Safb-flox 基因敲除小鼠

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产品名称

Safb-flox 基因敲除小鼠

产品编号

S-CKO-06795

品系全称

C57BL/6JCya-Safbem1flox/Cya

品系背景

C57BL/6JCya

品系编号

CKOCMP-224903-Safb-B6J-VA

品系状态

使用本品系发表的文献需注明: Safb-flox 基因敲除小鼠 mice (Strain S-CKO-06795) 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
scaffold attachment factor B
基因别称
3110021E02Rik,5330423C17Rik,E130307D12,HAP,HET,SAF-B1,SAFB1
染色体号
Chr 17 (Mouse)
转录本 ID
NCBI: NM_001374619 | Ensembl: ENSMUST00000182533
修饰方式
条件性基因敲除
靶向范围
Exon 2
敲除长度
~0.8 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:2146974Homozygous null mice display partial embryonic and neonatal lethality, neonatal cyanosis, impaired embryonic hematopoiesis, male sterility, azoospermia, reduced female fertility, impaired transport of embryos through the oviduct, reduced embryonic growth, testicular degeneration and ovarian atrophy.
SAFB,即支架附着因子B,是一种保守的RNA结合蛋白,在早期哺乳动物发育中起着关键作用。它通过结合RNA,参与调控基因表达、RNA加工和染色质修饰等多个生物学过程。SAFB与多种RNA相互作用,包括蛋白质编码基因的内含子、长链非编码RNA(lncRNA)和转座子RNA等,从而影响基因的转录、剪接和稳定性。SAFB还与染色质修饰复合物相互作用,参与调控染色质结构和基因表达。

SAFB在多种生物学过程中发挥重要作用,包括细胞分化和发育、DNA修复、细胞凋亡、细胞分裂和细胞迁移等。在神经干细胞(NSCs)中,SAFB通过结合Nfib mRNA并增强Drosha依赖性切割,阻止少突胶质细胞生成,促进神经元生成[4]。在急性髓细胞白血病(AML)中,SAFB与HOXA9形成抑制性染色质复合物,通过NuRD和HP1γ抑制分化相关基因的表达,维持AML的发生和发展[5]。此外,SAFB还与转座子RNA相互作用,抑制转座子的外显子化,保护基因组完整性[1,2]。SAFB在多种癌症中表达下调,与肿瘤的发生和发展密切相关[3,6]。

研究结果表明,SAFB是一种多功能的RNA结合蛋白,通过结合RNA和相互作用蛋白,参与调控基因表达、RNA加工和染色质修饰等多个生物学过程。SAFB在多种疾病中发挥重要作用,包括AML、神经干细胞分化异常和癌症等。SAFB的研究有助于深入理解RNA结合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. Ilık, İbrahim Avşar, Glažar, Petar, Tse, Kevin, Smith, Zachary D, Aktaş, Tuğçe. 2024. Autonomous transposons tune their sequences to ensure somatic suppression. In Nature, 626, 1116-1124. doi:10.1038/s41586-024-07081-0. https://pubmed.ncbi.nlm.nih.gov/38355802/
2. Hong, Yaqiang, Bie, Luyao, Zhang, Tao, Shen, Xiaohua, Liu, Nian. 2024. SAFB restricts contact domain boundaries associated with L1 chimeric transcription. In Molecular cell, 84, 1637-1650.e10. doi:10.1016/j.molcel.2024.03.021. https://pubmed.ncbi.nlm.nih.gov/38604171/
3. Jiao, Hong-Li, Ye, Ya-Ping, Yang, Run-Wei, Liao, Wen-Ting, Ding, Yan-Qing. 2017. Downregulation of SAFB Sustains the NF-κB Pathway by Targeting TAK1 during the Progression of Colorectal Cancer. In Clinical cancer research : an official journal of the American Association for Cancer Research, 23, 7108-7118. doi:10.1158/1078-0432.CCR-17-0747. https://pubmed.ncbi.nlm.nih.gov/28912140/
4. Forcella, Pascal, Ifflander, Niklas, Rolando, Chiara, Bock, Thomas, Taylor, Verdon. 2024. SAFB regulates hippocampal stem cell fate by targeting Drosha to destabilize Nfib mRNA. In eLife, 13, . doi:10.7554/eLife.74940. https://pubmed.ncbi.nlm.nih.gov/38722021/
5. Agrawal-Singh, Shuchi, Bagri, Jaana, Giotopoulos, George, Whetton, Anthony D, Huntly, Brian J P. . HOXA9 forms a repressive complex with nuclear matrix-associated protein SAFB to maintain acute myeloid leukemia. In Blood, 141, 1737-1754. doi:10.1182/blood.2022016528. https://pubmed.ncbi.nlm.nih.gov/36577137/
6. Yuan, Qihang, Ren, Jie, Wang, Zhizhou, Deng, Dawei, Shang, Dong. 2021. Identification of the Real Hub Gene and Construction of a Novel Prognostic Signature for Pancreatic Adenocarcinoma Based on the Weighted Gene Co-expression Network Analysis and Least Absolute Shrinkage and Selection Operator Algorithms. In Frontiers in genetics, 12, 692953. doi:10.3389/fgene.2021.692953. https://pubmed.ncbi.nlm.nih.gov/34490033/