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C57BL/6JCya-Soat2em1/Cya
Common Name:
Soat2-KO
Product ID:
S-KO-05760
Background:
C57BL/6JCya
Product Type
Age
Genotype
Sex
Quantity
Price:
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Basic Information
Strain Name
Soat2-KO
Strain ID
KOCMP-223920-Soat2-B6J-VA
Gene Name
Soat2
Product ID
S-KO-05760
Gene Alias
ACAT2; D15Wsu97e
Background
C57BL/6JCya
NCBI ID
223920
Modification
Conventional knockout
Chromosome
15
Phenotype
MGI:1332226
Document
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Application
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Rare Disease Data Center >>
Note
Note: When using this mouse strain in a publication, please cite “C57BL/6JCya-Soat2em1/Cya mice (Catalog S-KO-05760) were purchased from Cyagen.”
Strain Description
Ensembl Number
ENSMUST00000023806
NCBI RefSeq
NM_146064
Target Region
Exon 3~13
Size of Effective Region
~9.2 kb
Detailed Document
Click here to download >>
Overview of Gene Research
Soat2, also known as sterol O-acyltransferase 2, encodes acyl-coenzyme A: cholesterol acyltransferase 2 (ACAT2). This enzyme is crucial for synthesizing cholesteryl esters in hepatocytes and enterocytes, which are either stored or secreted into nascent triglyceride-rich lipoproteins, thus playing a significant role in cholesterol metabolism [1,3,4].

Genetic depletion of Soat2 in mice has revealed its multiple functions. In male mice, Soat2-/-mice showed improved glucose, insulin, HOMA-IR, OGTT, and insulin tolerance test results regardless of diet, along with a 30% increase in whole-body oxidation. The positive correlations between various lipid and glucose metabolism parameters in wild-type mice disappeared in Soat2-/-mice, indicating that ACAT2-generated cholesteryl esters negatively affect metabolic control by retaining TG in the liver, and genetic inhibition of Soat2 improves liver steatosis by partitioning lipids into secretory and oxidative pathways [1]. In female mice, Soat2-/-mice fed high-fat or high-carbohydrate, low-cholesterol diets had less hepatic steatosis, decreased expression of genes involved in de novo lipogenesis, and lower hepatic GLUT2 [3]. In intestine-specific Soat2 knockout (Soat2I-KO) mice, the development of dietary-induced obesity was prevented due to reduced intestinal lipid absorption [2]. In lysosomal acid lipase-deficient mice, loss of Soat2 function led to less hepatomegaly, reduced sequestration of esterified cholesterol, decreased liver transaminase activities, and lower hepatic mRNA expression levels for markers of inflammation, as well as curtailed esterified cholesterol entrapment in the small intestine [5].

In conclusion, Soat2 is essential for cholesterol metabolism and cholesteryl ester synthesis. Gene knockout mouse models have shown that Soat2 plays a role in metabolic control, hepatic steatosis, obesity, and the progression of lysosomal acid lipase-deficiency-related diseases. Understanding Soat2's function through these models provides insights into the mechanisms of related diseases and potential therapeutic targets.

References:

1. Pramfalk, Camilla, Ahmed, Osman, Pedrelli, Matteo, Eriksson, Mats, Parini, Paolo. 2022. Soat2 ties cholesterol metabolism to β-oxidation and glucose tolerance in male mice. In Journal of internal medicine, 292, 296-307. doi:10.1111/joim.13450. https://pubmed.ncbi.nlm.nih.gov/34982494/

2. Liang, Jingjia, Shao, Wentao, Ni, Pu, Jiang, Zhaoyan, Gu, Aihua. 2024. siRNA/CS-PLGA Nanoparticle System Targeting Knockdown Intestinal SOAT2 Reduced Intestinal Lipid Uptake and Alleviated Obesity. In Advanced science (Weinheim, Baden-Wurttemberg, Germany), 11, e2403442. doi:10.1002/advs.202403442. https://pubmed.ncbi.nlm.nih.gov/39297413/

3. Ahmed, O, Pramfalk, C, Pedrelli, M, Eriksson, M, Parini, P. 2018. Genetic depletion of Soat2 diminishes hepatic steatosis via genes regulating de novo lipogenesis and by GLUT2 protein in female mice. In Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver, 51, 1016-1022. doi:10.1016/j.dld.2018.12.007. https://pubmed.ncbi.nlm.nih.gov/30630736/

4. Pavanello, Chiara, Ossoli, Alice, Strazzella, Arianna, Parini, Paolo, Calabresi, Laura. 2022. Plasma FA composition in familial LCAT deficiency indicates SOAT2-derived cholesteryl ester formation in humans. In Journal of lipid research, 63, 100232. doi:10.1016/j.jlr.2022.100232. https://pubmed.ncbi.nlm.nih.gov/35598637/

5. Lopez, Adam M, Chuang, Jen-Chieh, Turley, Stephen D. 2017. Impact of loss of SOAT2 function on disease progression in the lysosomal acid lipase-deficient mouse. In Steroids, 130, 7-14. doi:10.1016/j.steroids.2017.11.015. https://pubmed.ncbi.nlm.nih.gov/29246491/

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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