Gnai3-flox Mouse
一般名
Gnai3-flox
製品ID
S-CKO-02675
背景情報
C57BL/6JCya
系統ID
CKOCMP-14679-Gnai3-B6J-VA
状況
このマウス系統を論文で使用する場合は、「Gnai3-flox Mouse（カタログ番号S-CKO-02675）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
Gnai3-flox
系統ID
CKOCMP-14679-Gnai3-B6J-VA
遺伝子名
製品ID
S-CKO-02675
遺伝子別名
Hg1a, Gnai-3, Galphai3
遺伝子別名
C57BL/6JCya
NCBI ID
修正
Conditional knockout
染色体
Chr 3
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
ENSMUST00000000001
NCBIトランスクリプトID
NM_010306
ターゲット領域
Exon 2~3
有効領域の大きさ
~1.9 kb
遺伝子研究の概要
Gnai3, also known as Guanine nucleotide binding protein, alpha inhibiting activity polypeptide 3, is involved in multiple biological processes. It plays roles in signal transduction pathways, such as those related to G-protein coupled receptors. Inhibitory G proteins like Gnai3 are crucial in regulating various cellular functions, including cell growth, differentiation, and inflammation [5,6,7,8,9]. Genetic models, like the Gnai3-iresGFP reporter mouse line, are valuable tools for studying Gnai3 expression patterns [3].
In a mouse model, GNAI1 and GNAI3 double-knockout (DKO) mice showed more severe colitis and significantly more colonic tumors compared to control mice. This indicates that GNAI3 suppresses DSS-plus-AOM-induced colon tumor development, possibly by blocking IL6 signaling and down-regulating GNAI2 expression [2]. In hepatocellular carcinoma (HCC), down-regulation of GNAI3 by miR-222 promoted cell migration and invasion, and low GNAI3 expression predicted poor prognosis in HCC patients [4,8]. In non-alcoholic fatty liver disease (NAFLD) mouse and cell models, GNAI3 knockout enhanced dysregulated hepatic lipid metabolism and liver damage, suggesting GNAI3 is a potential target for NAFLD treatment [6]. In periodontal stem cells, GNAI3, mediated by Lin28A, regulated lipopolysaccharide-induced inflammation and osteogenic differentiation via the NF-κB/NLRP3 inflammasome pathway [1]. Also, in osteoblast precursor cells, Gnai3 regulated cell proliferation, migration, osteogenic differentiation, and mineralization through the MAPK signaling pathway, and its mutation was related to congenital small jaw deformity [9].
In conclusion, Gnai3 is essential in regulating multiple biological processes. Model-based research, especially gene knockout mouse models, has revealed its significant roles in various disease areas, including colon cancer, HCC, NAFLD, periodontitis, and congenital mandibular defects. These findings provide potential therapeutic targets and a better understanding of the underlying disease mechanisms related to Gnai3.
References：
1. Guo, Ling, Sun, Hua, Pu, Jiao. 2024. GNAI3 mediated by Lin28A regulates lipopolysaccharide-induced inflammation and osteogenic differentiation in periodontal stem cells by mediating the NF-κB/NLRP3 inflammasome pathway. In Archives of oral biology, 163, 105974. doi:10.1016/j.archoralbio.2024.105974. https://pubmed.ncbi.nlm.nih.gov/38636252/
2. Li, Zhi-Wei, Sun, Beicheng, Gong, Ting, Zhou, Xiqiao, Chu, Wen-Ming. 2019. GNAI1 and GNAI3 Reduce Colitis-Associated Tumorigenesis in Mice by Blocking IL6 Signaling and Down-regulating Expression of GNAI2. In Gastroenterology, 156, 2297-2312. doi:10.1053/j.gastro.2019.02.040. https://pubmed.ncbi.nlm.nih.gov/30836096/
3. Leiss, Veronika, Reisinger, Ellen, Speidel, Annika, Beer-Hammer, Sandra, Nürnberg, Bernd. 2021. Analyses of Gnai3-iresGFP reporter mice reveal unknown Gαi3 expression sites. In Scientific reports, 11, 14271. doi:10.1038/s41598-021-93591-0. https://pubmed.ncbi.nlm.nih.gov/34253772/
4. Zhang, Yu, Yao, Jian, Huan, Lin, Liang, Linhui, He, Xianghuo. 2014. GNAI3 inhibits tumor cell migration and invasion and is post-transcriptionally regulated by miR-222 in hepatocellular carcinoma. In Cancer letters, 356, 978-84. doi:10.1016/j.canlet.2014.11.013. https://pubmed.ncbi.nlm.nih.gov/25444921/
5. Mishra, Chinmoy, Mohapatra, Swagat. . An integrative bioinformatics analysis of caprine GNAI3 gene. In Journal of genetics, 99, . doi:. https://pubmed.ncbi.nlm.nih.gov/32366735/
6. Zhu, Hanzhang, Ge, Ke, Lu, Jun, Jia, Changku. . Downregulation of GNAI3 Promotes the Pathogenesis of Methionine/Choline-Deficient Diet-Induced Nonalcoholic Fatty Liver Disease. In Gut and liver, 14, 492-499. doi:10.5009/gnl19115. https://pubmed.ncbi.nlm.nih.gov/31694365/
7. Young, Alejandra, Dandekar, Uma, Pan, Calvin, Lewis, Richard A, Farber, Debora B. 2016. GNAI3: Another Candidate Gene to Screen in Persons with Ocular Albinism. In PloS one, 11, e0162273. doi:10.1371/journal.pone.0162273. https://pubmed.ncbi.nlm.nih.gov/27607449/
8. Chen, Guodong, Li, Xiaoyan, He, Gengsheng, He, Jun, Huang, Zonghai. 2015. Low expression of GNAI3 predicts poor prognosis in patients with HCC. In International journal of clinical and experimental medicine, 8, 21482-6. doi:. https://pubmed.ncbi.nlm.nih.gov/26885096/
9. Meng, Li, Yuan, Lichan, Ni, Jieli, Ma, Junqing, Zhang, Yang. 2021. Mir24-2-5p suppresses the osteogenic differentiation with Gnai3 inhibition presenting a direct target via inactivating JNK-p38 MAPK signaling axis. In International journal of biological sciences, 17, 4238-4253. doi:10.7150/ijbs.60536. https://pubmed.ncbi.nlm.nih.gov/34803495/
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