Cks1b-KO 基因敲除小鼠

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产品名称

Cks1b-KO 基因敲除小鼠

产品编号

S-KO-16655

品系全称

C57BL/6JCya-Cks1bem1/Cya

品系背景

C57BL/6JCya

品系编号

KOCMP-54124-Cks1b-B6J-VA

品系状态

使用本品系发表的文献需注明: Cks1b-KO 基因敲除小鼠 mice (Strain S-KO-16655) 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
CDC28 protein kinase 1b
基因别称
2410005G18Rik,2610005D03Rik,Cks1,sid1334
染色体号
Chr 3 (Mouse)
转录本 ID
NCBI: NM_016904 | Ensembl: ENSMUST00000029679
修饰方式
全身性基因敲除
靶向范围
Exon 2~3
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:1889208Embryos homozygous for a knock-out allele exhibit a reduced body size that persists through adulthood while heterozygous mice are intermediate in size. Mutant mouse embryonic fibroblasts (MEFs) proliferate poorly and senesce earlier than wild-type MEFs.
CKS1B,也称为细胞周期蛋白依赖性激酶调节亚基1B,是细胞周期蛋白激酶家族的一个成员,在细胞周期的调控中发挥着重要作用。CKS1B与细胞周期蛋白依赖性激酶(CDKs)结合,促进CDKs的活性,进而影响细胞周期进程。CKS1B的异常表达与多种人类癌症的发生发展密切相关,并且在药物耐药性方面也发挥着重要作用。

多篇研究表明,CKS1B在多种人类癌症中表达上调,包括多发性骨髓瘤、胰腺癌和肝细胞癌等。在多发性骨髓瘤中,CKS1B基因扩增与患者的不良预后相关,如患者在接受自体造血干细胞移植后的无进展生存期和总生存期均较短[1]。此外,CKS1B基因扩增还与多发性骨髓瘤患者细胞遗传学异常有关,如13号染色体缺失等[2]。在胰腺癌中,CKS1B的表达水平与患者的预后相关,高表达的CKS1B预示着较差的生存期[3]。CKS1B的表达还与肿瘤微环境和免疫浸润相关,可能为胰腺癌的免疫治疗提供新的靶点[3]。在肝细胞癌中,CKS1B通过激活JAK/STAT3信号通路,促进肿瘤细胞的增殖和转移[4]。

CKS1B的异常表达还与细胞周期的调控密切相关。CKS1B的过表达可以导致细胞周期蛋白依赖性激酶的活性增加,进而导致细胞周期的异常进展。例如,在多发性骨髓瘤中,CKS1B的过表达可以促进细胞周期的进程,导致细胞增殖和生存的增加[8]。此外,CKS1B还与SKP2和p27Kip1的相互作用有关,影响细胞周期的进程。CKS1B可以通过与SKP2结合,促进p27Kip1的降解,进而导致细胞周期的异常进展[8]。

CKS1B的异常表达还与肿瘤免疫治疗相关。研究表明,CKS1B的表达水平与肿瘤的免疫原性和免疫细胞浸润程度相关。例如,在肺腺癌中,CKS1B的表达水平与肿瘤的免疫原性和免疫细胞浸润程度相关,可以作为免疫治疗的预测因子[7]。此外,CKS1B的表达水平还与肿瘤细胞的干性相关,可以作为免疫治疗的潜在靶点[7]。

综上所述,CKS1B是一种重要的细胞周期蛋白依赖性激酶调节亚基,在多种人类癌症中发挥着重要作用。CKS1B的异常表达与肿瘤的发生发展、细胞周期的调控和肿瘤免疫治疗相关。因此,CKS1B可能成为癌症治疗的新靶点,为癌症的治疗提供新的思路和策略。

参考文献:
1. Shi, Wenwen, Huang, Qiudi, Xie, Jiacui, Yu, Xiyong, Zhou, Yi. 2020. CKS1B as Drug Resistance-Inducing Gene-A Potential Target to Improve Cancer Therapy. In Frontiers in oncology, 10, 582451. doi:10.3389/fonc.2020.582451. https://pubmed.ncbi.nlm.nih.gov/33102238/
2. Bock, Fabian, Lu, Gary, Srour, Samer A, Champlin, Richard E, Qazilbash, Muzaffar H. 2016. Outcome of Patients with Multiple Myeloma and CKS1B Gene Amplification after Autologous Hematopoietic Stem Cell Transplantation. In Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation, 22, 2159-2164. doi:10.1016/j.bbmt.2016.09.003. https://pubmed.ncbi.nlm.nih.gov/27638366/
3. Li, Lincheng, Wang, Jing, Zhang, Zhuochao, Li, Chonghui, Liu, Rong. 2022. Identification of CKS1B as a prognostic indicator and a predictive marker for immunotherapy in pancreatic cancer. In Frontiers in immunology, 13, 1052768. doi:10.3389/fimmu.2022.1052768. https://pubmed.ncbi.nlm.nih.gov/36405738/
4. Liu, Xitao, Zhao, Defang. 2021. CKS1B promotes the progression of hepatocellular carcinoma by activating JAK/STAT3 signal pathway. In Animal cells and systems, 25, 227-234. doi:10.1080/19768354.2021.1953142. https://pubmed.ncbi.nlm.nih.gov/34408811/
5. Stella, Flavia, Pedrazzini, Estela, Baialardo, Edgardo, Schutz, Natalia, Slavutsky, Irma. 2014. Quantitative analysis of CKS1B mRNA expression and copy number gain in patients with plasma cell disorders. In Blood cells, molecules & diseases, 53, 110-7. doi:10.1016/j.bcmd.2014.05.006. https://pubmed.ncbi.nlm.nih.gov/24973170/
6. Tang, Yuzhu, Lan, Xiaohua, Yan, Maohui, Fu, Zhiguang, Li, Hongqi. . CKS1B as a potential target for prognostic assessment and intervention in pancreatic cancer and its role in abnormal proliferation and cellular phenotype through mediation of cell cycle signaling pathways. In Saudi medical journal, 45, 128-138. doi:10.15537/smj.2024.45.2.20230132. https://pubmed.ncbi.nlm.nih.gov/38309745/
7. Ye, Bicheng, Hongting, Ge, Zhuang, Wen, Jiang, Aimin, Zhong, Yating. . Deciphering lung adenocarcinoma prognosis and immunotherapy response through an AI-driven stemness-related gene signature. In Journal of cellular and molecular medicine, 28, e18564. doi:10.1111/jcmm.18564. https://pubmed.ncbi.nlm.nih.gov/39046884/
8. Zhan, Fenghuang, Colla, Simona, Wu, Xiaosong, Barlogie, Bart, Shaughnessy, John D. 2007. CKS1B, overexpressed in aggressive disease, regulates multiple myeloma growth and survival through SKP2- and p27Kip1-dependent and -independent mechanisms. In Blood, 109, 4995-5001. doi:. https://pubmed.ncbi.nlm.nih.gov/17303695/
9. Chang, Hong, Qi, Xiaoying, Trieu, Young, Ning, Yi, Reece, Donna. 2006. Multiple myeloma patients with CKS1B gene amplification have a shorter progression-free survival post-autologous stem cell transplantation. In British journal of haematology, 135, 486-91. doi:. https://pubmed.ncbi.nlm.nih.gov/16995883/
10. Zhang, Lianmin, Cui, Yanan, Mei, Jie, Zhang, Zhenfa, Zhang, Pengpeng. 2024. Exploring cellular diversity in lung adenocarcinoma epithelium: Advancing prognostic methods and immunotherapeutic strategies. In Cell proliferation, 57, e13703. doi:10.1111/cpr.13703. https://pubmed.ncbi.nlm.nih.gov/38946232/