UC Santa Cruz

The study of the cell cycle, specifically, understanding mechanistic regulation is fundamental for the development of therapeutic treatment in the event of disease. Limitless cell proliferation is a hallmark of cancer and often tied to cell cycle control. My research studied Cyclin- dependent kinases (Cdks) and their role in cell proliferation at the G1-S phase restriction point. I was able to shed insight on cyclin binding kinetics using Biolayer Interferometry (BLI) and the influence different types of inhibitors have on association of Cdks and cyclins. I reveal that Type I inhibitors increase binding affinity of CycA for Cdk2, whereas Type II inhibitors decrease affinity but differ in how they alter the CycA kinetic profile. Moreover, I explore an allosteric binding site of Cdk4-CycD that may be responsible for structural rearrangement to an active kinase configuration. My research as a whole gives insight into the development of a Cdk2 specific inhibitor and highlight the use of allosteric sites to understand mechanistic control of the cell cycle for Cdk inhibitor treatment therapy.