Pglyrp4-flox 基因敲除小鼠

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产品名称

Pglyrp4-flox 基因敲除小鼠

产品编号

S-CKO-11081

品系全称

C57BL/6JCya-Pglyrp4em1flox/Cya

品系背景

C57BL/6JCya

品系编号

CKOCMP-384997-Pglyrp4-B6J-VA

品系状态

使用本品系发表的文献需注明: Pglyrp4-flox 基因敲除小鼠 mice (Strain S-CKO-11081) 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
peptidoglycan recognition protein 4
基因别称
Gm1478,Gm413
染色体号
Chr 3 (Mouse)
转录本 ID
NCBI: NM_001165968.1 | Ensembl: ENSMUST00000169698
修饰方式
条件性基因敲除
靶向范围
Exon 6
敲除长度
~702 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:2686324Mice homozygous for a knock-out allele exhibit increased susceptibility to DSS-induced colitis.
Pglyrp4,也称为肽聚糖识别蛋白4,是一种重要的先天免疫分子,属于肽聚糖识别蛋白(PGRPs)家族。PGRPs是一类存在于哺乳动物中的模式识别受体,能够识别细菌细胞壁上的肽聚糖结构,从而参与宿主对细菌的免疫防御反应。PGLYRP4在宿主防御机制中发挥着重要作用,能够通过多种途径抑制细菌的生长和繁殖,保护宿主免受细菌感染。

PGLYRP4在多种疾病的发生和发展中发挥着重要作用。例如,研究发现PGLYRP4在头颈鳞状细胞癌(HNSCC)中具有预后价值,与患者的生存率相关[1]。PGLYRP4还能够影响宿主对细菌的清除和炎症反应,例如,PGLYRP4缺陷型小鼠在感染肺炎球菌时,肺部的细菌清除能力增强,免疫细胞招募增多,并且炎症反应加剧[5]。此外,PGLYRP4的表达水平还与多种疾病的易感性相关,例如,PGLYRP4基因多态性与帕金森病(PD)的风险和发病年龄相关[2,7],与哮喘病毒腹泻的易感性相关[6],与银屑病对生物疗法的响应相关[8]。

PGLYRP4在宿主防御机制中的重要作用是通过其与其他分子和信号通路的相互作用来实现的。例如,研究发现PGLYRP4能够通过诱导氧化应激、巯基消耗和金属应激来杀死细菌[3]。此外,PGLYRP4还能够抑制早期炎症反应,例如,PGLYRP4能够抑制百日咳杆菌感染后宿主组织的早期炎症病理反应[4]。PGLYRP4还能够通过控制肠道微生物组的组成和复杂性来影响宿主对细菌的清除和炎症反应[5]。

综上所述,PGLYRP4是一种重要的先天免疫分子,在宿主防御机制中发挥着重要作用。PGLYRP4能够通过多种途径抑制细菌的生长和繁殖,保护宿主免受细菌感染。PGLYRP4在多种疾病的发生和发展中发挥着重要作用,与患者的生存率、疾病的易感性和炎症反应相关。PGLYRP4的研究有助于深入理解宿主防御机制和疾病发生机制,为疾病的治疗和预防提供新的思路和策略。

参考文献:
1. Li, Zhuoqi, Zheng, Chunning, Liu, Hongtao, Zhang, Chi, Tian, Yuan. 2023. A novel oxidative stress-related gene signature as an indicator of prognosis and immunotherapy responses in HNSCC. In Aging, 15, 14957-14984. doi:10.18632/aging.205323. https://pubmed.ncbi.nlm.nih.gov/38157249/
2. Gorecki, Anastazja M, Bakeberg, Megan C, Theunissen, Frances, Mastaglia, Frank L, Anderton, Ryan S. 2020. Single Nucleotide Polymorphisms Associated With Gut Homeostasis Influence Risk and Age-at-Onset of Parkinson's Disease. In Frontiers in aging neuroscience, 12, 603849. doi:10.3389/fnagi.2020.603849. https://pubmed.ncbi.nlm.nih.gov/33328979/
3. Yang, Chun-Kai, Kashyap, Des R, Kowalczyk, Dominik A, Gupta, Dipika, Dziarski, Roman. 2021. Respiratory chain components are required for peptidoglycan recognition protein-induced thiol depletion and killing in Bacillus subtilis and Escherichia coli. In Scientific reports, 11, 64. doi:10.1038/s41598-020-79811-z. https://pubmed.ncbi.nlm.nih.gov/33420211/
4. Skerry, Ciaran, Goldman, William E, Carbonetti, Nicholas H. 2019. Peptidoglycan Recognition Protein 4 Suppresses Early Inflammatory Responses to Bordetella pertussis and Contributes to Sphingosine-1-Phosphate Receptor Agonist-Mediated Disease Attenuation. In Infection and immunity, 87, . doi:10.1128/IAI.00601-18. https://pubmed.ncbi.nlm.nih.gov/30510103/
5. Dabrowski, Alexander N, Shrivastav, Anshu, Conrad, Claudia, Hain, Torsten, Zahlten, Janine. 2019. Peptidoglycan Recognition Protein 4 Limits Bacterial Clearance and Inflammation in Lungs by Control of the Gut Microbiota. In Frontiers in immunology, 10, 2106. doi:10.3389/fimmu.2019.02106. https://pubmed.ncbi.nlm.nih.gov/31616404/
6. Membrive Jiménez, Cristina, Pérez Ramírez, Cristina, Sánchez Martín, Almudena, Ramírez Tortosa, María Del Carmen, Jiménez Morales, Alberto. 2021. Influence of Genetic Polymorphisms on Response to Biologics in Moderate-to-Severe Psoriasis. In Journal of personalized medicine, 11, . doi:10.3390/jpm11040293. https://pubmed.ncbi.nlm.nih.gov/33921427/
7. Chen, Laura, Munday, Rebecca M, Haque, Rashidul, Petri, William A, Duggal, Priya. 2024. Genetic Susceptibility to Astrovirus Diarrhea in Bangladeshi Infants. In Open forum infectious diseases, 11, ofae045. doi:10.1093/ofid/ofae045. https://pubmed.ncbi.nlm.nih.gov/38524222/
8. Sun, Chao, Mathur, Punam, Dupuis, Josée, Bowcock, Anne M, Carulli, John. 2005. Peptidoglycan recognition proteins Pglyrp3 and Pglyrp4 are encoded from the epidermal differentiation complex and are candidate genes for the Psors4 locus on chromosome 1q21. In Human genetics, 119, 113-25. doi:. https://pubmed.ncbi.nlm.nih.gov/16362825/