Pik3cg-flox 基因敲除小鼠

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产品名称

Pik3cg-flox 基因敲除小鼠

产品编号

S-CKO-10249

品系全称

C57BL/6NCya-Pik3cgem1flox/Cya

品系背景

C57BL/6NCya

品系编号

CKOCMP-30955-Pik3cg-B6N-VA

品系状态

使用本品系发表的文献需注明: Pik3cg-flox 基因敲除小鼠 mice (Strain S-CKO-10249) were purchased from Cyagen.
交付类型
周龄
性别
基因型
数量
cKO小鼠库模型
PI3K-Akt信号通路

基本信息

基因研究概述

质控标准

基因
基因全称
phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma
基因别称
5830428L06Rik,PI3Kgamma,p110gamma,p120-PI3K
染色体号
Chr 12 (Mouse)
转录本 ID
NCBI: NM_001146200 | Ensembl: ENSMUST00000053215
修饰方式
条件性基因敲除
靶向范围
Exon 3~4
敲除长度
~0.9 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:1353576Mice homozygous for disruptions in this gene display defects in thymocyte development, T cell activation, and neutrophil migration.
PIK3CG,即磷脂酰肌醇3激酶γ(Phosphoinositide 3-kinase gamma),是PI3K家族成员之一,属于一类重要的信号转导分子。PI3Kγ在多种生物学过程中发挥重要作用,包括细胞生长、分化和凋亡,以及免疫调节和炎症反应。PIK3CG基因的编码蛋白PI3Kγ主要在免疫细胞中表达,特别是巨噬细胞和T细胞。PI3Kγ的激活可以导致细胞内信号传导的级联反应,进而影响细胞的行为和功能。

PIK3CG基因的变异与多种疾病的发生和发展密切相关。例如,有研究表明,PIK3CG基因的某些单核苷酸多态性(SNPs)与注意力缺陷多动障碍(ADHD)的风险增加相关[1]。此外,PIK3CG基因的变异还与心脏衰竭的预后相关[2]。PI3Kγ在巨噬细胞中的作用研究表明,它是一种控制免疫抑制的分子开关,通过调节巨噬细胞的极化状态,影响炎症和癌症的发展[3]。此外,PI3Kγ的抑制可以保护心脏免受阿霉素诱导的毒性,并减少肿瘤生长[4]。在急性髓系白血病(AML)中,抑制PIK3CG/PI3KR5/p101信号通路可以抑制AML细胞的生长,并提高AML细胞对现有疗法的敏感性[5]。PI3Kδ/γ的抑制可以促进人CART细胞的表观遗传和代谢重编程,从而增强抗肿瘤细胞毒性[6]。此外,PIK3CG基因的变异还与自闭症[7]和原发性抗体缺乏症(PAD)[8]的发生相关。

PIK3CG基因的变异还与结直肠癌的免疫炎症表型相关[9]。此外,PIK3CG基因的变异还可能参与动脉粥样硬化和抑郁症之间的相互影响[10]。

综上所述,PIK3CG基因的变异与多种疾病的发生和发展密切相关,包括ADHD、心脏衰竭、炎症、癌症、自闭症和PAD等。PIK3CG基因的变异可能通过影响PI3Kγ的信号传导,进而影响细胞的行为和功能,从而参与疾病的发生和发展。因此,PIK3CG基因的研究有助于深入理解疾病的发病机制,为疾病的治疗和预防提供新的思路和策略。

参考文献:
1. Gu, Xue, Yuan, Fang-Fen, Huang, Xin, Lin, Jun, Wu, Jing. 2017. Association of PIK3CG gene polymorphisms with attention-deficit/hyperactivity disorder: A case-control study. In Progress in neuro-psychopharmacology & biological psychiatry, 81, 169-177. doi:10.1016/j.pnpbp.2017.10.020. https://pubmed.ncbi.nlm.nih.gov/29097255/
2. Hu, Dong, Xiao, Lei, Li, Shiyang. . A common variant in PIK3CG gene associated with the prognosis of heart failure. In Journal of cellular and molecular medicine, 28, e70069. doi:10.1111/jcmm.70069. https://pubmed.ncbi.nlm.nih.gov/39245801/
3. Kaneda, Megan M, Messer, Karen S, Ralainirina, Natacha, Cohen, Ezra E W, Varner, Judith A. 2016. PI3Kγ is a molecular switch that controls immune suppression. In Nature, 539, 437-442. doi:10.1038/nature19834. https://pubmed.ncbi.nlm.nih.gov/27642729/
4. Li, Mingchuan, Sala, Valentina, De Santis, Maria Chiara, Hirsch, Emilio, Ghigo, Alessandra. . Phosphoinositide 3-Kinase Gamma Inhibition Protects From Anthracycline Cardiotoxicity and Reduces Tumor Growth. In Circulation, 138, 696-711. doi:10.1161/CIRCULATIONAHA.117.030352. https://pubmed.ncbi.nlm.nih.gov/29348263/
5. Kelly, Lois M, Rutter, Justine C, Lin, Kevin H, Wood, Kris C, Puissant, Alexandre. 2024. Targeting a lineage-specific PI3Kɣ-Akt signaling module in acute myeloid leukemia using a heterobifunctional degrader molecule. In Nature cancer, 5, 1082-1101. doi:10.1038/s43018-024-00782-5. https://pubmed.ncbi.nlm.nih.gov/38816660/
6. Funk, Christopher Ronald, Wang, Shuhua, Chen, Kevin Z, Shanmugam, Mala, Waller, Edmund K. . PI3Kδ/γ inhibition promotes human CART cell epigenetic and metabolic reprogramming to enhance antitumor cytotoxicity. In Blood, 139, 523-537. doi:10.1182/blood.2021011597. https://pubmed.ncbi.nlm.nih.gov/35084470/
7. Serajee, F J, Nabi, R, Zhong, H, Mahbubul Huq, A H M. . Association of INPP1, PIK3CG, and TSC2 gene variants with autistic disorder: implications for phosphatidylinositol signalling in autism. In Journal of medical genetics, 40, e119. doi:. https://pubmed.ncbi.nlm.nih.gov/14627686/
8. Ramirez, Neftali J, Posadas-Cantera, Sara, Caballero-Oteyza, Andrés, Camacho-Ordonez, Nadezhda, Grimbacher, Bodo. 2021. There is no gene for CVID - novel monogenetic causes for primary antibody deficiency. In Current opinion in immunology, 72, 176-185. doi:10.1016/j.coi.2021.05.010. https://pubmed.ncbi.nlm.nih.gov/34153571/
9. Liu, Yong, Liang, Youcheng, Su, Yongjian, Zheng, Mingbin, Huang, Zunnan. 2023. Exploring the potential mechanisms of Yi-Yi-Fu-Zi-Bai-Jiang-San therapy on the immune-inflamed phenotype of colorectal cancer via combined network pharmacology and bioinformatics analyses. In Computers in biology and medicine, 166, 107432. doi:10.1016/j.compbiomed.2023.107432. https://pubmed.ncbi.nlm.nih.gov/37729701/
10. Huang, Peiying, Yan, Li, Li, Zhishang, Yu, Liyuan, Chen, Bojun. 2022. Potential shared gene signatures and molecular mechanisms between atherosclerosis and depression: Evidence from transcriptome data. In Computers in biology and medicine, 152, 106450. doi:10.1016/j.compbiomed.2022.106450. https://pubmed.ncbi.nlm.nih.gov/36565484/