Ranbp9-KO 基因敲除小鼠

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产品名称

Ranbp9-KO 基因敲除小鼠

产品编号

S-KO-17028

品系全称

C57BL/6JCya-Ranbp9em1/Cya

品系背景

C57BL/6JCya

品系编号

KOCMP-56705-Ranbp9-B6J-VA

品系状态

使用本品系发表的文献需注明: Ranbp9-KO 基因敲除小鼠 mice (Strain S-KO-17028) were purchased from Cyagen.
交付类型
周龄
性别
基因型
数量

基本信息

基因研究概述

质控标准

基因
基因全称
RAN binding protein 9
基因别称
IBAP-1,Ibap1,RanBPM
染色体号
Chr 13 (Mouse)
转录本 ID
NCBI: NM_019930 | Ensembl: ENSMUST00000144326
修饰方式
全身性基因敲除
靶向范围
Exon 3
敲除长度
~0.7 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:1928741Mice homozygous for a null mutation display partial neonatal lethality. Survivors display infertility with impaired spermatogenesis and oogenesis, azoospermia and premature ovarian failure.
Ranbp9,也称为Ran结合蛋白9,是一种重要的细胞骨架蛋白,参与细胞信号转导和细胞周期调控等多种生物学过程。Ranbp9基因编码的蛋白质与Ran GTPase相互作用,参与核质转运和细胞骨架的动态调控。此外,Ranbp9还与多种细胞表面受体和细胞内靶标结合,参与细胞增殖、分化和迁移等过程。

在多种肿瘤中,Ranbp9的表达水平发生改变,并与肿瘤的发生发展和预后相关。例如,在乳腺癌中,Ranbp9的表达水平升高,与患者的预后不良相关[1]。此外,Ranbp9还参与调节细胞周期进程,并与肿瘤免疫浸润相关。在喉癌中,circ-RANBP9的表达水平降低,与患者的预后良好相关[2]。circ-RANBP9抑制喉癌细胞的增殖、迁移和侵袭能力,并在上皮间质转化过程中发挥抑制作用。在骨肉瘤中,RanBP9在组织和细胞中呈阳性表达,主要分布在细胞质和细胞核中[3]。RanBP9的过表达促进Aβ生成,导致神经退行性变和细胞凋亡[4]。RanBP9基因敲除小鼠表现出脑发育缺陷,包括皮质板变小、侧脑室扩大和海马体积减少[5]。RanBP9通过RanBP9-cofilin通路促进Aβ诱导的细胞凋亡和神经退行性变[6]。RANBP9基因多态性与精神分裂症的发生风险相关[7]。CLOCK蛋白与RANBP9相互作用,参与精子发生过程中的选择性剪接[8]。RanBP9在视网膜发育中发挥重要作用,与Mind bomb蛋白相互作用,影响视网膜细胞的增殖和分化[9]。RanBP9的过表达加速了阿尔茨海默病模型小鼠脑中突触蛋白的丢失[10]。

综上所述,RanBP9在多种生物学过程中发挥重要作用,包括细胞信号转导、细胞周期调控、肿瘤发生发展和神经退行性变等。RanBP9的表达水平改变与多种疾病的预后相关,并可能作为疾病诊断和治疗的新靶点。

参考文献:
1. Meng, Yiling, Ying, Yingxia, Zhang, Meichao, Yao, Yuan, Li, Dong. 2021. A comprehensive bioinformatic analysis of RanBP9 expression and its relation to prognosis in human breast cancer. In Epigenomics, 14, 27-42. doi:10.2217/epi-2021-0464. https://pubmed.ncbi.nlm.nih.gov/34875851/
2. Wang, Zheng, Gu, Jia, Yan, Aihui, Li, Kai. . Downregulation of circ-RANBP9 in laryngeal cancer and its clinical significance. In Annals of translational medicine, 9, 484. doi:10.21037/atm-21-567. https://pubmed.ncbi.nlm.nih.gov/33850881/
3. Zhu, L L, Wang, C H, Yang, H P, Shu, W H. . Expression of cartilage antitumor component RanBP9 in osteosarcoma. In Journal of biological regulators and homeostatic agents, 30, 103-10. doi:. https://pubmed.ncbi.nlm.nih.gov/27049080/
4. Domingues, Sara C, Konietzko, Uwe, Henriques, Ana Gabriela, da Cruz E Silva, Edgar F, da Cruz E Silva, Odete A B. . RanBP9 modulates AICD localization and transcriptional activity via direct interaction with Tip60. In Journal of Alzheimer's disease : JAD, 42, 1415-33. doi:10.3233/JAD-132495. https://pubmed.ncbi.nlm.nih.gov/25024339/
5. Palavicini, Juan Pablo, Lloyd, Brandon Noel, Hayes, Crystal D, Dawson-Scully, Ken, Lakshmana, Madepalli K. 2013. RanBP9 Plays a Critical Role in Neonatal Brain Development in Mice. In PloS one, 8, e66908. doi:10.1371/journal.pone.0066908. https://pubmed.ncbi.nlm.nih.gov/23840553/
6. Woo, J A, Jung, A R, Lakshmana, M K, Mook-Jung, I, Kang, D E. 2012. Pivotal role of the RanBP9-cofilin pathway in Aβ-induced apoptosis and neurodegeneration. In Cell death and differentiation, 19, 1413-23. doi:10.1038/cdd.2012.14. https://pubmed.ncbi.nlm.nih.gov/22361682/
7. Bae, Joon Seol, Kim, Jason Yongha, Park, Byung-Lae, Shin, Hyoung Doo, Woo, Sung-Il. 2014. Investigating the potential genetic association between RANBP9 polymorphisms and the risk of schizophrenia. In Molecular medicine reports, 11, 2975-80. doi:10.3892/mmr.2014.3045. https://pubmed.ncbi.nlm.nih.gov/25482375/
8. Yang, Junbao, Zhang, Zhiwei, Zhang, Yingying, Liu, Yunqiang, Ma, Yongxin. 2017. CLOCK interacts with RANBP9 and is involved in alternative splicing in spermatogenesis. In Gene, 642, 199-204. doi:10.1016/j.gene.2017.11.007. https://pubmed.ncbi.nlm.nih.gov/29126923/
9. Yoo, Kyeong-Won, Thiruvarangan, Maivannan, Jeong, Yun-Mi, Kim, Hyung-Goo, Kim, Cheol-Hee. 2017. Mind Bomb-Binding Partner RanBP9 Plays a Contributory Role in Retinal Development. In Molecules and cells, 40, 271-279. doi:10.14348/molcells.2017.2308. https://pubmed.ncbi.nlm.nih.gov/28359144/
10. Wang, Hongjie, Wang, Ruizhi, Xu, Shaohua, Lakshmana, Madepalli K. 2014. RanBP9 overexpression accelerates loss of pre and postsynaptic proteins in the APΔE9 transgenic mouse brain. In PloS one, 9, e85484. doi:10.1371/journal.pone.0085484. https://pubmed.ncbi.nlm.nih.gov/24454876/