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Cell Cycle Proteins
Targeting subcellular localization through the polo-box domain: non-ATP competitive inhibitors recapitulate a PLK1 phenotype.
Involvement of base excision repair in response to therapy targeted at thymidylate synthase.
Uracil incorporation into genomic DNA does not predict toxicity caused by chemotherapeutic inhibition of thymidylate synthase.
Quinacrine has anticancer activity in breast cancer cells through inhibition of topoisomerase activity.
PLK1 as an oncology target: current status and future potential.
Lycopene synergistically enhances quinacrine action to inhibit Wnt-TCF signaling in breast cancer cells through APC.
SMUG1 but not UNG DNA glycosylase contributes to the cellular response to recovery from 5-fluorouracil induced replication stress.
Current assessment of polo-like kinases as anti-tumor drug targets.
Iterative conversion of cyclin binding groove peptides into druglike CDK inhibitors with antitumor activity.
Peptidomimetic Polo-Box-Targeted Inhibitors that Engage PLK1 in Tumor Cells and Are Selective against the PLK3 Tumor Suppressor.
Cell Cycle Checkpoints
Nonpeptidic, Polo-Box Domain-Targeted Inhibitors of PLK1 Block Kinase Activity, Induce Its Degradation and Target-Resistant Cells.
Structure-activity and mechanistic studies of non-peptidic inhibitors of the PLK1 polo box domain identified through REPLACE.