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, 13 bp deletion in exon 2 and 20 bp deletion in exon 2 and Insertion of the selection cassette in exon 2,
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-FASTK, 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.
FASTK also known as Fas-activated serine/threonine kinase is an enzyme that functions primarily in the mitochondria of cells. This protein weighs approximately 65 kDa. FASTK is ubiquitously expressed in various tissues but it shows higher levels in heart and skeletal muscle. FASTK plays a role in RNA processing especially in regulating the stability of specific RNA molecules in mitochondria.
Biological function summary
FASTK associates with a larger protein complex involved in mitochondrial RNA surveillance. This complex targets and stabilizes mitochondrial transcripts important for mitochondrial protein synthesis. Through its RNA-binding capability FASTK influences the production of ATP by maintaining proper mitochondrial function and energy metabolism.
Pathways
FASTK operates within mitochondrial gene expression and oxidative phosphorylation pathways. It is associated with proteins like FASTKD2 and TFB2M which also participate in mitochondrial RNA processing and ribosome biogenesis. This interplay is essential for responding to cellular energy demands and maintaining cellular homeostasis.
Disruptions in FASTK activity relate to mitochondrial myopathy and neurodegenerative disorders such as Charcot-Marie-Tooth disease. Mutations in proteins like FASTKD2 and other mitochondrial RNA-binding proteins can influence these conditions highlighting the significance of FASTK in maintaining mitochondrial integrity.
