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The previous studies suggested that Cdc25 homologues control the entry into mitosis through dephosphorylating and activating specific substrate cyclin-dependent kinases (CDK) to regulate the progression of cell division cycle and transition (Gould and Nurse, 1989; Dunphy and Kumagai, 1991; Gautier et al.
The compound, which specifically inhibits mitotic kinesin Eg5, arrests the cell division cycle of cancer cells at the mitotic phase and induces apoptosis.
An example of the TraFaC output for cell division cycle 25a (CDC25A) is shown in Figure 4.
With diseases such as cancer, the cell division cycle becomes deregulated, allowing tumor cells to proliferate uncontrolled.
Functional of metal-ion homeostasis in the cell division cycle, mitochondrial protein processing, sensitivity to mycobacterial infection and brain function.
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