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, 16 bp deletion in exon 5 and 5 bp deletion in exon 5,
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 and ERS Genomics Limited, and is developed with patented technology. For full details of the limited use licenses and relevant patents please refer to our
limited use license
patent pages
Properties and Storage Information:
Gene name-ACOX3, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, 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.
ACOX3 also known as acyl-CoA oxidase 3 or PRACOX3 is an enzyme that functions in the peroxisomal beta-oxidation of branched-chain fatty acids. It specifically catalyzes the first oxidation step introducing a double bond between alpha and beta carbon of Acyl-CoA esters. ACOX3 has a molecular mass of approximately 75 kDa. Expression of ACOX3 primarily occurs in liver and kidney tissues where it plays a significant role in lipid metabolism.
Biological function summary
ACOX3 contributes to the breakdown of pristanic acid a branched-chain fatty acid derived from phytanic acid. It functions as part of a peroxisomal enzyme system that efficiently oxidizes fatty acids that contain branches on their carbon chains which mitochondria can't oxidize. ACOX3 works alongside other enzymes like ACOX1 and ACOX2 which oxidize different substrates ensuring a specialized fatty acid metabolism in the cell.
Pathways
ACOX3 plays a critical role in the peroxisomal fatty acid beta-oxidation pathway also contributing to the catabolism of very-long-chain fatty acids. This pathway complements the mitochondrial beta-oxidation providing a synergistic approach for complete fatty acid degradation. ACOX3 works closely related to proteins like peroxisomal bifunctional enzyme and thiolase completing the sequential steps necessary for beta-oxidation and energy production from fatty acids.
Mutations or dysfunctions in ACOX3 can lead to disruptions in fatty acid metabolism particularly affecting the metabolism of branched-chain fatty acids and potentially contributing to conditions such as Refsum disease or Zellweger syndrome. These disorders often exhibit accumulation of toxic metabolites causing harmful effects in tissues. They link ACOX3 dysfunction to broader peroxisomal biogenesis issues that involve other enzymes such as the PEX proteins which are vital for normal peroxisomal function and maintenance.
