Csnk1g3-KO Mouse
一般名
Csnk1g3-KO
製品ID
S-KO-13337
背景情報
C57BL/6JCya
系統ID
KOCMP-70425-Csnk1g3-B6J-VA
状況
このマウス系統を論文で使用する場合は、「Csnk1g3-KO Mouse(カタログ番号S-KO-13337)はサイアジェンから購入しました。」と引用してください。
製品タイプ
年齢
遺伝子型
性別
数量
標準的な配送方法では、少なくとも3匹のヘテロ接合体キャリアを保証しています。ホモ接合体キャリアや指定された性別の個体の繁殖サービスも利用可能です。
基本情報
系統名
Csnk1g3-KO
系統ID
KOCMP-70425-Csnk1g3-B6J-VA
遺伝子名
製品ID
S-KO-13337
遺伝子別名
3300002K07Rik, C330049O21Rik
遺伝子別名
C57BL/6JCya
NCBI ID
修正
Conventional knockout
染色体
Chr 18
表現型
アプリケーション
--
さらに
系統詳細
EnsemblトランスクリプトID
ENSMUST00000069597
NCBIトランスクリプトID
NM_152809
ターゲット領域
Exon 5~10
有効領域の大きさ
~16.6 kb
遺伝子研究の概要
Csnk1g3, a member of the casein kinase 1γ subfamily, is involved in phosphorylation processes [10]. It likely participates in various cellular signaling pathways, though the exact pathways are not comprehensively detailed across the references. Understanding its function is crucial as it may be associated with multiple biological processes and diseases [1,3,4,5,6,7,10]. Genetic models, such as gene knockout in cultured HeLa cells, can be valuable for studying Csnk1g3 [2].
In colon cancers, there is intratumoral heterogeneity of CSNK1G3 mutations, suggesting its possible role in tumor development [1]. In triple-negative breast cancer, the curcumin derivative N17 exerts anti-cancer effects through the CSNK1G3/AKT axis, indicating CSNK1G3 is a key regulator in this cancer type [3]. In epileptic mice, the circRNA-Csnk1g3/Csnk1g3-85aa/CK1γ3/TNF-α signal pathway involving Csnk1g3 is associated with necroptosis and inflammation of hippocampal neurons, and Jiawei Chaihu Shugan decoction may act through regulating this pathway [7]. Also, CSNK1G3 was identified among genes with selection signals in Taiwanese Han people, potentially related to disease susceptibility and metabolic-related traits [4]. In geese, it was among genes potentially regulating feather color [5]. In C57BL/6 black mice, its gene expression was significantly low in lesional skin during autoimmune-induced depigmentation [6]. siRNAs targeting CSNK1G3 negatively regulate translation readthrough [8], and in cancer cells, siRNAs targeting CSNK1G3 enhanced an Akt inhibitor-mediated cell killing [9]. Additionally, gene variants of CSNK1G3 are associated with migraine susceptibility [10].
In summary, Csnk1g3 is involved in diverse biological processes and disease conditions. Studies using different models, including cell-based gene knockout and in vivo mouse models, have revealed its role in cancer, epilepsy, pigmentation-related processes, translation regulation, and migraine. These findings contribute to understanding the molecular mechanisms underlying these diseases and potentially offer new therapeutic targets.
References:
1. Son, Hyun Ji, Choi, Eun Ji, Yoo, Nam Jin, Lee, Sug Hyung. 2020. Intratumoral heterogeneity of CSNK1G3 mutations, a casein kinase 1, in colon cancers. In Pathology, research and practice, 216, 152936. doi:10.1016/j.prp.2020.152936. https://pubmed.ncbi.nlm.nih.gov/32241596/
2. Goto, Asako, Hanada, Kentaro. 2023. Protocol for casein kinase 1γ3 CSNK1G3 gene knockout and recombinant gene expression in cultured HeLa cells. In STAR protocols, 4, 102251. doi:10.1016/j.xpro.2023.102251. https://pubmed.ncbi.nlm.nih.gov/37119140/
3. Huai, Ziyou, Li, Zijian, Xue, Wei, Wei, Qinjun, Wang, Yuanyuan. 2024. Novel curcumin derivatives N17 exert anti-cancer effects through the CSNK1G3/AKT axis in triple-negative breast cancer. In Biochemical pharmacology, 229, 116472. doi:10.1016/j.bcp.2024.116472. https://pubmed.ncbi.nlm.nih.gov/39127154/
4. Lo, Yun-Hua, Cheng, Hsueh-Chien, Hsiung, Chia-Ni, Shen, Chen-Yang, Ko, Wen-Ya. . Detecting Genetic Ancestry and Adaptation in the Taiwanese Han People. In Molecular biology and evolution, 38, 4149-4165. doi:10.1093/molbev/msaa276. https://pubmed.ncbi.nlm.nih.gov/33170928/
5. Ren, Shuang, Lyu, Guangqi, Irwin, David M, Zhang, Shuyi, Wang, Zhe. 2021. Pooled Sequencing Analysis of Geese (Anser cygnoides) Reveals Genomic Variations Associated With Feather Color. In Frontiers in genetics, 12, 650013. doi:10.3389/fgene.2021.650013. https://pubmed.ncbi.nlm.nih.gov/34220935/
6. Al Robaee, Ahmad A, Alzolibani, Abdullateef A, Rasheed, Zafar. 2020. Autoimmune response against tyrosinase induces depigmentation in C57BL/6 black mice. In Autoimmunity, 53, 459-466. doi:10.1080/08916934.2020.1836489. https://pubmed.ncbi.nlm.nih.gov/33084421/
7. Wang, Qin, Qin, Baijun, Yu, Han, Zhou, Yanying, Diao, Limei. 2025. Mitigating effects of Jiawei Chaihu Shugan decoction on necroptosis and inflammation of hippocampal neurons in epileptic mice. In Scientific reports, 15, 4649. doi:10.1038/s41598-025-89275-8. https://pubmed.ncbi.nlm.nih.gov/39920301/
8. Chowdhury, H M, Siddiqui, M A, Kanneganti, S, Chowdhury, M W, Nasim, M Talat. . Aminoglycoside-mediated promotion of translation readthrough occurs through a non-stochastic mechanism that competes with translation termination. In Human molecular genetics, 27, 373-384. doi:10.1093/hmg/ddx409. https://pubmed.ncbi.nlm.nih.gov/29177465/
9. Morgan-Lappe, S, Woods, K W, Li, Q, Fesik, S W, Leverson, J D. . RNAi-based screening of the human kinome identifies Akt-cooperating kinases: a new approach to designing efficacious multitargeted kinase inhibitors. In Oncogene, 25, 1340-8. doi:. https://pubmed.ncbi.nlm.nih.gov/16247451/
10. Stuart, Shani, Benton, Miles C, Eccles, David A, Lea, Rodney A, Griffiths, Lyn R. 2017. Gene-centric analysis implicates nuclear encoded mitochondrial protein gene variants in migraine susceptibility. In Molecular genetics & genomic medicine, 5, 157-163. doi:10.1002/mgg3.270. https://pubmed.ncbi.nlm.nih.gov/28361102/
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