What does Cdc25 regulate?

CDC25C is a cyclin of the specific phosphatase family that activates the cyclin B1/CDK1 complex in cells for entering mitosis and regulates G2/M progression and plays an important role in checkpoint protein regulation in case of DNA damage, which can ensure accurate DNA information transmission to the daughter cells.

What activates Cdc25?

Cdc25 activates cyclin dependent kinases by removing phosphate from residues in the Cdk active site. In turn, the phosphorylation by M-Cdk (a complex of Cdk1 and cyclin B) activates Cdc25.

How does Cdc25 regulate CDK activity?

The activity of CDK is regulated by a series of phosphorylation and dephosphorylation of different residues. Cell Division Cycle-25 (CDC25) plays an important role in transitions between cell cycle phases by dephosphorylating these residues to activate CDKs [3, 4].

Is CAK a kinase?

The Cyclin-dependent kinase (CDK) Activating Kinase (CAK) is responsible for the activating phosphorylation of CDK1, CDK2, CDK4 and CDK6 and regulation of the cell cycle. The kinase is composed of three subunits: CDK7, Cyclin H and MAT1 (ménage a trois).

What is the activity of Cdc25 in fission yeast?

Cdc25 was identified initially in the fission yeast Schizosaccharomyces pombe [4]. In this organism, cells with conditional mutations in the Cdc25 protein are unable to enter mitosis at the restrictive temperature and thus continue to grow into highly elongated cells.

Does phosphorylation activate Cdc25?

In Xenopus eggs and early embryos a cdc25 homologue undergoes periodic phosphorylation and activation. Here we show that the catalytic activity of human cdc25-C phosphatase is also activated directly by phosphorylation in mitotic cells.

What is the function of Cdc25 during the G2 to M transition?

Cdc25 activates maturation promoting factor (MPF) and promotes mitosis by removing the inhibitory phosphate from the Tyr-15 of Cdc2 in human cells.

What happens when cyclin is overexpressed?

Taken together, this study reports that replication stress induced by overexpression of Cyclin E1 and Cdc25A results in the formation of lagging chromosomes and chromatin bridges, which is further exacerbated by inhibition of ATR or WEE1 kinases, and results in exacerbated tumor cell killing.