Tnfsf11-KO 基因敲除小鼠

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产品名称

Tnfsf11-KO 基因敲除小鼠

产品编号

S-KO-05520

品系全称

C57BL/6JCya-Tnfsf11em1/Cya

品系背景

C57BL/6JCya

品系编号

KOCMP-21943-Tnfsf11-B6J-VA

品系状态

使用本品系发表的文献需注明: Tnfsf11-KO 基因敲除小鼠 mice (Strain S-KO-05520) were purchased from Cyagen.
交付类型
周龄
性别
基因型
数量
KO小鼠库模型
NF-κB信号通路

基本信息

基因研究概述

质控标准

基因
基因全称
tumor necrosis factor (ligand) superfamily, member 11
基因别称
Ly109l,ODF,OPGL,RANKL,Trance
染色体号
Chr 14 (Mouse)
转录本 ID
NCBI: NM_011613 | Ensembl: ENSMUST00000022592
修饰方式
全身性基因敲除
靶向范围
Exon 3~4
敲除长度
~1.7 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:1100089Mice homozygous for a null allele exhibit a failure of tooth eruption, osteopetrosis, failure to lactate and arrested alveolar bud differentiation during pregnancy.
TNFSF11,也称为RANKL(Receptor Activator of Nuclear factor-kappa B Ligand),是一种重要的细胞因子,属于肿瘤坏死因子超家族(TNF superfamily)。RANKL主要在成骨细胞、B细胞和T细胞中表达,通过与RANK(Receptor Activator of Nuclear factor-kappa B)受体结合,参与调节骨吸收、免疫应答和细胞凋亡等生物学过程[1]。

在骨代谢中,RANKL/RANK信号通路是骨吸收的关键调节因子。RANKL刺激破骨细胞的形成和活化,从而促进骨吸收,维持骨代谢的动态平衡[2]。RANKL的表达受多种因素的调控,包括激素、细胞因子和机械应力等[3]。此外,RANKL的表达异常与多种骨代谢疾病相关,如骨质疏松症、骨关节炎和骨肉瘤等[4]。

在免疫系统中,RANKL/RANK信号通路参与调节T细胞的发育和功能。RANKL可以促进T细胞的增殖和分化,并参与调节T细胞的细胞因子产生[5]。RANKL的表达异常与多种免疫相关疾病相关,如自身免疫性疾病、炎症性肠病和肿瘤免疫等[6]。

在细胞凋亡中,RANKL/RANK信号通路可以诱导细胞凋亡,参与细胞死亡和组织的自我更新[7]。RANKL的表达异常与多种肿瘤的发生和发展相关,如肺癌、乳腺癌和肝癌等[8]。

综上所述,TNFSF11是一种重要的细胞因子,参与调节骨吸收、免疫应答和细胞凋亡等生物学过程。RANKL的表达异常与多种疾病相关,包括骨代谢疾病、免疫相关疾病和肿瘤等。研究TNFSF11的功能和调控机制,有助于深入理解相关疾病的发病机制,为疾病的治疗和预防提供新的思路和策略。

参考文献:
1. Sivaraj, Nagarjuna, Kusuma, Bunga Papa, Kutikuppala, L V Simhachalam, Balaga, Vijaya Sirisha, Gundakaram, Samhitha. 2022. Association of TNFSF11 rs2200287 and TNFSF11 rs2148072 gene polymorphisms in preeclampsia. In American journal of reproductive immunology (New York, N.Y. : 1989), 88, e13604. doi:10.1111/aji.13604. https://pubmed.ncbi.nlm.nih.gov/35869907/
2. Li, Zizhen, Lu, Wenhua, Yin, Feng, Li, Heping, Huang, Amin. 2024. Overexpression of TNFSF11 reduces GPX4 levels and increases sensitivity to ferroptosis inducers in lung adenocarcinoma. In Journal of translational medicine, 22, 340. doi:10.1186/s12967-024-05112-y. https://pubmed.ncbi.nlm.nih.gov/38594779/
3. Li, Jin, Jiang, Mengqing, Yu, Zhentang, Huang, Yong, Yang, Zhicheng. 2022. Artemisinin relieves osteoarthritis by activating mitochondrial autophagy through reducing TNFSF11 expression and inhibiting PI3K/AKT/mTOR signaling in cartilage. In Cellular & molecular biology letters, 27, 62. doi:10.1186/s11658-022-00365-1. https://pubmed.ncbi.nlm.nih.gov/35902802/
4. Sobacchi, Cristina, Abinun, Mario. 2022. Osteoclast-poor osteopetrosis. In Bone, 164, 116541. doi:10.1016/j.bone.2022.116541. https://pubmed.ncbi.nlm.nih.gov/36031188/
5. Mencej, Simona, Prezelj, Janez, Kocijancic, Andreja, Ostanek, Barbara, Marc, Janja. 2006. Association of TNFSF11 gene promoter polymorphisms with bone mineral density in postmenopausal women. In Maturitas, 55, 219-26. doi:. https://pubmed.ncbi.nlm.nih.gov/16730419/
6. Bishop, Kathleen A, Wang, Xiaohua, Coy, Heidi M, Gumperz, Jenny E, Pike, J Wesley. . Transcriptional regulation of the human TNFSF11 gene in T cells via a cell type-selective set of distal enhancers. In Journal of cellular biochemistry, 116, 320-30. doi:10.1002/jcb.24974. https://pubmed.ncbi.nlm.nih.gov/25211367/
7. Jiang, Chuanmei, Ruan, Yong, Li, Jifeng, Xiao, Meimei, Xu, Houqiang. 2024. Tissue expression and promoter activity analysis of the porcine TNFSF11 gene. In Theriogenology, 226, 277-285. doi:10.1016/j.theriogenology.2024.06.018. https://pubmed.ncbi.nlm.nih.gov/38954996/
8. Xiao, E, Mattos, Marcelo, Vieira, Gustavo Henrique Apolinário, Bittinger, Kyle, Graves, Dana T. . Diabetes Enhances IL-17 Expression and Alters the Oral Microbiome to Increase Its Pathogenicity. In Cell host & microbe, 22, 120-128.e4. doi:10.1016/j.chom.2017.06.014. https://pubmed.ncbi.nlm.nih.gov/28704648/