Cdh5-flox 基因敲除小鼠

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产品名称

Cdh5-flox 基因敲除小鼠

产品编号

S-CKO-01668

品系全称

C57BL/6JCya-Cdh5em1flox/Cya

品系背景

C57BL/6JCya

品系编号

CKOCMP-12562-Cdh5-B6J-VA

品系状态

使用本品系发表的文献需注明: Cdh5-flox 基因敲除小鼠 mice (Strain S-CKO-01668) 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
cadherin 5
基因别称
7B4,Cd144,VE-Cad,VECD,VEcad,Vec
染色体号
Chr 8 (Mouse)
转录本 ID
NCBI: NM_009868 | Ensembl: ENSMUST00000034339
修饰方式
条件性基因敲除
靶向范围
Exon 3~4
敲除长度
~2.1 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:105057Homozygous inactivation or cytosolic truncation of this gene causes embryonic growth retardation, abnormal somite and heart development, impaired remodeling and maturation of endothelial cells, increased endothelial apoptosis and severe vascular defects leading to embryonic death at midgestation. Inducible KO in endothelial cells affects retinal angiogenesis.
CDH5,也称为VE-钙粘蛋白(VE-cadherin),是一种钙粘蛋白,在血管内皮细胞中表达,参与血管形态发生、维持血管完整性和淋巴功能[1]。CDH5基因的突变可能与淋巴水肿的发病机制有关,因此被认为是淋巴水肿遗传检测的一个可能的新候选基因[1]。此外,CDH5基因还与心脏毒性、肿瘤免疫反应、内皮细胞功能障碍和卵品质有关[2,3,4,5,6,7,8]。

CDH5基因的突变可能导致淋巴水肿,但需要进一步的研究来证实这一假设[1]。在心脏毒性方面,CDH5基因与cGAS-STING信号通路有关,该通路在多柔比星诱导的心脏毒性中发挥重要作用[2]。在肿瘤免疫反应方面,CDH5基因与CD8+ T细胞的免疫反应有关,其表达异常可能与肿瘤预后相关[7]。在内皮细胞功能障碍方面,CDH5基因与自噬途径有关,自噬途径的失调可能导致内皮细胞功能障碍[4]。在卵品质方面,CDH5基因可能与钙离子转运有关,影响子宫上皮细胞中的钙离子浓度[8]。

综上所述,CDH5基因在多种生物学过程中发挥重要作用,包括淋巴水肿、心脏毒性、肿瘤免疫反应、内皮细胞功能障碍和卵品质。CDH5基因的研究有助于深入理解血管内皮细胞的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. Michelini, Sandro, Ricci, Maurizio, Amato, Bruno, Dautaj, Astrit, Bertelli, Matteo. 2021. CDH5, a Possible New Candidate Gene for Genetic Testing of Lymphedema. In Lymphatic research and biology, 20, 496-506. doi:10.1089/lrb.2020.0089. https://pubmed.ncbi.nlm.nih.gov/34882481/
2. Luo, Wei, Zou, Xiaoyi, Wang, Yidan, Sun, Aijun, Ge, Junbo. 2023. Critical Role of the cGAS-STING Pathway in Doxorubicin-Induced Cardiotoxicity. In Circulation research, 132, e223-e242. doi:10.1161/CIRCRESAHA.122.321587. https://pubmed.ncbi.nlm.nih.gov/37154056/
3. He, Qi, Li, Xiujuan, Singh, Kailash, Ulvmar, Maria, Welsh, Michael. 2019. The Cdh5-CreERT2 transgene causes conditional Shb gene deletion in hematopoietic cells with consequences for immune cell responses to tumors. In Scientific reports, 9, 7548. doi:10.1038/s41598-019-44039-z. https://pubmed.ncbi.nlm.nih.gov/31101877/
4. Niu, Chao, Chen, Zhiwei, Kim, Kyoung Tae, Jin, Litai, Li, Xiaokun. 2019. Metformin alleviates hyperglycemia-induced endothelial impairment by downregulating autophagy via the Hedgehog pathway. In Autophagy, 15, 843-870. doi:10.1080/15548627.2019.1569913. https://pubmed.ncbi.nlm.nih.gov/30653446/
5. Tombor, Lukas S, John, David, Glaser, Simone F, Abplanalp, Wesley T, Dimmeler, Stefanie. 2021. Single cell sequencing reveals endothelial plasticity with transient mesenchymal activation after myocardial infarction. In Nature communications, 12, 681. doi:10.1038/s41467-021-20905-1. https://pubmed.ncbi.nlm.nih.gov/33514719/
6. Katoh, Masaru. 2018. Multi‑layered prevention and treatment of chronic inflammation, organ fibrosis and cancer associated with canonical WNT/β‑catenin signaling activation (Review). In International journal of molecular medicine, 42, 713-725. doi:10.3892/ijmm.2018.3689. https://pubmed.ncbi.nlm.nih.gov/29786110/
7. Li, Yuantao, Wu, Qikai, Lv, Jiancheng, Gu, Junwei. 2023. A comprehensive pan-cancer analysis of CDH5 in immunological response. In Frontiers in immunology, 14, 1239875. doi:10.3389/fimmu.2023.1239875. https://pubmed.ncbi.nlm.nih.gov/37809080/
8. Zhang, Xianming, Jin, Hua, Huang, Xiaojia, Shanley, Thomas P, Zhao, You-Yang. . Robust genome editing in adult vascular endothelium by nanoparticle delivery of CRISPR-Cas9 plasmid DNA. In Cell reports, 38, 110196. doi:10.1016/j.celrep.2021.110196. https://pubmed.ncbi.nlm.nih.gov/34986352/