Description
Key facts
Species or organism:Human,
Form:LiquidSee storage information
Product details:
ab94222 is a 293T cell transfected lysate in which Human FEN1 has been transiently over-expressed using a pCMV-FEN1 plasmid. The lysate is provided in 1X Sample Buffer.
Properties and Storage Information:
Shipped at conditions-Dry Ice, Appropriate short-term storage conditions--20°C, Appropriate long-term storage conditions--20°C, Aliquoting information-Upon delivery aliquot, Storage information-Avoid freeze / thaw cycle
Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
Flap Endonuclease 1 known as FEN1 or FEN-1 is an important protein involved in DNA replication and repair. This protein shows a molecular weight of approximately 42 kDa. FEN1 functions as an endonuclease where it removes 5’ overhanging flaps in DNA products that occur during DNA replication and repair processes. It expresses in a wide range of human tissues with significant presence in the nucleus where DNA synthesis mainly occurs.
Biological function summary
FEN1 plays an important role in the Okazaki fragment maturation during lagging strand synthesis and long-patch base excision repair. FEN1 is not a solitary actor; it forms a part of larger complexes essential for maintaining genomic stability. It works closely with proliferating cell nuclear antigen (PCNA) to enhance its function and to interact with other proteins essential for the stability of the DNA.
Pathways
DNA replication and repair processes heavily rely on the activity of FEN1. It’s a component of the DNA replication fork protection and repair pathway and interacts with other proteins such as DNA polymerase and DNA ligase I to complete the repair process. Efficient DNA replication ensures accurate genomic duplication preventing mutations that could lead to severe cellular malfunction.
FEN1 is linked to the development of cancer and neurodegenerative diseases like Huntington's disease. FEN1 mutations or malfunction can result in genomic instability and an increased risk of tumorigenesis. In the context of neurodegenerative diseases deficiencies in FEN1 activity may disrupt the repair of oxidative DNA damage which is an important feature of disorders like Huntington's. These insights highlight the need for further research into FEN1's role and interactions to develop potential therapeutic strategies.
