C57BL/6JCya-Slfn2em1flox/Cya
Common Name:
Slfn2-flox
Product ID:
S-CKO-19064
Background:
C57BL/6JCya
Product Type
Age
Genotype
Sex
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Basic Information
Strain Name
Slfn2-flox
Strain ID
CKOCMP-20556-Slfn2-B6J-VA
Gene Name
Product ID
S-CKO-19064
Gene Alias
Shlf2
Background
C57BL/6JCya
NCBI ID
Modification
Conditional knockout
Chromosome
11
Phenotype
Document
Application
--
Note: When using this mouse strain in a publication, please cite “C57BL/6JCya-Slfn2em1flox/Cya mice (Catalog S-CKO-19064) were purchased from Cyagen.”
Strain Description
Ensembl Number
ENSMUST00000038038
NCBI RefSeq
NM_011408
Target Region
Exon 2
Size of Effective Region
~1.7 kb
Detailed Document
Overview of Gene Research
Slfn2, also known as Schlafen 2, is a cytoplasmic protein involved in multiple biological processes. It plays a crucial role in T cell-mediated immunity, type I interferon responses, and the regulation of cell quiescence. Associated pathways include those related to oxidative stress response in T cells, NF-κB signaling in the context of interferon responses, and cholesterol and lipid homeostasis in maintaining cell quiescence. Genetic mouse models, such as the elektra mouse with a Slfn2 mutation, have been valuable in studying its functions [1,2,3,4,5].
In T cells, Slfn2 deficiency leads to the accumulation of tRNA fragments due to stress-induced cleavage, inhibiting translation and promoting stress-granule formation. This renders T cells insensitive to interleukin-2's mitogenic effects, highlighting its importance in T cell expansion and immunity [1]. In the context of interferon responses, targeted disruption of Slfn2 leads to increased transcription of IFN-stimulated genes and enhanced type I IFN-mediated antiviral responses by modulating the NF-κB pathway [2]. In the elektra mouse model, Slfn2 mutation causes lymphoid and myeloid immunodeficiency due to loss of immune cell quiescence, and also disrupts cholesterol and lipid homeostasis in T cells and monocytes [3,4]. Moreover, in T-cell acute lymphoblastic leukemia (T-ALL), targeting Slfn2 to disrupt T-cell quiescence can prevent disease development and progression [6]. In osteoclastogenesis, Slfn2 is a positive regulator, and its loss-of-function in mice results in an osteopetrotic phenotype [7,8].
In conclusion, Slfn2 is essential for T cell-mediated immunity, the regulation of type I interferon responses, and the maintenance of cell quiescence in various cell types. The study of Slfn2 using gene knockout (KO) mouse models, like the elektra model, has provided valuable insights into its role in diseases such as immunodeficiency, T-ALL, and osteopetrosis. Understanding Slfn2 functions may offer new therapeutic strategies for these diseases.
References:
1. Yue, Tao, Zhan, Xiaoming, Zhang, Duanwu, Moresco, Eva Marie Y, Beutler, Bruce. . SLFN2 protection of tRNAs from stress-induced cleavage is essential for T cell-mediated immunity. In Science (New York, N.Y.), 372, . doi:10.1126/science.aba4220. https://pubmed.ncbi.nlm.nih.gov/33986151/
2. Fischietti, Mariafausta, Arslan, Ahmet D, Sassano, Antonella, Fish, Eleanor N, Platanias, Leonidas C. 2018. Slfn2 Regulates Type I Interferon Responses by Modulating the NF-κB Pathway. In Molecular and cellular biology, 38, . doi:10.1128/MCB.00053-18. https://pubmed.ncbi.nlm.nih.gov/29866656/
3. Omar, Ibrahim, Rom, Oren, Aviram, Michael, Parks, John S, Berger, Michael. 2017. Slfn2 mutation-induced loss of T-cell quiescence leads to elevated de novo sterol synthesis. In Immunology, 152, 484-493. doi:10.1111/imm.12785. https://pubmed.ncbi.nlm.nih.gov/28672048/
4. Berger, Michael, Krebs, Philippe, Crozat, Karine, Akira, Shizuo, Beutler, Bruce. 2010. An Slfn2 mutation causes lymphoid and myeloid immunodeficiency due to loss of immune cell quiescence. In Nature immunology, 11, 335-43. doi:10.1038/ni.1847. https://pubmed.ncbi.nlm.nih.gov/20190759/
5. Warsi, Sarah, Dahl, Maria, Smith, Emma M K, Karlsson, Goran, Karlsson, Stefan. 2022. Schlafen2 is a regulator of quiescence in adult murine hematopoietic stem cells. In Haematologica, 107, 2884-2896. doi:10.3324/haematol.2021.279799. https://pubmed.ncbi.nlm.nih.gov/35615926/
6. Goldshtein, Aviya, Zerbib, Shani Mistriel, Omar, Ibrahim, Popkin, Daniel, Berger, Michael. . Loss of T-cell quiescence by targeting Slfn2 prevents the development and progression of T-ALL. In Oncotarget, 7, 46835-46847. doi:10.18632/oncotarget.9390. https://pubmed.ncbi.nlm.nih.gov/27206675/
7. Omar, Ibrahim, Guterman-Ram, Gali, Rahat, Dolev, Berger, Michael, Levaot, Noam. 2018. Schlafen2 mutation in mice causes an osteopetrotic phenotype due to a decrease in the number of osteoclast progenitors. In Scientific reports, 8, 13005. doi:10.1038/s41598-018-31428-z. https://pubmed.ncbi.nlm.nih.gov/30158544/
8. Lee, Na Kyung, Choi, Han Kyung, Yoo, Hyun Joo, Shin, Jihye, Lee, Soo Young. 2008. RANKL-induced schlafen2 is a positive regulator of osteoclastogenesis. In Cellular signalling, 20, 2302-8. doi:10.1016/j.cellsig.2008.08.019. https://pubmed.ncbi.nlm.nih.gov/18796328/
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