Description
Key facts
Cell type:HeLa,
Species or organism:Human,
Tissue:Cervix,
Form:LiquidSee storage information,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, Homozygous: 1 bp insertion in exon 1,
Disease:Adenocarcinoma
Product details:
We will provide viable cells that proliferate on revival.
This product is subject to limited use licenses from The Broad Institute, ERS Genomics Limited and Sigma-Aldrich Co. LLC, and is developed with patented technology. For full details of the licenses and patents please refer to our
limited use license
patent pages
Properties and Storage Information:
Gene name-ACOT9, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Zygosity-Homozygous, Shipped at conditions-Dry Ice, Appropriate short-term storage conditions--196°C, Appropriate long-term storage conditions--196°C
Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
Acyl-CoA Thioesterase 9 (ACOT9) sometimes referred to as anti-CoA functions mechanically by hydrolyzing CoA esters into free fatty acids and CoA-SH playing a role in lipid metabolism. ACOT9 has a molecular mass of approximately 70 kDa. The expression of ACOT9 occurs in various tissues with higher levels observed in the liver and kidney contributing to the regulation of fatty acid and CoA concentrations within the cells.
Biological function summary
ACOT9 participates in the regulation of lipid metabolism and energy homeostasis. It does not form part of a known complex but performs a stand-alone role in converting activated fatty acids into their free form and CoA. This process contributes to the balance between synthesis and degradation of lipids impacting energy production and storage. ACOT9's action influences cellular metabolic states and can adapt them depending on the energy requirement of the organism.
Pathways
ACOT9 plays an important role in the peroxisomal and mitochondrial fatty acid oxidation pathways. In these pathways it interacts with enzymes such as Acyl-CoA oxidase and Carnitine palmitoyltransferase I facilitating the breakdown of long-chain fatty acids. ACOT9's hydrolytic activity helps reduce the build-up of acyl-CoA intermediates which is essential for maintaining cellular energy balance and supporting metabolic flexibility during fasting or exercise.
ACOT9 has been linked to metabolic syndromes including obesity and non-alcoholic fatty liver disease (NAFLD). Its modulation can influence the aberrant accumulation of lipids leading to these conditions. ACOT9's activity also connects it with proteins such as AMP-activated protein kinase (AMPK) in the regulation of energy homeostasis which is disrupted in metabolic disorders. Understanding the role of ACOT9 in these diseases may provide insights into therapeutic targets for managing metabolic imbalances.
