C57BL/6JCya-Trim38em1flox/Cya
Common Name:
Trim38-flox
Product ID:
S-CKO-05807
Background:
C57BL/6JCya
Product Type
Age
Genotype
Sex
Quantity
Price:
Contact for Pricing
Basic Information
Strain Name
Trim38-flox
Strain ID
CKOCMP-214158-Trim38-B6J-VA
Gene Name
Product ID
S-CKO-05807
Gene Alias
Gm23
Background
C57BL/6JCya
NCBI ID
Modification
Conditional knockout
Chromosome
13
Phenotype
Document
Application
--
Note: When using this mouse strain in a publication, please cite “C57BL/6JCya-Trim38em1flox/Cya mice (Catalog S-CKO-05807) were purchased from Cyagen.”
Strain Description
Ensembl Number
ENSMUST00000074067
NCBI RefSeq
NM_001029935
Target Region
Exon 3~5
Size of Effective Region
~2.3 kb
Detailed Document
Overview of Gene Research
TRIM38, a member of the tripartite motif (TRIM)-containing protein family, functions as a ubiquitin E3 protein ligase. It is involved in multiple intracellular physiological processes, including innate immune and inflammatory responses, cell proliferation, differentiation, apoptosis, and antiviral defense. It is associated with various signaling pathways such as TRAF6/TAK1/NF-κB, MYC, and RIG-I-mediated IFN-I regulation [1,2,3,4].
In a rat cardiomyoblast cell line (H9c2), TRIM38 knockdown activated the TAK1/NF-κB signaling pathway, reducing anti-apoptotic and anti-inflammatory capacity during hypoxia/reoxygenation (H/R) injury, while overexpression alleviated H/R-induced cell injury [1]. In colorectal cancer, decreased TRIM38, due to DNA hypermethylation of its promoter, was correlated with poor prognosis, and its overexpression inhibited cancer cell proliferation and metastasis by enhancing CCT6A ubiquitination to inhibit the MYC pathway [2]. In respiratory syncytial virus-infected cells, IFN-I promoted TRIM38 expression, which downregulated IFN-I production by competing with TRIM25 to bind RIG-I [3]. In chondrocytes, IL-1β stimulation decreased TRIM38 levels, and overexpression protected chondrocytes from IL-1β-induced apoptosis and degeneration by suppressing NF-κB signaling [5]. In the context of the maternal-fetal interface, TRIM38-mediated K48 ubiquitination of MITA in M2 macrophages inhibited pyroptosis, maintaining the immunosuppressed state [6]. In osteoclast and osteoblast differentiation, TRIM38 overexpression in precursor cells affected differentiation and function by regulating NF-κB activation through TAB2 degradation [7]. In human glioma cells, TRIM38 overexpression restricted Zika virus replication by upregulating the RIG-I/MDA5 pathway and promoting ubiquitin-mediated degradation of the viral NS3 protein [8]. In bladder cancer, low TRIM38 expression was associated with poor prognosis, and it restricted tumor progression by promoting GLUT1 ubiquitination and degradation [9]. In a NAFLD mouse model, TRIM38 depletion deteriorated hepatic steatosis, inflammation, and fibrosis, and TRIM38 overexpression mitigated these effects by promoting TAB2 degradation and inhibiting the MAPK signaling pathway [10].
In conclusion, TRIM38 plays crucial roles in various biological processes and diseases. Through gene-knockout or related loss-of-function models in different cell lines and animal models, it has been revealed that TRIM38 can regulate innate immune and inflammatory responses, cell apoptosis, differentiation, and tumor progression. These findings contribute to understanding the underlying mechanisms of related diseases and suggest TRIM38 as a potential therapeutic target for diseases such as myocardial ischemia/reperfusion injury, colorectal cancer, osteoarthritis, and NAFLD.
References:
1. Lu, Zhengri, Deng, Mengen, Ma, Genshan, Chen, Lijuan. 2022. TRIM38 protects H9c2 cells from hypoxia/reoxygenation injury via the TRAF6/TAK1/NF-κB signalling pathway. In PeerJ, 10, e13815. doi:10.7717/peerj.13815. https://pubmed.ncbi.nlm.nih.gov/36061751/
2. Zhang, Yue, Tan, Xinyu, Wang, Lu, Feng, Yifei, Sun, Yueming. 2025. TRIM38 Suppresses the Progression of Colorectal Cancer via Enhancing CCT6A Ubiquitination to Inhibit the MYC Pathway. In Advanced science (Weinheim, Baden-Wurttemberg, Germany), 12, e2411285. doi:10.1002/advs.202411285. https://pubmed.ncbi.nlm.nih.gov/40047371/
3. Sun, Qingqing, Han, Xiao, Meng, Lingtong, Wei, Lin, Ma, Cuiqing. 2024. TRIM38 Induced in Respiratory Syncytial Virus-infected Cells Downregulates Type I Interferon Expression by Competing with TRIM25 to Bind RIG-I. In Inflammation, 47, 1328-1343. doi:10.1007/s10753-024-01979-7. https://pubmed.ncbi.nlm.nih.gov/38630167/
4. Hu, Ming-Ming, Shu, Hong-Bing. 2017. Multifaceted roles of TRIM38 in innate immune and inflammatory responses. In Cellular & molecular immunology, 14, 331-338. doi:10.1038/cmi.2016.66. https://pubmed.ncbi.nlm.nih.gov/28194022/
5. Hu, Shouye, Li, Yanqi, Wang, Bo, Peng, Kan. 2021. TRIM38 protects chondrocytes from IL-1β-induced apoptosis and degeneration via negatively modulating nuclear factor (NF)-κB signaling. In International immunopharmacology, 99, 108048. doi:10.1016/j.intimp.2021.108048. https://pubmed.ncbi.nlm.nih.gov/34426118/
6. Liu, Jun, Deng, Yan, Wang, An, Chen, Jiao, Yang, Jing. 2023. Investigation into the role of the MITA-TRIM38 interaction in regulating pyroptosis and maintaining immune tolerance at the maternal-fetal interface. In Cell death & disease, 14, 780. doi:10.1038/s41419-023-06314-w. https://pubmed.ncbi.nlm.nih.gov/38012139/
7. Kim, Kabsun, Kim, Jung Ha, Kim, Inyoung, Seong, Semun, Kim, Nacksung. 2018. TRIM38 regulates NF-κB activation through TAB2 degradation in osteoclast and osteoblast differentiation. In Bone, 113, 17-28. doi:10.1016/j.bone.2018.05.009. https://pubmed.ncbi.nlm.nih.gov/29753717/
8. He, Jing, Kuang, Yulian, Xu, Kui, Yang, Jian, Yuan, Lei. 2025. TRIM38 Inhibits Zika Virus by Upregulating RIG-I/MDA5 Pathway and Promoting Ubiquitin-Mediated Degradation of Viral NS3 Protein. In Viruses, 17, . doi:10.3390/v17020199. https://pubmed.ncbi.nlm.nih.gov/40006954/
9. Wang, Xiaojing, He, Hongchao, Rui, Wenbin, Zhu, Yu, Xie, Xin. 2021. TRIM38 triggers the uniquitination and degradation of glucose transporter type 1 (GLUT1) to restrict tumor progression in bladder cancer. In Journal of translational medicine, 19, 508. doi:10.1186/s12967-021-03173-x. https://pubmed.ncbi.nlm.nih.gov/34906161/
10. Yao, Xinxin, Dong, Ruixiang, Hu, Sha, Li, Hongliang, Zhang, Peng. 2023. Tripartite motif 38 alleviates the pathological process of NAFLD-NASH by promoting TAB2 degradation. In Journal of lipid research, 64, 100382. doi:10.1016/j.jlr.2023.100382. https://pubmed.ncbi.nlm.nih.gov/37116711/
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