Gtf2h2-flox Mouse
一般名
Gtf2h2-flox
製品ID
S-CKO-08074
背景情報
C57BL/6JCya
系統ID
CKOCMP-23894-Gtf2h2-B6J-VA
状況
このマウス系統を論文で使用する場合は、「Gtf2h2-flox Mouse（カタログ番号S-CKO-08074）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
Gtf2h2-flox
系統ID
CKOCMP-23894-Gtf2h2-B6J-VA
遺伝子名
製品ID
S-CKO-08074
遺伝子別名
p44, 44kDa, Btf2p44, BTF2 p44, BTF2-p44
遺伝子別名
C57BL/6JCya
NCBI ID
修正
Conditional knockout
染色体
Chr 13
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
ENSMUST00000066984
NCBIトランスクリプトID
NM_022011
ターゲット領域
Exon 6~7
有効領域の大きさ
~1.0 kb
遺伝子研究の概要
Gtf2h2, also known as general transcription factor II subunit H2, functions in nucleotide excision repair (NER) and basal transcription [7]. It is involved in the estrogen-dependent estrogen receptor alpha (ERα) signaling pathway, and plays a role in maintaining NER-related genomic stability and affecting PAM/NF-κB signaling pathway [7].
In hepatocellular carcinoma (HCC), overexpressing Gtf2h2 had no direct effect on endothelial cell viability, migration, or permeability, but GTF2H2-enriched exosomes from Huh7 cells could inhibit human umbilical vein endothelial cells (HUVECs) phenotypes such as proliferation and migration, suggesting potential use as a novel drug for treating HCC [1]. In lung cancer, TEP linc-GTF2H2-1 was significantly downregulated in patients, and its combination with other lncRNAs could improve the diagnostic efficiency of lung cancer [2]. In spinal muscular atrophy (SMA), GTF2H2 gene deletions were analyzed in patients, and a significant difference was found between healthy and SMA subjects. Pediatric patients with GTF2H2 deletions demonstrated higher motor functions [3,5,8,9,10]. In addition, GTF2H2 was identified as one of the genes significantly differentially expressed in the tissue of patients with neuropathic pain, suggesting it may be a potential therapeutic target [6]. The N-terminal region of the transcription factor E2F1 can recruit GTF2H2, and overexpression of GTF2H2 enhanced E2F1 activation of tumor suppressor genes and induction of cell death [4].
In conclusion, Gtf2h2 has diverse functions in different biological processes and diseases. In HCC, its exosome-derived form may have anti-angiogenesis potential; in lung cancer, it could be a biomarker; in SMA, it may be related to disease severity and motor function; in neuropathic pain, it may serve as a therapeutic target. Its interaction with E2F1 also impacts tumor suppressor gene activation. These findings from various studies help to understand the biological significance of Gtf2h2 in different disease contexts.
References：
1. Li, Zhenkun, Li, Yanmeng, Ouyang, Qin, Li, Xiaojin, Huang, Jian. 2022. Exosome-derived GTF2H2 from Huh7 cells can inhibit endothelial cell viability, migration, tube formation, and permeability. In Tissue & cell, 79, 101922. doi:10.1016/j.tice.2022.101922. https://pubmed.ncbi.nlm.nih.gov/36116407/
2. Li, Xinyi, Liu, Lele, Song, Xingguo, Xie, Li, Song, Xianrang. 2021. TEP linc-GTF2H2-1, RP3-466P17.2, and lnc-ST8SIA4-12 as novel biomarkers for lung cancer diagnosis and progression prediction. In Journal of cancer research and clinical oncology, 147, 1609-1622. doi:10.1007/s00432-020-03502-5. https://pubmed.ncbi.nlm.nih.gov/33792796/
3. Karasu, Nilgun, Acer, Hamit, Akalin, Hilal, Canpolat, Mehmet, Dundar, Munis. 2024. Molecular analysis of SMN2, NAIP, and GTF2H2 gene deletions and relationships with clinical subtypes of spinal muscular atrophy. In Journal of neurogenetics, 38, 102-111. doi:10.1080/01677063.2024.2407332. https://pubmed.ncbi.nlm.nih.gov/39321203/
4. Zhao, Lin, Nakajima, Rinka, Zhou, Yaxuan, Araki, Keigo, Ohtani, Kiyoshi. 2024. The N-Terminal Region of the Transcription Factor E2F1 Contains a Novel Transactivation Domain and Recruits General Transcription Factor GTF2H2. In Biomolecules, 14, . doi:10.3390/biom14111357. https://pubmed.ncbi.nlm.nih.gov/39595534/
5. He, Jin, Zhang, Qi-Jie, Lin, Qi-Fang, Wang, Ning, Chen, Wan-Jin. 2013. Molecular analysis of SMN1, SMN2, NAIP, GTF2H2, and H4F5 genes in 157 Chinese patients with spinal muscular atrophy. In Gene, 518, 325-9. doi:10.1016/j.gene.2012.12.109. https://pubmed.ncbi.nlm.nih.gov/23352792/
6. Hu, Ling, Yin, Wei, Ma, Yao, Zhang, Qiushi, Xu, Qingbang. 2023. Gene expression signature of human neuropathic pain identified through transcriptome analysis. In Frontiers in genetics, 14, 1127167. doi:10.3389/fgene.2023.1127167. https://pubmed.ncbi.nlm.nih.gov/36816032/
7. Li, Yanmeng, Ouyang, Qin, Chen, Zhibin, Jia, Jidong, Huang, Jian. 2025. Novel role of general transcript factor IIH subunit 2 (GTF2H2) in the development and sex disparity of hepatocellular carcinoma. In Oncogene, 44, 1323-1335. doi:10.1038/s41388-025-03301-7. https://pubmed.ncbi.nlm.nih.gov/39972070/
8. Theodorou, L, Nicolaou, P, Koutsou, P, Zamba-Papanicolaou, E, Christodoulou, K. 2015. Genetic findings of Cypriot spinal muscular atrophy patients. In Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 36, 1829-34. doi:10.1007/s10072-015-2263-5. https://pubmed.ncbi.nlm.nih.gov/26017350/
9. Zhuri, Drenushe, Gurkan, Hakan, Eker, Damla, Demir, Selma, Atli, Emine Ikbal. 2022. Investigation on the Effects of Modifying Genes on the Spinal Muscular Atrophy Phenotype. In Global medical genetics, 9, 226-236. doi:10.1055/s-0042-1751302. https://pubmed.ncbi.nlm.nih.gov/36071912/
10. Liu, Zhidai, Zhang, Penghui, He, Xiaoyan, Hong, Siqi, Zou, Lin. 2016. New multiplex real-time PCR approach to detect gene mutations for spinal muscular atrophy. In BMC neurology, 16, 141. doi:10.1186/s12883-016-0651-y. https://pubmed.ncbi.nlm.nih.gov/27534852/
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