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-ACAD9, 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.
The protein ACAD9 also known as acyl-CoA dehydrogenase family member 9 plays a role in mitochondrial fatty acid β-oxidation. It functions as an enzyme that catalyzes the initial step of this fatty acid metabolism process assisting in breaking down long-chain fatty acids. The mass of ACAD9 is approximately 71 kDa. This protein mainly expresses in tissues with high energy demands such as heart and skeletal muscle indicating its involvement in energy metabolism.
Biological function summary
ACAD9 participates in key enzymatic activities important for energy production. It forms part of a larger enzyme complex known as the electron transfer flavoprotein (ETF)-ubiquinone oxidoreductase complex which is essential for the transfer of electrons in the mitochondrial respiratory chain. This protein aids in converting stored fatty acids into acetyl-CoA which is then funneled into the Krebs cycle for further energy generation.
Pathways
ACAD9 is intricately linked to mitochondrial fatty acid oxidation and energy metabolism. It plays a central role in the β-oxidation pathway which is critical for converting fatty acids into usable energy. ACAD9 interacts with related proteins such as electron transfer flavoprotein (ETF) and ETF-ubiquinone oxidoreductase facilitating the transfer of electrons derived from fatty acid metabolism into the respiratory chain thereby producing ATP efficiently.
Mutations or deficiencies in ACAD9 can lead to fatty acid oxidation disorders such as multiple acyl-CoA dehydrogenase deficiency. These conditions manifest with severe metabolic myopathies and cardiomyopathies. ACAD9's role connects it to other proteins involved in mitochondrial function such as ETF which also associates with similar disorders. Understanding ACAD9's function aids in diagnosing and developing therapeutic approaches for these metabolic conditions.
