C57BL/6JCya-Timp2em1flox/Cya
Common Name
Timp2-flox
Product ID
S-CKO-06302
Backgroud
C57BL/6JCya
Strain ID
CKOCMP-21858-Timp2-B6J-VA
Status
When using this mouse strain in a publication, please cite “Timp2-flox Mouse (Catalog S-CKO-06302) were purchased from Cyagen.”
Product Type
Age
Genotype
Sex
Quantity
The standard delivery applies for a guaranteed minimum of three heterozygous carriers. Breeding services for homozygous carriers and/or specified sex are available.
Basic Information
Strain Name
Timp2-flox
Strain ID
CKOCMP-21858-Timp2-B6J-VA
Gene Name
Product ID
S-CKO-06302
Gene Alias
Timp-2, D11Bwg1104e
Background
C57BL/6JCya
Gene Full Name
tissue inhibitor of metalloproteinase 2
Modification
Conditional knockout
NCBI ID
Phenotype
Chromosome
Chr 11 (Mouse)
Application
--
Datasheet
Strain Description
Ensembl Transcript ID
ENSMUST00000017610
NCBI Transcript ID
NM_011594
Target Region
Exon 2
Size of Effective Region
~1.3 kb
Overview of Gene Research
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/
Quality Control Standard
Sperm Test
Pre-cryopreservation: Measurement of sperm concentration, determination of sperm viability.
Post-cryopreservation: A vial of cryopreserved sperms is selected for in-vitro fertilization from each batch.
Environmental Standards:SPF
Available Region:Global
Source:Cyagen
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