Thbs4-flox 基因敲除小鼠

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产品名称

Thbs4-flox 基因敲除小鼠

产品编号

S-CKO-06265

品系全称

C57BL/6JCya-Thbs4em1flox/Cya

品系背景

C57BL/6JCya

品系编号

CKOCMP-21828-Thbs4-B6J-VA

品系状态

使用本品系发表的文献需注明: Thbs4-flox 基因敲除小鼠 mice (Strain S-CKO-06265) were purchased from Cyagen.
交付类型
周龄
性别
基因型
数量
cKO小鼠库模型
PI3K-Akt信号通路

基本信息

基因研究概述

质控标准

基因
基因全称
thrombospondin 4
基因别称
TSP4
染色体号
Chr 13 (Mouse)
转录本 ID
NCBI: NM_011582 | Ensembl: ENSMUST00000022213
修饰方式
条件性基因敲除
靶向范围
Exon 5~8
敲除长度
~3.1 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:1101779Mice homozygous for a targeted allele exhibit increased sensitivity to cardiac pressure overload, including increased hypertrophy, decreased ejection fraction, decreased microvessel number, increased extracellular matrix deposition and increased fibrosis. Homozygous KO leads to impaired wound healing and delayed retinal vasculature development and affects macrophage differentiation. Homozygosity for the p.A389P mutation leads to enhanced wound healing and accelerated retinal vasculature development and affects macrophage differentiation.
Thbs4,也称为Thrombospondin-4,是一种重要的细胞外基质蛋白,属于血栓蛋白家族。血栓蛋白家族是一组分泌性细胞外基质蛋白,参与细胞粘附动力学和细胞外基质蛋白的生成。Thbs4在多种生物学过程中发挥作用,包括炎症反应、细胞粘附、细胞迁移、细胞分化和细胞外基质重塑。

Thbs4在多种疾病中发挥重要作用。在心脏疾病中,Thbs4的表达与心脏纤维化和肥厚相关。研究表明,Thbs4在心脏组织中的表达与心脏纤维化和肥厚呈正相关[5]。此外,Thbs4还与心脏疾病的发生和发展相关。例如,Thbs4的表达与心脏肥厚和心力衰竭的发生相关[3]。Thbs4在脑疾病中也发挥重要作用。研究表明,Thbs4的表达与阿尔茨海默病的发生和发展相关。Thbs4的表达与阿尔茨海默病患者的脑灰质体积和基因表达相关[1]。此外,Thbs4还与脑卒中后的恢复相关。研究表明,Thbs4的表达与脑卒中后的恢复相关。Thbs4的表达与脑卒中后的神经功能和神经再生相关[2]。

Thbs4的表达与肿瘤的发生和发展相关。研究表明,Thbs4的表达与结直肠癌的发生和发展相关。Thbs4的表达与结直肠癌患者的预后相关。Thbs4的表达与结直肠癌患者的肿瘤生长和转移相关[4]。此外,Thbs4还与胃癌的发生和发展相关。Thbs4的表达与胃癌患者的预后相关。Thbs4的表达与胃癌患者的肿瘤生长和转移相关[6]。

Thbs4的表达与皮肤疾病的发生和发展相关。研究表明,Thbs4的表达与皮肤疾病的发生和发展相关。Thbs4的表达与皮肤疾病的炎症反应和细胞迁移相关[7]。

Thbs4在多种生物学过程中发挥作用,包括炎症反应、细胞粘附、细胞迁移、细胞分化和细胞外基质重塑。Thbs4在多种疾病中发挥重要作用,包括心脏疾病、脑疾病、肿瘤和皮肤疾病。Thbs4的研究有助于深入理解细胞外基质蛋白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. Cagliani, Rachele, Guerini, Franca R, Rubio-Acero, Raquel, Clerici, Mario, Sironi, Manuela. 2013. Long-standing balancing selection in the THBS4 gene: influence on sex-specific brain expression and gray matter volumes in Alzheimer disease. In Human mutation, 34, 743-53. doi:10.1002/humu.22301. https://pubmed.ncbi.nlm.nih.gov/23420636/
2. Stokowska, Anna, Aswendt, Markus, Zucha, Daniel, Pekny, Milos, Pekna, Marcela. 2023. Complement C3a treatment accelerates recovery after stroke via modulation of astrocyte reactivity and cortical connectivity. In The Journal of clinical investigation, 133, . doi:10.1172/JCI162253. https://pubmed.ncbi.nlm.nih.gov/36995772/
3. Meng, Xiang-Min, Pang, Qiu-Yu, Zhou, Zhen-Fang, Feng, Qi-Pu, Zhu, Bing-Mei. 2024. Histone methyltransferase MLL4 protects against pressure overload-induced heart failure via a THBS4-mediated protection in ER stress. In Pharmacological research, 205, 107263. doi:10.1016/j.phrs.2024.107263. https://pubmed.ncbi.nlm.nih.gov/38876442/
4. Greco, Sonia A, Chia, June, Inglis, Kelly J, Leggett, Barbara A, Whitehall, Vicki L J. 2010. Thrombospondin-4 is a putative tumour-suppressor gene in colorectal cancer that exhibits age-related methylation. In BMC cancer, 10, 494. doi:10.1186/1471-2407-10-494. https://pubmed.ncbi.nlm.nih.gov/20846368/
5. McLellan, Micheal A, Skelly, Daniel A, Dona, Malathi S I, Rosenthal, Nadia A, Pinto, Alexander R. 2020. High-Resolution Transcriptomic Profiling of the Heart During Chronic Stress Reveals Cellular Drivers of Cardiac Fibrosis and Hypertrophy. In Circulation, 142, 1448-1463. doi:10.1161/CIRCULATIONAHA.119.045115. https://pubmed.ncbi.nlm.nih.gov/32795101/
6. Chen, Xiangbo, Huang, Yisen, Wang, Yubin, Hong, Shunzhong, Huang, Zicheng. 2019. THBS4 predicts poor outcomes and promotes proliferation and metastasis in gastric cancer. In Journal of physiology and biochemistry, 75, 117-123. doi:10.1007/s13105-019-00665-9. https://pubmed.ncbi.nlm.nih.gov/30746617/
7. Mäemets-Allas, Kristina, Klaas, Mariliis, Cárdenas-León, Claudia Griselda, Kankuri, Esko, Jaks, Viljar. 2022. Stimulation with THBS4 activates pathways that regulate proliferation, migration and inflammation in primary human keratinocytes. In Biochemical and biophysical research communications, 642, 97-106. doi:10.1016/j.bbrc.2022.12.052. https://pubmed.ncbi.nlm.nih.gov/36566568/