C57BL/6JCya-Acsm5em1/Cya
Common Name:
Acsm5-KO
Product ID:
S-KO-17363
Background:
C57BL/6JCya
Product Type
Age
Genotype
Sex
Quantity
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Contact for Pricing
Basic Information
Strain Name
Acsm5-KO
Strain ID
KOCMP-272428-Acsm5-B6J-VB
Gene Name
Product ID
S-KO-17363
Gene Alias
C730019D22; C730027J19Rik
Background
C57BL/6JCya
NCBI ID
Modification
Conventional knockout
Chromosome
7
Phenotype
Document
Application
--
Note: When using this mouse strain in a publication, please cite “C57BL/6JCya-Acsm5em1/Cya mice (Catalog S-KO-17363) were purchased from Cyagen.”
Strain Description
Ensembl Number
ENSMUST00000066465
NCBI RefSeq
NM_178758
Target Region
Exon 3~4
Size of Effective Region
~3.1 kb
Detailed Document
Overview of Gene Research
Acsm5, or Acyl-CoA Synthetase Medium-Chain Family Member 5, is involved in fatty acid metabolism. It plays a role in activating medium-chain fatty acids, which are then available for processes such as β-oxidation, lipid synthesis, and energy production. This gene is associated with pathways related to lipid metabolism and is of biological importance in various tissues and disease contexts [2,3,4].
In the context of ligamentum flavum (LF) hypertrophy, a major cause of lumbar spinal canal stenosis, Acsm5 was found to be significantly down-regulated in LF tissues. In vitro cell experiments showed that overexpression of Acsm5 inhibited free fatty acid (FFA)-induced lipid accumulation and fibrosis in LF cells. In vivo mouse experiments further confirmed that overexpression of Acsm5 inhibited LF thickening, lipid accumulation, and fibrosis. Mechanistically, Acsm5 inhibited lipid accumulation of LF cells by inhibiting the FABP4-mediated PPARγ signaling pathway, thus improving LF hypertrophy and fibrosis [1]. In hepatocellular carcinoma (HCC), Acsm5 was down-regulated in tumor tissues compared with non-tumor tissues. Overexpression of Acsm5 in HCC cell lines reduced fatty acid accumulation, decreased cell proliferation, migration, and invasion in vitro, and inhibited tumor growth in mouse xenografts. ACSM5 overexpression also decreased STAT3 phosphorylation, affecting downstream cytokine levels [2].
In conclusion, Acsm5 is crucial in regulating lipid accumulation through its role in fatty acid metabolism. Its dysregulation is associated with diseases like LF hypertrophy and HCC. Studies using overexpression models in cells and in vivo mouse models have revealed its role in these disease conditions, highlighting its potential as a biomarker and therapeutic target for related diseases.
References:
1. Cao, Yanlin, Li, Jianjun, Qiu, Sujun, Ni, Songjia, Duan, Yang. 2023. ACSM5 inhibits ligamentum flavum hypertrophy by regulating lipid accumulation mediated by FABP4/PPAR signaling pathway. In Biology direct, 18, 75. doi:10.1186/s13062-023-00436-z. https://pubmed.ncbi.nlm.nih.gov/37957699/
2. Yang, Lei, Pham, Kien, Xi, Yibo, Robertson, Keith D, Liu, Chen. 2024. Acyl-CoA Synthetase Medium-Chain Family Member 5-Mediated Fatty Acid Metabolism Dysregulation Promotes the Progression of Hepatocellular Carcinoma. In The American journal of pathology, 194, 1951-1966. doi:10.1016/j.ajpath.2024.07.002. https://pubmed.ncbi.nlm.nih.gov/39069168/
3. Rinaldi, Anna, Lazareth, Hélène, Poindessous, Virginie, Cippà, Pietro E, Pallet, Nicolas. 2022. Impaired fatty acid metabolism perpetuates lipotoxicity along the transition to chronic kidney injury. In JCI insight, 7, . doi:10.1172/jci.insight.161783. https://pubmed.ncbi.nlm.nih.gov/35998043/
4. Mizuno, Yumi, Tamaru, Shunsuke, Tochigi, Hideno, Ishihara, Osamu, Kajihara, Takeshi. 2024. Decidualized Endometrial Stromal Cells Promote Mitochondrial Beta-Oxidation to Produce the Octanoic Acid Required for Implantation. In Biomolecules, 14, . doi:10.3390/biom14081014. https://pubmed.ncbi.nlm.nih.gov/39199401/
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