Fbxo11-flox 基因敲除小鼠

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产品名称

Fbxo11-flox 基因敲除小鼠

产品编号

S-CKO-18849

品系全称

C57BL/6JCya-Fbxo11em1flox/Cya

品系背景

C57BL/6JCya

品系编号

CKOCMP-225055-Fbxo11-B6J-VB

品系状态

使用本品系发表的文献需注明: Fbxo11-flox 基因敲除小鼠 mice (Strain S-CKO-18849) 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
F-box protein 11
基因别称
Jf
染色体号
Chr 17 (Mouse)
转录本 ID
NCBI: NM_001081034 | Ensembl: ENSMUST00000005504
修饰方式
条件性基因敲除
靶向范围
Exon 4
敲除长度
~0.6 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:2147134Mice homozygous for ENU-induced mutations exhibit cleft palate, facial clefting, and perinatal lethality. Mice homozygous for a knock-out allele show neonatal lethality, thick epidermis, decreased hair follicle number, absent keratohyalin granules, and increased epidermal Snail protein levels.
Fbxo11,也称为F-box only protein 11,是一种重要的F-box蛋白。F-box蛋白是Skp1-Cullin1-F-box (SCF) E3泛素连接酶复合物中的底物识别亚基,参与调控多种生物学过程,包括细胞周期、细胞凋亡、信号传导和蛋白质降解等。Fbxo11通过与SCF复合物中的Skp1和Cullin1结合,识别并泛素化底物蛋白,进而将其降解。Fbxo11在多种生物学过程中发挥重要作用,包括免疫调节、骨发育、脂质代谢和血液系统发育等。

在免疫调节方面,Fbxo11通过泛素化MHC class II转录激活因子CIITA,降低MHC class II的表达水平,从而抑制免疫反应[1]。此外,Fbxo11的突变还与智力障碍和行为问题相关[2]。在骨发育方面,Fbxo11通过调节Snail1蛋白的表达水平,影响骨形成和骨矿化[3]。在脂质代谢方面,Fbxo11通过调节hnRNPA2B1蛋白的表达水平,影响脂质代谢和肝癌的发生[4]。在血液系统发育方面,Fbxo11通过调节BAHD1蛋白的表达水平,影响红细胞生成和PRC2依赖性转录抑制[5]。

Fbxo11还与多种疾病的发生发展相关。例如,Fbxo11的突变与慢性中耳炎、复发性中耳炎和淋巴增殖性疾病等相关[6,7,8]。此外,Fbxo11的缺失还与听力丧失相关[6,7]。Fbxo11的突变还与智力障碍和行为问题相关,例如自闭症谱系障碍、注意力缺陷/多动障碍、焦虑和攻击行为等[2,9]。在肿瘤方面,Fbxo11的缺失与淋巴瘤的发生发展相关,Fbxo11的缺失导致BCL6蛋白水平升高,进而导致淋巴增殖性疾病[8]。

综上所述,Fbxo11是一种重要的F-box蛋白,参与调控多种生物学过程,包括免疫调节、骨发育、脂质代谢和血液系统发育等。Fbxo11的突变与多种疾病的发生发展相关,包括慢性中耳炎、复发性中耳炎、淋巴增殖性疾病、智力障碍、行为问题和淋巴瘤等。Fbxo11的研究有助于深入理解F-box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. Kasuga, Yusuke, Ouda, Ryota, Watanabe, Masashi, Hatakeyama, Shigetsugu, Kobayashi, Koichi S. 2023. FBXO11 constitutes a major negative regulator of MHC class II through ubiquitin-dependent proteasomal degradation of CIITA. In Proceedings of the National Academy of Sciences of the United States of America, 120, e2218955120. doi:10.1073/pnas.2218955120. https://pubmed.ncbi.nlm.nih.gov/37279268/
2. Jansen, Sandra, van der Werf, Ilse M, Innes, A Micheil, Vissers, Lisenka E L M, de Vries, Bert B A. 2019. De novo variants in FBXO11 cause a syndromic form of intellectual disability with behavioral problems and dysmorphisms. In European journal of human genetics : EJHG, 27, 738-746. doi:10.1038/s41431-018-0292-2. https://pubmed.ncbi.nlm.nih.gov/30679813/
3. Huang, Hong, Lu, Jianrong, Aukhil, Ikramuddin, Pirih, Flavia, Chang, Jia. 2023. FBXO11 regulates bone development. In Bone, 170, 116709. doi:10.1016/j.bone.2023.116709. https://pubmed.ncbi.nlm.nih.gov/36863499/
4. Zhang, Hao, Xia, Peng, Yang, Zhangshuo, Zhang, Zhonglin, Yuan, Yufeng. . Cullin-associated and neddylation-dissociated 1 regulate reprogramming of lipid metabolism through SKP1-Cullin-1-F-boxFBXO11 -mediated heterogeneous nuclear ribonucleoprotein A2/B1 ubiquitination and promote hepatocellular carcinoma. In Clinical and translational medicine, 13, e1443. doi:10.1002/ctm2.1443. https://pubmed.ncbi.nlm.nih.gov/37837399/
5. Chan, Kah Lok, Gomez, Juliana, Cardinez, Chelisa, Burr, Marian L, Dawson, Mark A. 2022. Inhibition of the CtBP complex and FBXO11 enhances MHC class II expression and anti-cancer immune responses. In Cancer cell, 40, 1190-1206.e9. doi:10.1016/j.ccell.2022.09.007. https://pubmed.ncbi.nlm.nih.gov/36179686/
6. Xu, Peng, Scott, Daniel C, Xu, Beisi, Schulman, Brenda A, Weiss, Mitchell J. . FBXO11-mediated proteolysis of BAHD1 relieves PRC2-dependent transcriptional repression in erythropoiesis. In Blood, 137, 155-167. doi:10.1182/blood.2020007809. https://pubmed.ncbi.nlm.nih.gov/33156908/
7. Segade, Fernando, Daly, Kathleen A, Allred, Dax, Rich, Stephen S, Bowden, Donald W. . Association of the FBXO11 gene with chronic otitis media with effusion and recurrent otitis media: the Minnesota COME/ROM Family Study. In Archives of otolaryngology--head & neck surgery, 132, 729-33. doi:. https://pubmed.ncbi.nlm.nih.gov/16847180/
8. Schneider, Christof, Kon, Ning, Amadori, Letizia, Basso, Katia, Dalla-Favera, Riccardo. 2016. FBXO11 inactivation leads to abnormal germinal-center formation and lymphoproliferative disease. In Blood, 128, 660-6. doi:10.1182/blood-2015-11-684357. https://pubmed.ncbi.nlm.nih.gov/27166359/
9. Gregor, Anne, Meerbrei, Tanja, Gerstner, Thorsten, Sticht, Heinrich, Zweier, Christiane. . De novo missense variants in FBXO11 alter its protein expression and subcellular localization. In Human molecular genetics, 31, 440-454. doi:10.1093/hmg/ddab265. https://pubmed.ncbi.nlm.nih.gov/34505148/