C57BL/6JCya-Selenowem1flox/Cya
Common Name:
Selenow-flox
Product ID:
S-CKO-05005
Background:
C57BL/6JCya
Product Type
Age
Genotype
Sex
Quantity
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Basic Information
Strain Name
Selenow-flox
Strain ID
CKOCMP-20364-Selenow-B6J-VA
Gene Name
Product ID
S-CKO-05005
Gene Alias
Sepw1; selW
Background
C57BL/6JCya
NCBI ID
Modification
Conditional knockout
Chromosome
7
Phenotype
Document
Application
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Note: When using this mouse strain in a publication, please cite “C57BL/6JCya-Selenowem1flox/Cya mice (Catalog S-CKO-05005) were purchased from Cyagen.”
Strain Description
Ensembl Number
ENSMUST00000044355
NCBI RefSeq
NM_009156
Target Region
Exon 2~5
Size of Effective Region
~2.6 kb
Detailed Document
Overview of Gene Research
SELENOW, also known as selenoprotein W and SEPW1, is a selenocysteine-containing selenoprotein. It is involved in various biological processes and is part of the thioredoxin-like family of selenoproteins [5,7]. SELENOW plays a role in redox-related functions, and its expression and function are associated with multiple pathways and biological systems [7]. Genetic models, especially KO mouse models, have been crucial in understanding its functions.
In muscle-related studies, SELENOW KO in mouse models of dexamethasone-induced muscle atrophy and age-related sarcopenia aggravated muscle mass loss. Mechanistically, it suppressed the RAC1-mTOR cascade through interaction with RAC1, leading to an imbalance in protein synthesis and degradation [1].
In an Alzheimer's disease mouse model, SELENOW deficiency led to synaptic defects, tau dysregulation, and memory deficits, while overexpression ameliorated memory impairment and tau-related pathologies, as SELENOW promotes tau degradation through the ubiquitin-proteasome system [2].
In non-alcoholic fatty liver disease, loss of SelW alleviated hepatic steatosis induced by a high-fat diet, and SelW modulated the translocation of Pyruvate Kinase M2 into the nucleus, mediating mitochondrial apoptosis and related inflammatory responses [3].
In experimental colitis, Selenow KO mice showed exacerbated acute colitis, with loss of epithelial barrier integrity and decreased expression of key epithelial-related proteins, indicating Selenow's role in resolving inflammation and promoting intestinal epithelial repair [4].
In bone remodeling, SELENOW-deficient mice exhibited a high bone mass phenotype, as SELENOW regulates osteoclastogenic genes and its deficiency suppresses osteoclast formation [6].
In conclusion, SELENOW is essential in multiple biological processes such as muscle mass maintenance, tau homeostasis, liver lipid metabolism, intestinal epithelial repair, and bone remodeling. Studies using KO mouse models have revealed its significance in age-related sarcopenia, Alzheimer's disease, non-alcoholic fatty liver disease, experimental colitis, and osteoporosis, providing insights into potential therapeutic strategies for these diseases.
References:
1. Yang, Jia-Cheng, Liu, Meng, Huang, Rong-Hui, Lei, Xin Gen, Sun, Lv-Hui. 2024. Loss of SELENOW aggravates muscle loss with regulation of protein synthesis and the ubiquitin-proteasome system. In Science advances, 10, eadj4122. doi:10.1126/sciadv.adj4122. https://pubmed.ncbi.nlm.nih.gov/39303039/
2. Ren, Bingyu, Situ, Jiaxin, Huang, Xuelian, Ni, Jiazuan, Liu, Qiong. 2024. Selenoprotein W modulates tau homeostasis in an Alzheimer's disease mouse model. In Communications biology, 7, 872. doi:10.1038/s42003-024-06572-0. https://pubmed.ncbi.nlm.nih.gov/39020075/
3. Miao, Zhiruo, Wang, Wei, Miao, Zhiying, Cao, Qiyuan, Xu, Shiwen. 2024. Role of Selenoprotein W in participating in the progression of non-alcoholic fatty liver disease. In Redox biology, 71, 103114. doi:10.1016/j.redox.2024.103114. https://pubmed.ncbi.nlm.nih.gov/38460355/
4. Nettleford, Shaneice K, Liao, Chang, Short, Sarah P, Singh, Vishal, Prabhu, K Sandeep. 2023. Selenoprotein W Ameliorates Experimental Colitis and Promotes Intestinal Epithelial Repair. In Antioxidants (Basel, Switzerland), 12, . doi:10.3390/antiox12040850. https://pubmed.ncbi.nlm.nih.gov/37107231/
5. Gladyshev, Vadim N, Arnér, Elias S, Berry, Marla J, Whanger, Philip D, Zhang, Yan. 2016. Selenoprotein Gene Nomenclature. In The Journal of biological chemistry, 291, 24036-24040. doi:. https://pubmed.ncbi.nlm.nih.gov/27645994/
6. Kim, Hyunsoo, Lee, Kyunghee, Kim, Jin Man, Choi, Yongwon, Jeong, Daewon. 2021. Selenoprotein W ensures physiological bone remodeling by preventing hyperactivity of osteoclasts. In Nature communications, 12, 2258. doi:10.1038/s41467-021-22565-7. https://pubmed.ncbi.nlm.nih.gov/33859201/
7. Zhang, Li, Zhu, Jian-Hong, Zhang, Xiong, Cheng, Wen-Hsing. 2018. The Thioredoxin-Like Family of Selenoproteins: Implications in Aging and Age-Related Degeneration. In Biological trace element research, 188, 189-195. doi:10.1007/s12011-018-1521-9. https://pubmed.ncbi.nlm.nih.gov/30229511/
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