Description
Key facts
Cell type:HEK-293T,
Species or organism:Human,
Tissue:Kidney,
Form:LiquidSee storage information,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, Homozygous: 2 bp deletion in exon 4
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-AKR1A1, 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.
AKR1A1 also known as aldehyde reductase or aldo-keto reductase is a member of the aldo-keto reductase family. It functions mechanically as a reductase enzyme that converts aldehydes and ketones to their corresponding alcohols via NADPH as a cofactor. The enzyme has a molecular mass of approximately 36 kDa. AKR1A1 is expressed in a wide range of tissues including liver kidney and brain indicating its broad role in metabolic processes.
Biological function summary
AKR1A1 is involved in the detoxification of aldehydes produced during metabolism and oxidative stress. This function occurs as part of a larger detoxification system. Being part of the aldo-keto reductase family it contributes to maintaining homeostasis by regulating the levels of reactive aldehydes. Through this activity it affects cellular responses to stress and the metabolism of xenobiotics.
Pathways
AKR1A1 has significant involvement in metabolic and detoxification pathways notably in glycolysis and xenobiotic metabolism. It interacts with various aldehydes formed as intermediates in these pathways. Related proteins in these pathways include AKR1B1 which also plays a role in reducing sugar-derived aldehydes emphasizing the importance of AKR1A1 in controlling toxic aldehyde levels and protecting cellular components from damage.
AKR1A1 has been linked to diabetic complications due to its role in polyol pathway where it contributes to the conversion of glucose to sorbitol. This pathway can lead to osmotic and oxidative stress when dysregulated contributing to retinal and renal dysfunctions in diabetes. Additionally AKR1A1 is connected to cancer development where it affects oxidative stress levels and tumor progression alongside proteins like AKR1C1 which are also involved in lipid and steroid metabolism further influencing disease outcomes.
