Large Scale Docking of Chemical Compound Against CDK20
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Regulation of the eukaryotic cell cycle is directed by the activation of cyclin-dependent kinases (CDKs). CDK’s are known to interact with cyclins and are inhibited by enzymes like p27. Literature has identified CDK20 as an interesting target for cancer treatment because a CDK20 knockout causes cell growth reduction and eventually termination. By using CDK2, CDK5, and CDK7 structures a computational homology model for CDK20 was previously generated. I hypothesize that if the computational model of CDK20 is docked against a library of chemical lead-like compounds; then some of those compounds might inhibit the CDK20 complexing with a Cyclin or an Enzyme Inhibitor (like KIP1). I computationally docked molecules from a ZINC database using Autodock-Vina to score CDK20/inhibitor complexes. I mapped protein amino acid side chain interactions with the small molecule in the docked complex and ranked drug leads for analysis. This research has significant impact if one of these drug leads can be matured into a drug candidate and used in a cancer therapy. It also has near term impact by providing small molecule disrupters of CDK20 that can be used in basic research in our function studies of lung cancer using H1437, H2122, and A549 cell lines.