Eif3c-KO Mouse
一般名
Eif3c-KO
製品ID
S-KO-10778
背景情報
C57BL/6NCya
系統ID
KOCMP-56347-Eif3c-B6N-VA
状況
このマウス系統を論文で使用する場合は、「Eif3c-KO Mouse（カタログ番号S-KO-10778）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
Eif3c-KO
系統ID
KOCMP-56347-Eif3c-B6N-VA
遺伝子名
製品ID
S-KO-10778
遺伝子別名
110kDa, 3230401O13Rik, Eif3s8, NIPIL(A3), NipilA3, Xs, Xsl
遺伝子別名
C57BL/6NCya
遺伝子正式名称
eukaryotic translation initiation factor 3, subunit C
NCBI ID
修正
Conventional knockout
染色体
Chr 7
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
ENSMUST00000032992
NCBIトランスクリプトID
NM_146200
ターゲット領域
Exon 3~15
有効領域の大きさ
~8.5 kb
遺伝子研究の概要
Eif3c, short for eukaryotic translation initiation factor 3 subunit C, is a component of the protein translation initiation factor EIF3. It is crucial for the initiation of protein translation, a fundamental process in cells. Dysregulation of Eif3c can impact various biological pathways related to cell growth, proliferation, and apoptosis, making it of great biological importance. Genetic models, such as gene knockout (KO) and conditional knockout (CKO) mouse models, are valuable tools for studying Eif3c's functions [1-10].
In multiple cancer types, Eif3c has been found to play significant roles. In ovarian cancer, the m6A reader YTHDF1 augments Eif3c translation in an m6A-dependent manner, promoting tumorigenesis and metastasis [1]. In lung cancer, Eif3c is overexpressed, and its silencing suppresses cell proliferation and promotes apoptosis, possibly by regulating the APP/HSPA1A/LMNB1 axis [2]. In intrahepatic cholangiocarcinoma, elevated Eif3c expression promotes cancer development, and its combination with KI67 is a valuable predictor of survival and recurrence [3]. Similar findings exist in nasopharyngeal carcinoma, pancreatic cancer, prostate cancer, and renal cell carcinoma, where knockdown of Eif3c inhibits cell proliferation, promotes apoptosis, and suppresses tumor growth [4,5,9,10]. In hepatocellular carcinoma, Eif3C-enhanced exosome secretion promotes angiogenesis and tumorigenesis [8]. In rheumatoid arthritis, Complement factor H upregulates Eif3C to attenuate TNF-α-induced inflammation [6]. In prostate cancer, circPDE5A blocks the WTAP-dependent m6A methylation of Eif3C mRNA, disrupting its translation and restraining cancer progression [7].
In conclusion, Eif3c is essential for protein translation initiation. Model-based research, especially KO/CKO mouse models, has revealed its critical roles in cancer development, progression, and in the context of rheumatoid arthritis. Understanding Eif3c's functions provides potential therapeutic targets for these diseases.
References:
1. Liu, Tao, Wei, Qinglv, Jin, Jing, Zou, Dongling, Yi, Ping. . The m6A reader YTHDF1 promotes ovarian cancer progression via augmenting EIF3C translation. In Nucleic acids research, 48, 3816-3831. doi:10.1093/nar/gkaa048. https://pubmed.ncbi.nlm.nih.gov/31996915/
2. Ding, Xiaoli, Hou, Lanlan, Zhang, Huijuan, Tang, Zhixian, Hu, Rong. 2022. EIF3C Promotes Lung Cancer Tumorigenesis by Regulating the APP/HSPA1A/LMNB1 Axis. In Disease markers, 2022, 9464094. doi:10.1155/2022/9464094. https://pubmed.ncbi.nlm.nih.gov/36157221/
3. Xu, Ya-Ping, Dong, Ze-Ning, Zhou, Ying-Qun, Huang, Xiao-Yong, Guo, Chuan-Yong. 2021. Role of eIF3C Overexpression in Predicting Prognosis of Intrahepatic Cholangiocarcinoma. In Digestive diseases and sciences, 67, 559-568. doi:10.1007/s10620-021-06878-7. https://pubmed.ncbi.nlm.nih.gov/33576946/
4. Zhao, Qian, Luo, Xuehui, Li, Honghui, Xu, Chongwen, Han, Suxia. 2022. Targeting EIF3C to suppress the development and progression of nasopharyngeal carcinoma. In Frontiers in bioengineering and biotechnology, 10, 994628. doi:10.3389/fbioe.2022.994628. https://pubmed.ncbi.nlm.nih.gov/36147539/
5. Jiao, Heng, Zeng, Lingxiao, Yang, Shengsheng, Zhang, Jianpeng, Lou, Wenhui. 2020. Knockdown EIF3C Suppresses Cell Proliferation and Increases Apoptosis in Pancreatic Cancer Cell. In Dose-response : a publication of International Hormesis Society, 18, 1559325820950061. doi:10.1177/1559325820950061. https://pubmed.ncbi.nlm.nih.gov/32973416/
6. Jia, Yimeng, Feng, Bin, Ji, Xin, Fei, Yunyun, Wu, Xunyao. 2023. Complement factor H attenuates TNF-α-induced inflammation by upregulating EIF3C in rheumatoid arthritis. In Journal of translational medicine, 21, 846. doi:10.1186/s12967-023-04730-2. https://pubmed.ncbi.nlm.nih.gov/37996918/
7. Ding, Lifeng, Wang, Ruyue, Zheng, Qiming, Cheng, Sheng, Li, Gonghui. 2022. circPDE5A regulates prostate cancer metastasis via controlling WTAP-dependent N6-methyladenisine methylation of EIF3C mRNA. In Journal of experimental & clinical cancer research : CR, 41, 187. doi:10.1186/s13046-022-02391-5. https://pubmed.ncbi.nlm.nih.gov/35650605/
8. Lee, Hsin-Yi, Chen, Chi-Kuan, Ho, Chun-Ming, Chen, Kuan-Ju, Jou, Yuh-Shan. 2018. EIF3C-enhanced exosome secretion promotes angiogenesis and tumorigenesis of human hepatocellular carcinoma. In Oncotarget, 9, 13193-13205. doi:10.18632/oncotarget.24149. https://pubmed.ncbi.nlm.nih.gov/29568350/
9. Hu, Jianxin, Luo, Heng, Xu, Yuangao, Sun, Zhaolin, Kuang, Youlin. 2019. The Prognostic Significance of EIF3C Gene during the Tumorigenesis of Prostate Cancer. In Cancer investigation, 37, 199-208. doi:10.1080/07357907.2019.1618322. https://pubmed.ncbi.nlm.nih.gov/31181967/
10. Fan, Min, Wang, Kai, Wei, Xiaohui, Chen, Zhen, He, Xiaozhou. 2019. Upregulated expression of eIF3C is associated with malignant behavior in renal cell carcinoma. In International journal of oncology, 55, 1385-1395. doi:10.3892/ijo.2019.4903. https://pubmed.ncbi.nlm.nih.gov/31638200/
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凍結後の精子では、各バッチから1本の凍結保存された精子を選び出し、体外受精に使用します。
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