Cdk5r2-flox 基因敲除小鼠

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产品名称

Cdk5r2-flox 基因敲除小鼠

产品编号

S-CKO-01676

品系全称

C57BL/6JCya-Cdk5r2em1flox/Cya

品系背景

C57BL/6JCya

品系编号

CKOCMP-12570-Cdk5r2-B6J-VA

品系状态

使用本品系发表的文献需注明: Cdk5r2-flox 基因敲除小鼠 mice (Strain S-CKO-01676) 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
cyclin dependent kinase 5, regulatory subunit 2
基因别称
B230310J22Rik,p39
染色体号
Chr 1 (Mouse)
转录本 ID
NCBI: NM_009872.3 | Ensembl: ENSMUST00000160379
修饰方式
条件性基因敲除
靶向范围
Exon 1
敲除长度
~1140 bp
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:1330828Homozygous mutation of this gene does not appear to result in a phenotype.
CDK5R2,也称为p39,是一种重要的细胞周期素依赖性激酶5(Cdk5)的调节蛋白。Cdk5是一种丝氨酸/苏氨酸激酶,它在多种生物学过程中发挥重要作用,包括神经元发育、突触可塑性、细胞迁移和细胞周期调控。Cdk5通常需要与调节蛋白结合才能被激活,而CDK5R2正是Cdk5的调节蛋白之一,它通过与其他蛋白质相互作用,参与调控Cdk5的活性。

CDK5R2在多种疾病中发挥重要作用。例如,在HIV感染相关的脑炎(HIVE)中,CDK5R2作为一种关键基因,与HIVE的发生发展密切相关[1]。此外,CDK5R2还与甲状腺髓样癌(MTC)的免疫特征相关,它在MTC中高表达,并与患者的预后不良相关[2]。在胰腺癌中,CDK5R2作为一种负相关基因,与淋巴节转移和患者生存期相关,它通过抑制β-连环蛋白通路,抑制胰腺癌细胞的迁移和侵袭[3]。

CDK5R2在神经系统中也发挥重要作用。例如,在甲状腺功能亢进症中,CDK5R2的表达水平降低,与学习和记忆功能障碍相关[4]。此外,CDK5R2的过表达与焦虑和抑郁行为相关,而CDK5R2基因敲除小鼠表现出较少的焦虑和抑郁行为[5]。

CDK5R2还与其他生物学过程相关。例如,在肝细胞癌(HCC)中,CDK5R2作为一种与自噬相关的基因,其表达水平与患者的预后相关[6]。在非小细胞肺癌(NSCLC)中,CDK5R2的过表达与肿瘤分级和分期相关,它可能作为一种潜在的肺癌分级和分期生物标志物[7]。此外,CDK5R2还与HCC中的肿瘤浸润免疫细胞相关,它可能通过调节CDK5R2和NK细胞,影响HCC的血管侵袭[8]。

综上所述,CDK5R2是一种重要的Cdk5调节蛋白,参与调控多种生物学过程,包括神经元发育、突触可塑性、细胞迁移和细胞周期调控。CDK5R2在多种疾病中发挥重要作用,包括HIVE、MTC、胰腺癌、HCC和NSCLC。此外,CDK5R2还与焦虑和抑郁行为相关,可能作为一种潜在的神经精神疾病治疗靶点。CDK5R2的研究有助于深入理解Cdk5的调控机制和生物学功能,为疾病的治疗和预防提供新的思路和策略。

参考文献:
1. Wang, Shitao, Ding, Xiangqian, Li, Zongyou, Zhang, Mengen, Xie, Zhenrong. 2023. Comprehensive analyses identify potential biomarkers for encephalitis in HIV infection. In Scientific reports, 13, 18418. doi:10.1038/s41598-023-45922-6. https://pubmed.ncbi.nlm.nih.gov/37891420/
2. Weng, Danfeng, He, Long, Chen, Xiangna, Ao, Lu, Wang, Shenglin. 2023. Integrated analysis of transcription factor-mRNA-miRNA regulatory network related to immune characteristics in medullary thyroid carcinoma. In Frontiers in immunology, 13, 1055412. doi:10.3389/fimmu.2022.1055412. https://pubmed.ncbi.nlm.nih.gov/36713370/
3. Qin, Cheng, Li, Tianhao, Wang, Yuanyang, Zhao, Yutong, Wang, Weibin. 2022. CHRNB2 represses pancreatic cancer migration and invasion via inhibiting β-catenin pathway. In Cancer cell international, 22, 340. doi:10.1186/s12935-022-02768-8. https://pubmed.ncbi.nlm.nih.gov/36344976/
4. Sahin, Leyla, Keloglan Müsüroglu, Seval, Selin Cevik, Ozge, Cevik, Kenan, Orekici Temel, Gulhan. 2022. Hyperthyroidism leads learning and memory impairment possibly via GRIN2B expression alterations. In Brain research, 1802, 148209. doi:10.1016/j.brainres.2022.148209. https://pubmed.ncbi.nlm.nih.gov/36563833/
5. Arif, Abul. 2012. Extraneuronal activities and regulatory mechanisms of the atypical cyclin-dependent kinase Cdk5. In Biochemical pharmacology, 84, 985-93. doi:10.1016/j.bcp.2012.06.027. https://pubmed.ncbi.nlm.nih.gov/22795893/
6. Liu, Bo, Li, Likun, Yang, Guang, Broom, Bradley, Thompson, Timothy C. 2019. PARP Inhibition Suppresses GR-MYCN-CDK5-RB1-E2F1 Signaling and Neuroendocrine Differentiation in Castration-Resistant Prostate Cancer. In Clinical cancer research : an official journal of the American Association for Cancer Research, 25, 6839-6851. doi:10.1158/1078-0432.CCR-19-0317. https://pubmed.ncbi.nlm.nih.gov/31439587/
7. Wu, Yingmin, Li, Lian, Wang, Long, Li, Haiyang, Chen, Tengxiang. 2024. m1A regulator-mediated methylation modification patterns correlated with autophagy to predict the prognosis of hepatocellular carcinoma. In BMC cancer, 24, 506. doi:10.1186/s12885-024-12235-4. https://pubmed.ncbi.nlm.nih.gov/38649860/
8. Pérez-Morales, Jaileene, Mejías-Morales, Darielys, Rivera-Rivera, Stephanie, Koomen, John M, Santiago-Cardona, Pedro G. 2018. Hyper-phosphorylation of Rb S249 together with CDK5R2/p39 overexpression are associated with impaired cell adhesion and epithelial-to-mesenchymal transition: Implications as a potential lung cancer grading and staging biomarker. In PloS one, 13, e0207483. doi:10.1371/journal.pone.0207483. https://pubmed.ncbi.nlm.nih.gov/30452490/