Description
Key facts
Cell type:HeLa,
Species or organism:Human,
Tissue:Cervix,
Form:LiquidSee storage information,
Knockout validation:Sanger Sequencing,Western blot,
Mutation description:Knockout achieved by using CRISPR/Cas9, 1 bp insertion in exon 2 and 2 bp insertion in exon 2,
Antibiotic resistance:Puromycin 1µg/mL,
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-CDC25C, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Western blot, 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.
Cdc25C also known as dual specificity phosphatase Cdc25C is a 65-kDa protein that acts as a cell cycle regulator controlling the transition from the G2 to M phase. The protein is expressed in various tissues but has higher expression levels in actively dividing cells. Cdc25C is important for cell division due to its ability to activate cyclin-dependent kinases (CDKs) by dephosphorylating the inactive phosphorylated forms. This action makes Cdc25C an important target for regulating the cell cycle and ensuring proper cell proliferation.
Biological function summary
The proper function of Cdc25C involves facilitating proper cell cycle progression by coordinating with other cell cycle regulators. It participates in a complex network where it dephosphorylates and activates CDK1/cyclin B1 complexes promoting the mitotic entry. This function is important for maintaining genomic stability during cell division. Misregulation of Cdc25C can lead to cell cycle arrest or uncontrolled cell proliferation highlighting its essential role in cell cycle control mechanisms.
Pathways
Cdc25C fits into the cell cycle checkpoint pathways and is also a part of the DNA damage response pathways. It connects with the p53 and ATM/ATR signaling proteins while responding to DNA damage ensuring a temporary pause in cell cycle progression for repair mechanisms to act. Proper interaction with these pathways is essential for maintaining cellular integrity and preventing the proliferation of damaged cells with CDK1 and Wee1 kinase serving as major interacting proteins in these processes.
Misregulation or overexpression of Cdc25C can relate to cancer and various cell proliferation disorders. In cancer Cdc25C's disordered expression often links to unchecked cell division and tumor progression commonly involving proteins such as p53 which act as tumor suppressors. Furthermore abnormalities in Cdc25C function may lead to issues related to cell cycle progression errors implicating it in other proliferative disorders such as hyperplasia where it acts in conjunction with and alters the activities of proteins like cyclin B1.
