Micall2-flox Mouse
一般名
Micall2-flox
製品ID
S-CKO-07493
背景情報
C57BL/6JCya
系統ID
CKOCMP-231830-Micall2-B6J-VA
状況
このマウス系統を論文で使用する場合は、「Micall2-flox Mouse（カタログ番号S-CKO-07493）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
Micall2-flox
系統ID
CKOCMP-231830-Micall2-B6J-VA
遺伝子名
製品ID
S-CKO-07493
遺伝子別名
JRAB, MICAL-L2, mFLJ00139, A930021H16Rik
遺伝子別名
C57BL/6JCya
NCBI ID
修正
Conditional knockout
染色体
Chr 5
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
ENSMUST00000044642
NCBIトランスクリプトID
NM_174850
ターゲット領域
Exon 4
有効領域の大きさ
~0.8 kb
遺伝子研究の概要
Micall2, also known as molecule interacting with CasL-like protein 2, is believed to regulate cytoskeleton dynamics, tight junction formation, and neurite outgrowth. It has been associated with multiple biological processes and diseases, and is involved in pathways such as the Wnt/β -catenin signaling pathway [2,3]. Genetic models are valuable for studying its functions.
In clear cell renal cell carcinoma (ccRCC), Micall2 was highly expressed in cancer tissues and cell lines compared to normal tissues. Overexpression promoted, while gene silencing inhibited, the proliferation, migration, and invasion of ccRCC cells, suggesting it contributes to ccRCC malignancy [1].
In colorectal cancer, its overexpression was correlated with poor prognosis, and it enhanced cell growth and migration via the Wnt/β -catenin pathway. Ubiquitin E3 ligase TRIM21 mediated its ubiquitination and degradation [2].
In pulmonary fibrosis, knockdown of Micall2 in mice and cells restrained the epithelial-mesenchymal transition (EMT) process by impeding β -catenin nuclear translocation [3].
In ovarian cancer, bioinformatics analysis showed its high expression in advanced-stage tissues, and it participated in immune infiltration and invasion, preventing EGFR degradation in a Rac1-dependent manner [4].
In Ashidan yaks, copy number variations in the Micall2 gene were associated with growth traits [5].
In children with attention deficit hyperactivity disorder (ADHD), a locus regulating Micall2 expression was associated with executive inhibition, and reducing the expression of its homologous gene in zebrafish induced hyperactive-impulsive-like behavior [6].
In conclusion, Micall2 plays crucial roles in various biological processes and diseases. Studies using gene-manipulation models, such as gene knockdown in mice and cells, have revealed its pro-tumorigenic role in cancers like ccRCC, colorectal cancer, and ovarian cancer. It also has implications in pulmonary fibrosis, animal growth traits, and ADHD. These findings provide valuable insights into understanding disease mechanisms and potential therapeutic targets related to Micall2.
References：
1. Zeng, Xianyou, Wang, Hongquan, Yang, Jia, Hu, Jing. 2023. Micall2 Is Responsible for the Malignancy of Clear Cell Renal Cell Carcinoma. In Yonago acta medica, 66, 171-179. doi:10.33160/yam.2023.02.021. https://pubmed.ncbi.nlm.nih.gov/36811029/
2. Wen, Pushuai, Wang, Huade, Li, Yi, Wang, Yu, Gao, Jing. 2022. MICALL2 as a substrate of ubiquitinase TRIM21 regulates tumorigenesis of colorectal cancer. In Cell communication and signaling : CCS, 20, 170. doi:10.1186/s12964-022-00984-3. https://pubmed.ncbi.nlm.nih.gov/36307841/
3. Chen, Yingying, Song, Wei, Zhang, He, Ji, Xinping. 2023. MICALL2 participates in the regulation of epithelial-mesenchymal transition in alveolar epithelial cells - Potential roles in pulmonary fibrosis. In Archives of biochemistry and biophysics, 747, 109730. doi:10.1016/j.abb.2023.109730. https://pubmed.ncbi.nlm.nih.gov/37690696/
4. Xia, Tianxiang, Ye, Fengwen, Zhao, Weizhen, Zhang, Yujie, Du, Jun. 2023. Comprehensive Analysis of MICALL2 Reveals Its Potential Roles in EGFR Stabilization and Ovarian Cancer Cell Invasion. In International journal of molecular sciences, 25, . doi:10.3390/ijms25010518. https://pubmed.ncbi.nlm.nih.gov/38203692/
5. Liu, Modian, Huang, Chun, Dai, Rongfeng, Yan, Ping, Liang, Chunnian. 2022. Copy Number Variations in the MICALL2 and MOGAT2 Genes Are Associated with Ashidan Yak Growth Traits. In Animals : an open access journal from MDPI, 12, . doi:10.3390/ani12202779. https://pubmed.ncbi.nlm.nih.gov/36290165/
6. Yang, L, Chang, S, Lu, Q, Wang, Y, Lu, L. 2017. A new locus regulating MICALL2 expression was identified for association with executive inhibition in children with attention deficit hyperactivity disorder. In Molecular psychiatry, 23, 1014-1020. doi:10.1038/mp.2017.74. https://pubmed.ncbi.nlm.nih.gov/28416812/
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