CDKs is dependent upon a regulatory subunit called cyclin. Members of the cyclin family bind to and activate their CDK partners. For example, cyclins A and B activate CDK1, cyclins A and E regulate the activity of CDK2, and the D-type cyclins are associated with CDK4. While the concentration of the CDKs remains relatively constant throughout the cell cycle, cyclin expression and degradation occur in a periodic fashion. The rise and fall of cyclin concentrations are timed to provide specific CDK activities, as they are needed for progression through the various stages of the cell cycle.
The recognition of the importance of CDKs to the process of cell division has stimulated an interest in them as potential targets for proliferative diseases such as cancer, psoriasis, and restenosis, and for the prevention of chemotherapy- associated side effects such as alopecia. A number of small-molecules, which act as, inhibitors of CDKs have been identified and are described in recent reviews.
Thus, our interest is in developing new cyclin-dependent kinase 2 inhibitors. In particular, we want to study the effect of a phenylpentyl moeity at the 4th position.
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