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C57BL/6JCya-S1pr2em1flox/Cya
Common Name:
S1pr2-flox
Product ID:
S-CKO-02713
Background:
C57BL/6JCya
Product Type
Age
Genotype
Sex
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Basic Information
Strain Name
S1pr2-flox
Strain ID
CKOCMP-14739-S1pr2-B6J-VA
Gene Name
S1pr2
Product ID
S-CKO-02713
Gene Alias
1100001A16Rik; Edg5; Gpcr13; H218; LPb2; S1P2
Background
C57BL/6JCya
NCBI ID
14739
Modification
Conditional knockout
Chromosome
9
Phenotype
MGI:99569
Document
Click here to download >>
Application
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More
Rare Disease Data Center >>
Note
Note: When using this mouse strain in a publication, please cite “C57BL/6JCya-S1pr2em1flox/Cya mice (Catalog S-CKO-02713) were purchased from Cyagen.”
Strain Description
Ensembl Number
ENSMUST00000054197
NCBI RefSeq
NM_010333
Target Region
Exon 2
Size of Effective Region
~1.8 kb
Detailed Document
Click here to download >>
Overview of Gene Research
S1pr2, or sphingosine 1-phosphate receptor 2, is a key receptor that binds to sphingosine-1-phosphate, regulating various biological processes. It is involved in multiple signaling pathways such as RhoA/ROCK1, p38 MAPK/YAP, and Wnt3a/RhoA/ROCK1/β-catenin, which are crucial for functions like cell migration, activation, and barrier function regulation, and are of great biological importance in processes including angiogenesis, immune cell regulation, and tissue repair [1,2,3,7]. Genetic models, especially KO/CKO mouse models, are valuable tools for studying S1pr2.

In IBD, knockdown or pharmacological inhibition of S1pr2 in mice reversed intestinal vascular endothelial barrier damage and M1 macrophage polarization, suggesting its role in IBD pathogenesis through the S1PR2/RhoA/ROCK1 pathway [1]. In cholestatic liver fibrosis, S1pr2 deficiency in mice attenuated liver injury and collagen accumulation, indicating its role in promoting hepatic stellate cell activation via the S1PR2/p38 MAPK/YAP signaling pathway [2]. In cerebral infarction, activating S1pr2 in the thalamus augmented vascular autophagy, suppressing angiogenesis and aggravating neuronal damage, while knockdown of Rtn4 (which interacts with S1pr2) enhanced angiogenesis and improved cognitive function [3]. In biliary atresia, selective knockdown of macrophage S1pr2 in mice decreased ZBP1/p-MLKL-mediated necroptosis and collagen deposition [4]. In peripheral artery disease, EC-specific S1pr2 loss-of-function in mice enhanced post-ischemic angiogenesis and blood flow recovery, as S1pr2 inhibits the AKT/eNOS signaling pathway [5]. In cardiac ischemia-reperfusion injury, EC-specific S1pr2 loss-of-function lessened inflammatory responses and diminished injury, while gain-of-function aggravated injury, with S1pr2 initiating excessive mitochondrial fission via the RHO/ROCK1/DRP1 pathway [6]. In diabetic nephropathy, knockdown or pharmacological inhibition of S1pr2 in mice reversed endothelial mesenchymal transition and endothelial barrier dysfunction in glomerular endothelial cells [7].

In conclusion, model-based research, especially using KO/CKO mouse models, has revealed that S1pr2 plays essential roles in various biological processes. It is involved in the pathogenesis of multiple diseases including IBD, cholestatic liver fibrosis, cerebral infarction, biliary atresia, peripheral artery disease, cardiac ischemia-reperfusion injury, and diabetic nephropathy. Understanding S1pr2's functions provides insights into disease mechanisms and potential therapeutic targets for these conditions.

References:
1. Wang, Xuewen, Chen, Shuhua, Xiang, Hong, Chen, Alex F, Lu, Hongwei. 2022. S1PR2/RhoA/ROCK1 pathway promotes inflammatory bowel disease by inducing intestinal vascular endothelial barrier damage and M1 macrophage polarization. In Biochemical pharmacology, 201, 115077. doi:10.1016/j.bcp.2022.115077. https://pubmed.ncbi.nlm.nih.gov/35537530/
2. Yang, Jing, Tang, Xujiao, Liang, Zhu, Chen, Mingzhu, Sun, Lixin. 2023. Taurocholic acid promotes hepatic stellate cell activation via S1PR2/p38 MAPK/YAP signaling under cholestatic conditions. In Clinical and molecular hepatology, 29, 465-481. doi:10.3350/cmh.2022.0327. https://pubmed.ncbi.nlm.nih.gov/36800698/
3. Xiao, Peiyi, Gu, Jinmin, Xu, Wei, Zeng, Jinsheng, Xing, Shihui. 2022. RTN4/Nogo-A-S1PR2 negatively regulates angiogenesis and secondary neural repair through enhancing vascular autophagy in the thalamus after cerebral cortical infarction. In Autophagy, 18, 2711-2730. doi:10.1080/15548627.2022.2047344. https://pubmed.ncbi.nlm.nih.gov/35263212/
4. Yang, Shen, Chang, Na, Li, Weiyang, Huang, Jinshi, Li, Liying. 2023. Necroptosis of macrophage is a key pathological feature in biliary atresia via GDCA/S1PR2/ZBP1/p-MLKL axis. In Cell death & disease, 14, 175. doi:10.1038/s41419-023-05615-4. https://pubmed.ncbi.nlm.nih.gov/36859525/
5. Zhou, Caixia, Kuang, Yashu, Li, Qinyu, Zhang, Yuzhen, Zhang, Lin. 2022. Endothelial S1pr2 regulates post-ischemic angiogenesis via AKT/eNOS signaling pathway. In Theranostics, 12, 5172-5188. doi:10.7150/thno.71585. https://pubmed.ncbi.nlm.nih.gov/35836816/
6. Duan, Yunhao, Li, Qinyu, Wu, Jinjin, Zhang, Yuzhen, Zhang, Lin. 2024. A detrimental role of endothelial S1PR2 in cardiac ischemia-reperfusion injury via modulating mitochondrial dysfunction, NLRP3 inflammasome activation, and pyroptosis. In Redox biology, 75, 103244. doi:10.1016/j.redox.2024.103244. https://pubmed.ncbi.nlm.nih.gov/38909407/
7. Zhang, Jing, Chen, Shuhua, Xiang, Hong, Chen, Alex F, Lu, Hongwei. 2023. S1PR2/Wnt3a/RhoA/ROCK1/β-catenin signaling pathway promotes diabetic nephropathy by inducting endothelial mesenchymal transition and impairing endothelial barrier function. In Life sciences, 328, 121853. doi:10.1016/j.lfs.2023.121853. https://pubmed.ncbi.nlm.nih.gov/37307963/
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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