Timp2-flox Mouse
一般名
Timp2-flox
製品ID
S-CKO-06302
背景情報
C57BL/6JCya
系統ID
CKOCMP-21858-Timp2-B6J-VA
状況
このマウス系統を論文で使用する場合は、「Timp2-flox Mouse（カタログ番号S-CKO-06302）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
Timp2-flox
系統ID
CKOCMP-21858-Timp2-B6J-VA
遺伝子名
製品ID
S-CKO-06302
遺伝子別名
D11Bwg1104e, Timp-2
遺伝子別名
C57BL/6JCya
遺伝子正式名称
tissue inhibitor of metalloproteinase 2
NCBI ID
修正
Conditional knockout
染色体
Chr 11
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
ENSMUST00000017610
NCBIトランスクリプトID
NM_011594
ターゲット領域
Exon 2
有効領域の大きさ
~1.3 kb
遺伝子研究の概要
Timp2, short for Tissue inhibitor of metalloproteinase-2, is a protein-coding gene. It has dual functions of inhibiting MMP (matrix metalloproteinase) activity and cytokine-like activity via receptor binding. It is involved in regulating extracellular matrix (ECM) structure and composition [5]. Genetic models, such as knockout (KO) and conditional knockout (CKO) mouse models, have been crucial in studying its functions.
In the context of traumatic brain injury (TBI), both TIMP2 and a TIMP2 mutant without MMP-inhibiting activity attenuated neurological deficits and BBB leakage in TBI mice, by inhibiting Src-dependent VE-cadherin internalization [1]. In sepsis-associated acute kidney injury (SA-AKI), kidney tubule-specific Timp2 knockout mice showed more severe kidney injury and elevated pyroptosis markers, while exogenous TIMP2 protected against kidney damage [2]. In renal fibrogenesis following ischemia-reperfusion injury, tubule-specific Timp2 knockout markedly attenuated renal fibrosis, and Timp2 was found to exacerbate Hedgehog (Hh) signaling, promoting mitochondrial fragmentation and metabolic reprogramming [3]. In sepsis-induced acute kidney injury, TIMP2-deficient mice had lower serum creatinine levels and decreased endoplasmic reticulum (ER) stress-mediated apoptosis compared to wild-type mice [4]. Also, downregulation of TIMP2 in stable, kidney-specific TIMP2 knockdown mice ameliorated cecal ligation and puncture (CLP)-induced proinflammatory cytokines, kidney dysfunction, and histopathological changes, through inhibition of the nuclear factor (NF)-κB pathway [6].
In conclusion, Timp2 plays diverse roles in multiple biological processes and disease conditions. Model-based research, especially using Timp2 KO/CKO mouse models, has revealed its significance in diseases like TBI, SA-AKI, and renal fibrogenesis. It is involved in processes such as maintaining blood-brain barrier integrity, regulating pyroptosis, mitochondrial function, and inflammation, providing potential therapeutic targets for these diseases.
References：
1. Tang, Jingshu, Kang, Yuying, Zhou, Yujun, Wu, Lei, Peng, Ying. 2023. TIMP2 ameliorates blood-brain barrier disruption in traumatic brain injury by inhibiting Src-dependent VE-cadherin internalization. In The Journal of clinical investigation, 134, . doi:10.1172/JCI164199. https://pubmed.ncbi.nlm.nih.gov/38015626/
2. Xu, Dongxue, Jiang, Jun, Liu, Ye, Li, Yiming, Peng, Zhiyong. 2024. TIMP2 protects against sepsis-associated acute kidney injury by cAMP/NLRP3 axis-mediated pyroptosis. In American journal of physiology. Cell physiology, 326, C1353-C1366. doi:10.1152/ajpcell.00577.2023. https://pubmed.ncbi.nlm.nih.gov/38497110/
3. Pang, Jingjing, Xu, Dongxue, Zhang, Xiaoyu, Li, Yiming, Peng, Zhiyong. 2025. TIMP2-mediated mitochondrial fragmentation and glycolytic reprogramming drive renal fibrogenesis following ischemia-reperfusion injury. In Free radical biology & medicine, 232, 244-259. doi:10.1016/j.freeradbiomed.2025.02.020. https://pubmed.ncbi.nlm.nih.gov/39986488/
4. Jiang, Nanhui, Huang, Rong, Zhang, Jiahao, Su, Lianjiu, Peng, Zhiyong. . TIMP2 mediates endoplasmic reticulum stress contributing to sepsis-induced acute kidney injury. In FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 36, e22228. doi:10.1096/fj.202101555RR. https://pubmed.ncbi.nlm.nih.gov/35218571/
5. Peeney, David, Liu, Yueqin, Lazaroff, Carolyn, Gurung, Sadeechya, Stetler-Stevenson, William G. . Unravelling the distinct biological functions and potential therapeutic applications of TIMP2 in cancer. In Carcinogenesis, 43, 405-418. doi:10.1093/carcin/bgac037. https://pubmed.ncbi.nlm.nih.gov/35436325/
6. Li, Yi-Ming, Zhang, Jing, Su, Lian-Jiu, Kellum, John A, Peng, Zhi-Yong. 2018. Downregulation of TIMP2 attenuates sepsis-induced AKI through the NF-κb pathway. In Biochimica et biophysica acta. Molecular basis of disease, 1865, 558-569. doi:10.1016/j.bbadis.2018.10.041. https://pubmed.ncbi.nlm.nih.gov/30562560/
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