Tinagl1-KO Mouse
一般名
Tinagl1-KO
製品ID
S-KO-20854
背景情報
C57BL/6JCya
系統ID
KOCMP-94242-Tinagl1-B6J-VD
状況
このマウス系統を論文で使用する場合は、「Tinagl1-KO Mouse（カタログ番号S-KO-20854）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
Tinagl1-KO
系統ID
KOCMP-94242-Tinagl1-B6J-VD
遺伝子名
製品ID
S-KO-20854
遺伝子別名
AZ1, AZ-1, Arg1, Lcn7, TARP, Tinagl, 1110021J17Rik
遺伝子別名
C57BL/6JCya
NCBI ID
修正
Conventional knockout
染色体
Chr 4
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
ENSMUST00000105998
NCBIトランスクリプトID
NM_023476
ターゲット領域
Exon 2~3
有効領域の大きさ
~2.2 kb
遺伝子研究の概要
Tinagl1, also known as Tubulointerstitial nephritis antigen-like 1, is a matricellular protein. It is involved in multiple biological functions such as cell adhesion, and modulates cell proliferation, migration, and differentiation. It is associated with pathways like integrin/FAK, EGFR, TGF-β, and ERK signaling, which are crucial for normal development and disease-related processes [1,2,5,6].
In breast cancer, Tinagl1 has been well-studied. Ectopic expression and therapeutic delivery of Tinagl1 protein suppress triple-negative breast cancer (TNBC) progression and metastasis by directly binding to integrin α5β1, αvβ1, and EGFR, simultaneously inhibiting FAK and EGFR signaling pathways [1]. Low TINAGL1 mRNA expression is associated with significantly shorter disease-free survival and overall survival in breast cancer patients, and is an independent poor prognostic factor for disease-free survival in invasive breast cancer patients when combined with lymph node positivity [3]. In addition, Tinagl1 can restore tamoxifen sensitivity in tamoxifen-resistant breast cancer cells by blocking the EGFR and β1-integrin/FAK signaling pathways [7].
In Crohn's Disease, mesenteric adipose-derived exosomal TINAGL1 enhances intestinal fibrosis via SMAD4 in the TGF-β signaling pathway [2].
In diabetes, decreased TINAGL1 expression in fibroblasts impairs wound healing, while exogenous TINAGL1 promotes wound healing in diabetic mice [4].
In muscle development, Tinagl1-deficient mice exhibit reduced body mass, calf muscle weights, and a decreasing trend in capillary density in the soleus muscle, indicating that Tinagl1 is required for normal muscle and capillary development through the activation of ERK signaling [6].
In conclusion, Tinagl1 plays essential roles in multiple biological processes and diseases. Studies using gene-knockout or conditional-knockout mouse models, along with other functional studies, have revealed its significance in breast cancer, Crohn's Disease, diabetes-related wound healing, and muscle development. These findings contribute to a better understanding of the molecular mechanisms underlying these diseases and suggest Tinagl1 as a potential therapeutic target [1-4,9,10].
References：
1. Shen, Minhong, Jiang, Yi-Zhou, Wei, Yong, Shao, Zhi-Ming, Kang, Yibin. 2019. Tinagl1 Suppresses Triple-Negative Breast Cancer Progression and Metastasis by Simultaneously Inhibiting Integrin/FAK and EGFR Signaling. In Cancer cell, 35, 64-80.e7. doi:10.1016/j.ccell.2018.11.016. https://pubmed.ncbi.nlm.nih.gov/30612941/
2. Chen, Yidong, Li, Junrong, Zhang, Xiaopeng, Li, Jiamin, Zhu, Liangru. 2024. Mesenteric adipose-derived exosomal TINAGL1 enhances intestinal fibrosis in Crohn's Disease via SMAD4. In Journal of advanced research, 70, 139-158. doi:10.1016/j.jare.2024.05.016. https://pubmed.ncbi.nlm.nih.gov/38750695/
3. Kato, Akiko, Kondo, Naoto, Wanifuchi-Endo, Yumi, Takahashi, Satoru, Toyama, Tatsuya. 2022. Low TINAGL1 expression is a marker for poor prognosis in breast cancer. In Journal of cancer research and clinical oncology, 149, 4771-4782. doi:10.1007/s00432-022-04394-3. https://pubmed.ncbi.nlm.nih.gov/36229542/
4. Tian, Wen-Qing, Chen, Si-Yu, Chuan, Feng-Ning, Zhao, Wen-Rui, Zhou, Bo. . Down-regulated TINAGL1 in fibroblasts impairs wound healing in diabetes. In FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 36, e22235. doi:10.1096/fj.202101438RR. https://pubmed.ncbi.nlm.nih.gov/35199864/
5. Sun, Lu, Dong, Zihui, Gu, Hongli, Guo, Zhixian, Yu, Zujiang. 2019. TINAGL1 promotes hepatocellular carcinogenesis through the activation of TGF-β signaling-medicated VEGF expression. In Cancer management and research, 11, 767-775. doi:10.2147/CMAR.S190390. https://pubmed.ncbi.nlm.nih.gov/30697069/
6. Sato, Yoriko, Kawashima, Keisuke, Fukui, Emiko, Yoshizawa, Fumiaki, Sato, Yusuke. 2022. Functional analysis reveals that Tinagl1 is required for normal muscle development in mice through the activation of ERK signaling. In Biochimica et biophysica acta. Molecular cell research, 1869, 119294. doi:10.1016/j.bbamcr.2022.119294. https://pubmed.ncbi.nlm.nih.gov/35597451/
7. Yuan, Jie, Yuan, Li, Yang, Li, Wei, Changsheng, Luo, Chengyu. . Tinagl1 restores tamoxifen sensitivity and blocks fibronectin-induced EMT by simultaneously blocking the EGFR and β1-integrin/FAK signaling pathways in tamoxifen-resistant breast cancer cells. In IUBMB life, 77, e2940. doi:10.1002/iub.2940. https://pubmed.ncbi.nlm.nih.gov/39817673/
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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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