov/31918161/

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