C57BL/6JCya-Smpd3em1flox/Cya
Common Name:
Smpd3-flox
Product ID:
S-CKO-12462
Background:
C57BL/6JCya
Product Type
Age
Genotype
Sex
Quantity
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Basic Information
Strain Name
Smpd3-flox
Strain ID
CKOCMP-58994-Smpd3-B6J-VA
Gene Name
Product ID
S-CKO-12462
Gene Alias
4631433G07Rik; Nsm2; fro; nSMase2
Background
C57BL/6JCya
NCBI ID
Modification
Conditional knockout
Chromosome
8
Phenotype
Document
Application
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Note: When using this mouse strain in a publication, please cite “C57BL/6JCya-Smpd3em1flox/Cya mice (Catalog S-CKO-12462) were purchased from Cyagen.”
Strain Description
Ensembl Number
ENSMUST00000067512
NCBI RefSeq
NM_021491
Target Region
Exon 4~5
Size of Effective Region
~0.8 kb
Detailed Document
Overview of Gene Research
Smpd3, sphingomyelin phosphodiesterase 3, is a lipid-metabolizing enzyme. It is crucial for sphingomyelin hydrolysis to produce ceramide, thus playing a role in sphingolipid metabolism pathways. It has significance in multiple biological processes such as embryonic development, bone formation, and is associated with various diseases [2,3,4]. Genetic models, like knockout (KO) and conditional knockout (CKO) mouse models, are valuable for studying its functions.
In KO mouse models, Smpd3 deficiency leads to various phenotypes. In Smpd3flox/flox ; Osx-Cre mice where Smpd3 was ablated in Osx-expressing chondrocytes and osteoblasts during early skeletogenesis, there were delayed extracellular matrix mineralization and severe skeletal deformities. Postnatal ablation in 3-month-old Smpd3flox/flox ; Osx-Cre mice resulted in a milder bone mineralization defect but marked increase of unmineralized osteoid in fractured tibiae [3]. In smpd3-/-mouse brain, absence of SMPD3 in the Golgi compartment of neurons led to inhibition of Golgi vesicular protein transport and progressive cognitive impairment [5]. In hepatocyte-specific Smpd3 gene disruption, it alleviated metabolic-dysfunction-associated steatohepatitis (MASH) [1].
In conclusion, Smpd3 is essential for normal endochondral bone development, ECM mineralization, chondrocyte apoptosis, and neuronal proteostasis. Mouse KO/CKO models have revealed its role in diseases such as skeletal disorders, neurodegeneration, and MASH, providing insights into potential therapeutic targets for these conditions.
References:
1. Jiang, Jie, Gao, Yuqing, Wang, Jiang, Xie, Qing, Xie, Cen. 2025. Hepatic sphingomyelin phosphodiesterase 3 promotes steatohepatitis by disrupting membrane sphingolipid metabolism. In Cell metabolism, 37, 1119-1136.e13. doi:10.1016/j.cmet.2025.01.016. https://pubmed.ncbi.nlm.nih.gov/40015281/
2. Piacentino, Michael L, Fasse, Aria J, Camacho-Avila, Alexis, Grabylnikov, Ilya, Bronner, Marianne E. 2023. SMPD3 expression is spatially regulated in the developing embryo by SOXE factors. In Developmental biology, 506, 31-41. doi:10.1016/j.ydbio.2023.11.011. https://pubmed.ncbi.nlm.nih.gov/38052296/
3. Manickam, Garthiga, Moffatt, Pierre, Murshed, Monzur. 2019. Role of SMPD3 during Bone Fracture Healing and Regulation of Its Expression. In Molecular and cellular biology, 39, . doi:10.1128/MCB.00370-18. https://pubmed.ncbi.nlm.nih.gov/30530524/
4. Li, Jingjing, Manickam, Garthiga, Ray, Seemun, Moffatt, Pierre, Murshed, Monzur. 2016. Smpd3 Expression in both Chondrocytes and Osteoblasts Is Required for Normal Endochondral Bone Development. In Molecular and cellular biology, 36, 2282-99. doi:10.1128/MCB.01077-15. https://pubmed.ncbi.nlm.nih.gov/27325675/
5. Stoffel, Wilhelm, Jenke, Britta, Schmidt-Soltau, Inga, Brodesser, Susanne, Hammels, Ina. 2018. SMPD3 deficiency perturbs neuronal proteostasis and causes progressive cognitive impairment. In Cell death & disease, 9, 507. doi:10.1038/s41419-018-0560-7. https://pubmed.ncbi.nlm.nih.gov/29725009/
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