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, 2 bp deletion in exon 3 and 2 bp insertion in exon 3 and 8 bp deletion in exon 3
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-CDC14B, 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.
Cdc14B also known as Cell Division Cycle 14B is a serine/threonine-protein phosphatase with a molecular mass of approximately 62 kDa. This protein localizes mainly to the nucleolus but can also be found in the cytoplasm during the cell cycle. It plays a significant role in dephosphorylating substrates involved in cell cycle regulation. Cdc14B is widely expressed across various human tissues including high expression levels in the testes where it serves essential regulatory functions.
Biological function summary
Cdc14B regulates exit from mitosis and cytokinesis. It functions as part of a regulatory network that controls the transition from mitosis to interphase. In this process Cdc14B dephosphorylates key proteins involved in spindle disassembly and chromosome segregation ensuring proper cell cycle progression. While it does not form a complex on its own Cdc14B interacts with other regulatory proteins to maintain cellular homeostasis and genomic stability.
Pathways
Cdc14B plays a critical role in the DNA damage response and the mitotic exit network. It interacts with proteins such as Cdh1 and Securin to mediate cell cycle checkpoints and ensure proper timing of mitotic exit. Cdc14B's ability to dephosphorylate specific substrates allows it to regulate these pathways effectively placing it centrally within the regulatory framework that safeguards cell cycle accuracy.
Alterations in Cdc14B expression or function have been linked to cancer development due to its role in cell cycle regulation and genomic stability. Aberrant Cdc14B activity can contribute to unchecked cell division a hallmark of many cancers. Additionally its dysfunction associates with neurodegenerative diseases where improper cell cycle re-entry of neurons leads to cell death. In cancer Cdc14B's interaction with proteins like p53 and Mdm2 highlights its importance in tumor suppression pathways.
